causes of left ventricular hypertrophy

hy Left Ventricular Hypertrophy Left Ventricular Hypertrophy (LVH) causes a similar pattern of repolarization abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, a VL, V5-6).

The ST Segment

The ST Segmentby Edward Burns, Last updated November 15, 2017The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave. It represents the interval between ventricular depolarization and repolarization. The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia or infarction.

Causes of ST Segment Elevation Acute myocardial infarction Coronary vasospasm (Printzmetal’s angina)Pericarditis Benign early repolarization Left bundle branch block Left ventricular hypertrophy Ventricular aneurysm Brugada syndrome Ventricular paced rhythm Raised intracranial pressure Morphology of the Elevated ST segment Myocardial Infarction Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology.

ST Segment Morphology in Other Conditions Patterns of ST Elevation Acute ST elevation myocardial infarction (STEMI)Causes ST segment elevation and Q-wave formation in contiguous leads, either: Septal (V1-2)Anterior (V3-4)Lateral (I + a VL, V5-6)Inferior (II, III, a VF)Right ventricular (V1, V4R)Posterior (V7-9)There is usually reciprocal ST depression in the electrically opposite leads. For example, STE in the high lateral leads I + a VL typically produces reciprocal ST depression in lead III (see example below).

Follow the links above to find out more about the different STEMI patterns. Anterolateral STEMICoronary Vasospasm (Prinzmetal’s angina)This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis.

It may be impossible to differentiate these two conditions based on the ECG alone. Pericarditis Pericarditis Acute Pericarditis causes widespread concave (“saddleback”) ST segment elevation with PR segment depression in multiple leads, typically involving I, II, III, a VF, a VL, and V2-6.

There is reciprocal ST depression and PR elevation in leads a VR and V1. Spodick’s sign was first described by David H. Spodick in 1974 as a downward sloping TP segment with specificity for acute pericarditis. Concave “saddleback” ST elevation in leads I, II, III, a VF, V5-6 with depressed PR segments. There is reciprocal ST depression and PR elevation in a VR. Spodick’s sign is present. Benign Early Repolarization Benign Early Repolarization Benign Early Repolarization (BER) causes mild ST elevation with tall T-waves mainly in the precordial leads.

Is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point — the “fish-hook” pattern. The ST changes may be more prominent at slower heart rates and disappear in the presence of tachycardia.

There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)Left Bundle Branch Block Left Bundle Branch Block In Left bundle branch block (LBBB), the ST segments and T waves show “appropriate discordance” — i.e.

they are directed opposite to the main vector of the QRS complex. This produces ST elevation and upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave). Note the ST elevation in leads with deep S waves — most apparent in V1-3. Also note the ST depression in leads with tall R waves — most apparent in I and a VL. Left Ventricular Hypertrop

Deep S waves with ST elevation in V1-3ST depression and T-wave inversion in the lateral leads V5-6Note in this this case there is also right axis deviation, which is unusual for LVH and may be due to associated left posterior fascicular block. Ventricular Aneurysm Ventricular Aneurysm This is an ECG pattern of Ventricular Aneurysm – residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It is associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.

There is ST elevation with deep Q waves and inverted T waves in V1-3. This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI. Brugada Syndrome Brugada syndrome Brugada Syndrome is an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients.

The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.

There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”. Ventricular Paced Rhythm AV Sequential Pacing Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.

Raised Intracranial Pressure ST elevation due to traumatic brain injury Raised Intracranial Pressure (ICP) (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis.

More commonly, raised ICP is associated with widespread, deep T-wave inversions (“cerebral T waves”). Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.

Less Common Causes of ST segment Elevation Pulmonary embolism and acute cor pulmonale (usually in lead III)Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)Hyperkalaemia Sodium-channel blocking drugs (secondary to QRS widening)J-waves ( hypothermia , hypercalcaemia)Following electrical cardioversion Others: Cardiac tumour, myocarditis, pancreas or gallbladder disease Transient ST elevation after DC cardioversion from VFJ waves in hypothermia simulating ST elevation Causes of ST Depression Myocardial ischaemia / NSTEMIReciprocal change in STEMIPosterior MIDigoxin effect Hypokalaemia Supraventricular tachycardia Right bundle branch block Right ventricular hypertrophy Left bundle branch block Left ventricular hypertrophy Ventricular paced rhythm Morphology of ST Depression ST depression can be either upsloping, downsloping, or horizontal.

Horizontal or downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia ( according to the 2007 Task Force Criteria ).

Upsloping ST depression in the precordial leads with prominent “De Winter’s” T waves is highly specific for occlusion of the LAD. Reciprocal change has a morphology that resembles “upside down” ST elevation and is seen in leads electrically opposite to the site of infarction.

Posterior MI manifests as horizontal ST depression in V1-3 and is associated with upright T waves and tall R waves. ST depression: upsloping (A), downsloping (B), horizontal (C)ST segment morphology in myocardial ischaemia Reciprocal change ST segment morphology in posterior MIPatterns of ST depression Myocardial Ischaemia ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology.

It is often most prominent in the left precordial leads V4-6 plus leads I, II and a VL. Widespread ST depression with ST elevation in a VR is seen in left main coronary artery occlusion and severe triple vessel disease.

LMCA Occlusion NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. This concept is discussed further here.

Reciprocal Change ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads: Inferior STEMI produces reciprocal ST depression in a VL (± lead I). Lateral or anterolateral STEMI produces reciprocal ST depression in III and a VF (± lead II). Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).

Reciprocal ST depression in a VL with inferior STEMIReciprocal ST depression in III and a VF with high lateral STEMIPosterior Myocardial Infarction Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9. Posterior MIDe Winters T Waves De Winter’s T waves: a pattern of up-sloping ST depression with symmetrically peaked T waves in the precordial leads is considered to be a STEMI equivalent, and is highly specific for an acute occlusion of the LAD.

De Winter’s T Waves Digoxin Effect Digoxin Effect: Treatment with digoxin causes downsloping ST depression with a “sagging” morphology, reminiscent of Salvador Dali’s moustache.

Digoxin reverse tick salvador dali moustache Hypokalaemia Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval. Hypokalaemia Right ventricular hypertrophy Right ventricular hypertrophy (RVH) causes ST depression and T-wave inversion in the right precordial leads V1-3. Right ventricular hypertrophy Right Bundle Branch Block Right Bundle Branch Block (RBBB) may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.

Right bundle branch block Supraventricular tachycardia Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6).

This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia, provided that it resolves with treatment. AV-nodal re-entry tachycardia Related Topics P Wave PR Interval PR Segment Q Wave QRS Segment QT Interval J Point R Wave T Wave U Wave Osborne Wave Epsilon Wave Delta Wave References Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II.

BMJ. 2002 Apr 20;324 (7343):963-6. Review. Pub Med PMID: 11964344; Pub Med Central PMCID: PMC1122906 . Full text. Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction.

Am J Emerg Med. 2005 May;23 (3):279-87. Pub Med PMID: 15915398. Advanced Reading Brady WJ, Truwit JD. Critical Decisions in Emergency and Acute Care Electrocardiography Hampton, JR. The ECG In Practice, 6e Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice: Adult and Pediatric, 6e Wagner, GS.

Marriott’s Practical Electrocardiography 12e Chan, TC. ECG in Emergency Medicine and Acute Care Wang, K. Atlas of Electrocardiography Mattu, A. ECG’s for the Emergency Physician LITFL Further Reading ECG BASICS — Waves, Intervals, Segments and Clinical Interpretation ECG A to Z by diagnosis –alphabetical diagnostic approach to the ECGECG CLINICAL CASES — ECG’s placed in clinical context with a challenging Q&A approach100 ECG Quiz — Self-assessment tool for examination practice ECG Reference SITES and BOOKS — the best of the rest LITFL ECG IMAGE Database — Searchable database of LITFL ECG’s ECG and Cardiology Eponymous Syndromes — Cheats guide to eponymous emancipation ECG Exam Template — a framework for answering ECG exam questions. Last update: [last-modified]Share this: Facebook Linked In Twitter About Edward Burns Ed Burns is an Emergency Physician working in Prehospital & Retrieval Medicine in Sydney, Australia. He has a passion for ECG interpretation and medical education. Ed is the force behind the LITFL ECG library | + Edward Burns | @edjamesburns

Hypertensive cardiovascular disease also known as hypertensive heart disease occurs due to the complication of hypertension or high blood pressure. In this condition the workload of the heart is increased manifold and with time this causes the heart muscles to thicken. The heart continues pumping blood against this increased pressure and over a period of time the left ventricle of the heart enlarges and this in turn causes the blood pumped by heart to reduce.

Hypertensive Cardiovascular Disease

Hypertensive Cardiovascular Disease High blood pressure is commonly seen in most people these days. But do you know that it has a very close connection with cardiovascular diseases? Read on to learn about hypertensive cardiovascular disease. By Ashwini Ambekar | Thursday, October 09, 2008

If proper treatment is not taken at this stage then symptoms of congestive heart failure may be observed. High blood pressure or hypertension is among the top most factors associated with cardiovascular diseases.

This can result in ischemic heart disease. High blood pressure is also a contributing factor to the eventual thickening of walls of blood vessels. This increases the possibility of heart attacks and strokes. Hypertensive cardiovascular disease is among the leading killers in present times. Around 7 people out of every 1000 suffer from this disease. Heredity is an important factor so far as people suffering from hypertension are concerned.

Other factors include excessive consumption of salt and excessive stress. Symptoms It usually takes some time for the problem of high blood pressure to eventually lead to hypertensive cardiovascular disease and therefore high blood pressure is often called the silent killer.

Eventually hypertensive heart disease can also lead to congestive heart failure. Some symptoms of hypertension and the eventual congestive heart failure include arrhythmias, shortness of breath, weakness and fatigue, swelling in lower extremities and greater frequency of urination during the night.

However, some cases with less right ventricular hypertrophy than the maximal one had a more advanced associated left ventricular hypertrophy (cases 8, 10, 22, 24, 25, 26), the thickness of the left ventricular wall ranging from 15 to 20 millimeters. Left ventricular hypertrophy was absent in one case only (case 2).

Bilateral Ventricular Hypertrophy Due to Chronic Pulmonary Disease

Bilateral Ventricular Hypertrophy Due to Chronic Pulmonary Disease NICHOLAS MICHELSON, M. D., F. C. C. PBilateral Ventricular Hypertrophy Due to Chronic Pulmonary Disease DOI: https://doi.org/10.1378/chest.38.4.435Abstract Full Text Images References Article Outline Introduction Heart Weight Atrial Hypertrophy Hypertrophy of the Right Ventricle Left Ventricular Hypertrophy The Proportion of Right to Left and Left to Right Ventricular Hypertrophy Percentage Increase of Ventricular Thickness Above Normal Introduction to the Electrocardiographic Observations The Atrial Wave in Atrial Hypertrophy The Atrial Wave without Atrial Hypertrophy Discussion of the Electrical Axis Discussion of the QRS Pattern Discussion of ST Segment Discussion of the T Wave Discussion of the U Wave Review and Discussion of the Literature SUMMARYRESUMENRESUMÉZUSAMMENFASSUNGACKNOWLEDGEMENTREFERENCESIntroduction Eighty autopsy protocols derived from adult men and containing the diagnosis: “Cor pulmonale” have been reviewed at Castle Point, N. Y.

In the overwhelming majority of the cases right ventricular hypertrophy was associated with left ventricular hypertrophy; that is to say, the width of the left ventricular wall at its thickest portion exceeded 12 millimeters. The pathologist, the late Dr. Bernard Barshay had been most careful not to include any trabeculated part of the myocardium or the papillary muscles.

The diagnosis of right ventricular hypertrophy was made only when the maximal width of the wall was five millimeters or over. This standard was adopted in the year 1946 arbitrarily and with full knowledge that for adult males the normal value ascribed to the thickness of the right ventricular wall ranged from two to three millimeters.

These figures are still considered to be valid. 1This presentation is restricted to cases for which the following aspects could be verified by clinical and post mortem data: 1. Presence of chronic pulmonary disease, and 2. Absence of any congenital cardiac malformation, valvular disease, coronary occlusion, myocardial infarction, nephrosclerosis, systemic hypertension, or any medical condition definitely known to cause left ventricular hypertrophy.

Not excluded were cases where the histopathological investigation disclosed microscopic evidence of slight focal replacement fibrosis in the myocardium.

Also included were a few records where the autopsy protocol mentioned arteriosclerotic changes of the aorta and the coronary arteries ascribable to physiologic age processes, provided the coronaries had remained patent. This limited series embraces thirty-two cases. For twenty-seven individuals electrocardiograms were obtained in the absence of digitalis therapy.

For five patients electrocardiograms were either not available or had to be omitted from this study in view of a possible drug effect on the tracing. This pertains to cases 4, 5, 11, 21 and 26. Table 1 shows the age at death, body length, body weight, heart weight and the pulmonary diseases as found on necropsy.

TABLE 1Case No. Age Height in Inc. Weight in lbs. Heart Weight in Grams Diagnosis on Necropsy1 56 65 1/2 100 325 Pulm. tbc. Pulm. emphysema.2 43 Not rec. 130 350 Pulm. tbc. Pulm. emphysema.3 60 67 140 450 Primary progressive pulm. emphysema. Pulm. tbc.4 28 65 1/2 150 370 Pulm. tbc.5 61 66 1/2 145 360 Bronchogenic carcinoma. Pulm.

emphysema.6 34 Not rec. 125 300 Pulm. tbc. Focal. pulm. emphysema.7 68 66 118 225 Primary progressive pulm. emphysema. Pulm. tbc.8 53 66 100 365 Pulm. tbc. Pulm. emphysema.9 52 63 135 275 Pulm. tbc. Silicosis.10 58 66 170 400 Bronchogenic carcinoma. Pulm. tbc. Pulm. interstitial emphysema. Bronchiectasis.11 58 60 96 275 Bronchiectasis, Pulm. emphysema. Pulm. fibrosis.12 50 71 150 550 Pulm. tbc., inactive. Pulm. emphysema.13 59 Not rec. 131 450 Pulm. tbc., inactive. Pulm. emphysema. Pulm. fibrosis. Bronchiectasis.14 47 67 140 450 Pulm. tbc. Pulm.

emphysema. Pulm. fibrosis.15 41 Not rec. 115 450 Pulm. tbc. Pulm. fibrosis. Pulm. emphysema.16 61 69 120 350 Pulm. tbc. Carcinoma of lung. Pulm. emphysema.17 57 Not rec. 135 400 Pulm. tbc. Pulm. emphysema.18 57 70 115 400 Pulm. tbc. Pulm. emphysema.19 59 66 100 400 Pulm. tbc. Pulm. emphysema.20 53 68 180 550 Pulm. tbc. Bronchiectasis. Pulm. fibrosis. Pulm. emphysema.21 59 Not rec. 100 425 Pulm. tbc. Bronchiectasis.

Pulm. emphysema.22 59 Not rec. 120 475 Pulm. tbc. Carcinoma of lung. Pulm. emphysema. Pulm. fibrosis.23 52 60 178 650 Pulm. tbc. Pulm. emphysema. Fibrosis of pulmonary vessels.24 45 60 Estimated less than 100 400 Bullous pulm. emphysema. Pulm. arteriolar sclerosis.25 62 69 170 450 Bronchiectasis. Pulm. emphysema. Pulm.

fibr. Bronchogenic carcinoma.26 58 66 110 450 Pulm. tbc. Bronchogenic carcinoma. Pulm. emphysema.27 58 72 150 550 Pulm. emphysema. Pulm. fibrosis. Bronchogenic carcinoma.28 64 64 120 360 Pulm. tbc. Pulm. emphysema.29 37 70 150 550 Primary pulm. atherosclerosis and thrombosis of pulm. arteries. Pulm. emphysema. Pulm. Tbc.30 48 67 100 375 Pulm.

tbc. Pulm. emphysema. Bronchiectasis.31 52 Not rec. 100 400 Pulm. tbc. Pulm. emphysema. Pulm. fibrosis.32 47 73 100 400 Pulm. tbc. Pulm. emphysema. Bronchiectasis. View Table in HTMLTable 2 shows the abnormal atrial findings on necropsy.

TABLE 2ATRIAL HYPERTROPHY. THICKNESS OF WALL IN MM. (Normal Value: 1 to 2 mm. )Case No. Right Atrium Left Atrium1 2–3 2–312 3–4 2–318 2–3 Normal20 2–3 2–323 1–3 Normal29 3–5 Normal View Table in HTMLTable 3 shows the thickness of the ventricular walls.

TABLE 3THICKNESS OF VENTRICULAR WALL (in millimeters)Case Right Left1 3 to 5 10 to 152 Minimal not recorded — 6 103 3 to 6 10 to 154 Minimal not recorded — 6 155 Minimal not recorded — 6 156 5 to 7 10 to 157 3 to 7 10 to 158 5 to 7 15 to 209 3 to 8 10 to 1510 5 to 8 15 to 2011 5 to 8 10 to 1512 5 to 10 10 to 1513 5 to 10 10 to 1514 5 to 10 10 to 1515 5 to 10 10 to 1516 5 to 10 10 to 1517 5 to 10 10 to 1518 5 to 10 10 to 1519 5 to 10 10 to 1520 5 to 10 10 to 1521 5 to 10 10 to 1522 5 to 10 15 to 2023 5 to 10 10 to 2024 5 to 10 15 to 2025 5 to 10 15 to 2026 5 to 10 15 to 2027 5 to 10 10 to 2028 Minimal not recorded —12 1829 8 to 13 10 to 1530 10 to 15 10 to 1531 8 to 15 10 to 1532 8 to 15 10 to 20View Table in HTMLTable 4 shows the left to right ratio for the thickness of the ventricular walls.

TABLE 4RATIO FOR THICKNESS OF VENTRICULAR WALLS (Calculation Based on Values for Maximal Thickness)Case Left to Right1 3.02 1.673 2.504 2.505 2.506 2.147 2.148 2.869 1.8810 2.5011 1.8812 1.5013 1.5014 1.5015 1.5016 1.5017 1.5018 1.5019 1.5020 1.5021 1.5022 2.0023 2.0024 2.0025 2.0026 2.0027 2.0028 1.5029 1.1530 1.0031 1.0032 1.33View Table in HTMLTable 5 shows the percentage increase above normal for the thickness of the ventricular walls.

Table 6 shows the electrocardiographic abnormalities as regards the axis, the ST segment, the T wave and the QRS complex.

On Table 6 the occurrence of the U wave is also listed. TABLE 5PERCENTAGE INCREASE OF VENTRICULAR THICKNESS ABOVE NORMAL (As normal value used for right ventricle: 3 millimeters; as normal value used for left ventricle: 12 millimeters Case Right Ventricle Left Ventricle1 0.66 0.252 100 No increase3 100 254 100 255 100 256 133 257 133 258 133 669 166 2510 166 6611 166 2512 233 2513 233 2514 233 2515 233 2516 233 2517 233 2518 233 2519 233 2520 233 2521 233 2522 233 6623 233 6624 233 6625 233 6626 233 6627 233 6628 300 5029 333 2530 400 2531 400 2532 400 66View Table in HTMLTABLE 6A.

THE ELECTRICAL AXISRight axis deviation: 30 patients No axis deviation: 1 patient Combination of right and left axis factors with a predominating shift to the right: 1 patient B.

THE rs R' PATTERNa. In the absence of a hypertrophied crista supraventricularis:1. (Case 18.) QRS in V 2 0.10 second. Onset of r to peak of R' 0.05 second. Duration of the initial r wave 0.02 second. Onset of R' to its peak 0.02 second.

R' 8 mm. high.2. (Case 19.) QRS in V 2 and V 3 0.10 second. Onset of r to peak of R' 0.06 second. Duration of initial r wave less than 0.02 second. Onset of R' to its peak 0.02 second. R' 7 mm. high.3.

(Case 24.) QRS in V 2 0.10 second. Onset of r to peak of R' 0.07 second. Duration of initial r wave 0.02 second. Onset of R' to its peak less than 0.02 second. R' 4 mm. high.b. In the presence of hypertrophied crista supraventricularis: rs R' pattern absent: cases 3, 12, 13, 14, 23, 30, 31.

C. THE ST SEGMENT Normal in 20 individuals. Abnormal in 7 individuals. II III AVF AVL V 2V 3V 4V 5V 6a. ST depressed 4* 1 1 1 2 1 1 1b. ST elevated 1 2 1 1*The numbers signify the incidence in the various leads for seven individuals.

D. THE T WAVENormal in 12 individuals. Abnormal in 15 individuals.a. Shallow or isoelectric Shallow, isoelectric or diphasic Lead I Lead II Lead III V 15** 11 8 1b. Inverted Lead III V 1V 2V 3V 4CF 42** 2 5 4 1 1The numbers signify the incidence in the various leads for fifteen individuals.

E. THE PROTODIASTOLIC WAVEUpright U wave present: 6 individualsabsent: 21 individuals View Table in HTMLThe atrial electrocardiographic findings are summed up in the text. The study is supplemented by a report of a case with left ventricular hypertrophy without right ventricular hypertrophy. This addition was prompted by an electrocardiographic pattern which conforms with one of the criteria claimed in the literature to be characteristic for right ventricular hypertrophy.

The observation was made at the Veterans Hospital, Lyons, N. J., and it is cited in order to emphasize the elusiveness and uncertainty of electrocardiographic criteria for right ventricular hypertrophy. The age at death of the youngest person was 28 years and the oldest 68 years. The duration of the pulmonary diseases ranged from not less than five years to several decades. The tabulated data demonstrate the concurrence of bilateral ventricular hypertrophy in protracted and severe pulmonary diseases. It is the author's impression that there is little awareness as regards its existence. This is understandable because a concentric thickening of the myocardium without obvious dilatation of the ventricles will not be identified on the routine chest roentgenogram, when pulmonary emphysema is present. Among the 32 cases of the series the autopsy revealed pulmonary emphysema in 30, with or without additional pulmonary diseases. Heart Weight In order to compare the weight of an abnormal heart with averages deduced from healthy persons one must make the choice between computations based on body height or body weight. Each method of correlation shows a substantial variability as regards the weight of the normal heart. A standard value quoted by Gould 1 reads: “The weight of the normal heart in the adult male is stated to be between 275 and 325 grams.”Among the thirty-two cases of this study there were twenty-seven with the heart weight over 325 grams, as can be seen on Table 1. The weight of the heaviest heart was 650 grams (case 23). The second highest weight was 550 grams, and this applies to four cases (12, 20, 27 and 29). There was no significant relationship between the weight of the heart and body weight or body height. Graybiel et al 2 have shown in experiments on dogs that loss of body weight did not influence ventricular weight. In the present series the high heart weights are the expression of a pathological process and they came about irrespective of chronic emaciation and avoidance of physical exertion during prolonged hospitalization, and those conditions applied to an overwhelming majority of patients represented by this investigation. Atrial Hypertrophy Out of the 32 necropsies there were six instances where the thickness of the atrial walls exceeded the normal range of 1 to 2 millimeters. These data are shown on Table 2. Three individuals had bilateral atrial hypertrophy and three hypertrophy of the right atrial wall only. The abnormal width of the atrial walls ranged from 3 to 5 millimeters. Hypertrophy of the Right Ventricle Table 3 shows the thickness of the right ventricular wall. In the mildest degree of right ventricular hypertrophy the thickness of the right ventricular wall ranged from 3 to 5 millimeters (case 1); and in the severest (case 30) from 10 to 15 millimeters. Left Ventricular Hypertrophy Gould quotes Saphir 1 in citing the value for normal thickness of the left ventricular wall, namely 8 to 10 millimeters. Anderson 3 recommends higher figures: 10 to 12 millimeters. Table 3 shows that the abnormal thickness of the left ventricular wall in the mildest case of cor pulmonale (case 1) measured 10 to 15 millimeters. In the severest case of cor pulmonale (case 30) the left ventricular wall measured also from 10 to 15 millimeters.

However, some cases with less right ventricular hypertrophy than the maximal one had a more advanced associated left ventricular hypertrophy (cases 8, 10, 22, 24, 25, 26), the thickness of the left ventricular wall ranging from 15 to 20 millimeters. Left ventricular hypertrophy was absent in one case only (case 2).

The Proportion of Right to Left and Left to Right Ventricular Hypertrophy For the calculation of the ratio between the thickness of the right and left ventricular walls and vice versa, there were computed the measurements for the maximal width and not the range.

The question of interest was: Does increasing right ventricular hypertrophy disclose a quantitatively parallel increase in left ventricular hypertrophy? The figures on Table 4 do not reveal any consistent pattern. Percentage Increase of Ventricular Thickness Above Normal As normal thickness of the right ventricular wall the author used again: 3 millimeters, and of the left ventricular wall: 12 millimeters.

The thickness of the right ventricular wall shows a percentage increase over normal amounting to 0.66 per cent in the mildest case, and 400 per cent in the severest cases (case 1 versus cases 30, 31, and 32 on Table 5 ). The thickness of the left ventricular wall shows a percentage increase over normal amounting to 0.25 per cent in the mildest case of right ventricular hypertrophy (case 1 of Table 5) and very variable increases for the whole series, the maximum being 66 per cent (cases 8, 10, 22, 23, 24, 25, 26, 27 and 32).

In relation to the normal values the hypertrophy was very much greater in the right than the left ventricle. Introduction to the Electrocardiographic Observations There are elements of incompatibility if not of absurdity in an attempt to correlate electrocardiographic and anatomical findings.

For example: It is logical to assume that with the clinical evidence of cor pulmonale the appearance of an abnormal atrial wave, such as a tall peaked P wave, implies distention of the right atrium. However, the in vivo haemodynamic event does not need to be represented in the autopsy by either atrial dilatation or hypertrophy.

A dilatation of the atrium may resolve pre mortem or post mortem. Furthermore, in the living individual the position of the atrium may be reflected in the P wave, but that position might not be the same after breathing and cardiac action have ceased.

The following report should be read with these reservations in mind. The Atrial Wave in Atrial Hypertrophy This section is devoted to an analysis of the six cases listed on Table 2 . Case 1. Equal bilateral atrial hypertrophy. Twelve days prior to death: peaked P in lead II, 3 millimeters high. Case 12. Marked bilateral atrial hypertrophy with predominance on the right. One year and eight months prior to death: normal P waves. Case 20. Equal bilateral atrial hypertrophy. Two months prior to death: normal P waves. Case 18.

Right atrial hypertrophy. One year and six months prior to death: normal P waves. Eleven months prior to death: slightly peaked P in lead II, 3 millimeters high. The last cited electrocardiogram showed a heart rate of 115, and the tachycardia may or may not have influenced the form and size of the P wave.

Case 23. Right atrial hypertrophy and dilatation. Four days prior to death: normal P waves. Case 29. The most marked right atrial hypertrophy of the series. One year and five months prior to death: peaked P, lead II, 3 millimeters high.

Prominent upright P wave in V 2, 3 millimeters high. Thus, as regards atrial hypertrophy, there was no consistent correlation between electrocardiographic manifestations and the anatomical findings on autopsy. The Atrial Wave without Atrial Hypertrophy Among the twenty-one subjects with electrocardiograms in the absence of digitalis therapy and without atrial hypertrophy there were fifteen persons whose tracings showed normal P waves.

Six had abnormal P waves: Case 7: Two months prior to the patient's death: P in lead II and lead III and AVF peaked and 3 millimeters high. Case 14. Sixteen months prior to the patient's death: asymmetric P with a relatively broad descending limb which slants, without a horizontal base line, directly toward the QRS complex in lead II, lead III and AVF.

The depth of the descending limb is 3 millimeters. Similar P in V 2, V 3, V 4 and V 5. In AVR the summit of P is flattened and slightly notched. Case 15. One year and four months prior to the patient's death: P in lead II peaked, 4 millimeters high.

Prominent upright P in V 2, V 3 and V 5, 2 millimeters high. Heart shifted to the left. Case 19. Six months prior to the patient's death: P slightly peaked and 3 millimeters high in lead II, lead III and AVF.

Case 24. One year and 11 months before the patient's death a severe asthmatic attack. Heart rate: 115, P peaked, with deep descending limb, in lead II, lead III and AVF. Prominent P with deep descending limb in V 4. Subsequently, during absence of asthma and with a heart rate of 79, normal P waves, one year and one month prior to the patient's death.

Case 30. Five weeks prior to the patient's death: P peaked, 4 to 5 millimeters high, in lead II, lead III and AVF. Peaked upright P and 3 to 4 millimeters high, in V 3. Peaked upright P and 3 millimeters high, in V 4.

Peaked upright P and 2 1/2 millimeters high, with descending limb 4 millimeters deep, in V 5. Heart shifted to the left. Attention is being drawn to the prominent P waves in the precordial leads (cases 15 and 30 with shift of the mediastinum to the left, and cases 24 and 29 without such a cardiac displacement).

While with pulmonary heart disease the very rare occurrence of a prominent P wave in the precordial leads has been observed before (Michelson), 4 case 24 is the only instance where the author found this formation to be transient. Such an instability of the P wave supports the concept that acute right atrial dilatation, induced by pulmonary insufficiency, can recede with the abatement of the pulmonary insufficiency.

The clinical aspects of cases 15, 24 and 29 have been reported in a previous publication. 4Discussion of the Electrical Axis With one exception (case 19) all of the electrocardiograms showed right axis deviation. In view of the bilateral ventricular hypertrophy in this series, the right axis deviation cannot be explained by the effect of a clock wise rotation of the heart on its long axis and a backward displacement of the apex.

The autopsy material presented here dispells the notion that right ventricular hypertrophy must achieve or surpass the thickness of the left ventricular wall in order to produce right axis deviation. The predominance of the mass of the left ventricular wall over the mass of the right ventricular wall has been demonstrated.

Therefore there arises the hypothetical question whether the great muscular performance of the hypertrophied right ventricle may possibly cause an alteration of the electrical potential resulting in right axis deviation. Discussion of the QRS Pattern Among twenty-seven patients an abnormal QRS complex was observed in three individuals.

An rs R' pattern with a delayed intrinsicoid deflection occurred in V 2 and V 3 without a hypertrophied crista supraventricularis. In contrast to these three instances there was no rs R' pattern and no widening of the QRS complex in the electrocardiograms of seven subjects whose hearts showed on necropsy a hypertrophy of the crista supraventriculars. These observations throw doubt on the concept that the electrocardiographic pattern under discussion is to be regarded as pathognomonic for right ventricular hypertrophy.

At this point an autopsy finding (R-15785, July 3, 1958) at Lyons, N. J., may perhaps be pertinent. The subject's age at death was 59 years. Height: 68 inches. Weight: 90 lbs. History of arterial hypertension. Cause of death: pneumonia. Heart weight: 290 grams. There was left but no right ventricular hypertrophy.

The thickness of the right ventricular wall measured up to 3 millimeters and the thickness of the left ventricular wall up to 15 millimeters. Between the year 1950 and October 1957 eight routine electrocardiograms showed a stable rs R' pattern in V 1 and V 2, the duration of QRS being 0.10 second.

There was a delay of 0.06 second in the onset of the intrinsicoid deflection (beginning of r to peak of R').

The duration of the initial r was 0.02 second (this excluding the application of an electrocardiographic classification of “partial right bundle branch block” [ Fig. 1 ]). FIGURE 1Case R15785: Left ventricular hyperthrophy. Delayed onset of the intrinsicoid deflection in lead V 2. View Large Image| Download Power Point Slide Thus, the frequent absence of the delayed intrinsicoid deflection in V 1 and V 2 in the presence of right ventricular hypertrophy and the occurrence of that pattern in association with a normal right ventricle, raise questions as regards the origin and electrocardiographic specificity of that pattern.

Is its formation possibly induced or influenced by the activation of the left ventricle? Discussion of ST Segment Seven individuals among the series of 27 patients showed abnormalities.

They occurred in nine leads as a whole. Hypoxia, associated with pulmonary insufficiency, may be incriminated in the present series because coronary artery disease could be ruled out as a causative factor. Discussion of the T Wave Fifteen individuals among the series of 27 patients showed abnormalities.

They occurred in eight leads as a whole. Leads two and three were chiefly affected. T 2 was shallow, isoelectric or diphasic eleven times; T 3 was shallow, isoelectric, diphasic or inverted ten times.

Inversion of T in V 2 and V 3 summed up to nine instances. In the opinion of the author these findings are not pathognomonic for cor pulmonale but may be considered as a clue when harmonizing with clinical criteria. Discussion of the U Wave The present series of 27 patients with the occurrence of a normal U wave in six individuals is too small for any interpretative attempt.

That the U wave represents “an electrical, i.e. biochemical process occurring during the protodiastolic phase of the heart cycle” has been demonstrated by Groedel and Miller 5 in support of the theory of Maekawa (quoted from Groedel and Miller) who believed the U wave to be a dilatation potential.

Review and Discussion of the Literature Kounitz, Alexander and Prinzmetal 6 reported in 1936 that among seventeen autopsied cases of pulmonary emphysema there was thickening and dilatation of the right ventricle as well as thickening of the left ventricular wall.

From the methodological point of view that study is of great value because the weight of the ventricles was compared after sectioning the heart according to Hermann and Wilson 7 whose material was used for normal controls. Parker 8 stated in 1940 that a post mortem examination on 32 cases with essential pulmonary emphysema revealed in 11 instances the combination of right and left ventricular enlargement.

While Kounitz and his co-authors could not offer an explanation for their observation, Parker surmised that in his series the work hypertrophy of the left ventricle could be explained most logically on the basis of hypertension in the systemic circulation which was not detected clinically. Harvey, Ferrer, Richards, Jr. and Cournand 9 declared in 1951: “The left ventricle is not compromised even with chronic cor pulmonale in cardiac failure.

There was no enlargement of this chamber radiographically.” These authors add that post mortem examinations in eight cases of the investigated series confirmed their impression. In 1951 Zimmerman and Ryan 10 reviewed 50 cases for cor pulmonale autopsied at Cleveland City Hospital and reported in 1941 by Scott and Garvin. 11 To that series Zimmerman and Ryan added 52 new cases from the same hospital. Zimmerman and Ryan confirmed the findings of Scott and Garvin and stated: “The left ventricle as first reported showed varying grades of hypertrophy.

In 93 per cent the left ventricle measured 12 mm. or more and in 41 cases (78 per cent) it measured 15 mm.

or more. The cause of this hypertrophy is not clear. However, the recent work of Mc Michael and Sharpey-Shaffer 12 may tend to elucidate this problem since they showed thta patients with cor pulmonale had increased cardiac outputs which tended to remain elevated even when cardiac failure occurred”Boettner et al 13 claimed in 1957 that among 38 cases of cor pulmonale the autopsy showed eight cases of dilatation of the left heart.

However, this statement is not specified as regards atrial or ventricular location. While discussing the pathology of cor pulmonale Shepers 14 writes in 1957: “Studies based on ratios of right and left ventricles break down when one considers the recent evidence that the left ventricle may hypertrophy either in sympathy with the enlarging right ventricle or in order to fulfill some function compensatory to the increasing embarrassment of the lesser circulation.” He states that a hypertrophy of the left ventricle has been propounded either on an anoxic basis (Spain and Handler) 15 or on the basis of the continuity of the muscle fibre bundles of the right ventricle across the septum to the left myocardium.

Armen, Kantor and Weiser 16 mentioned in 1958 one post mortem case of cor pulmonale in which there was left ventricular hypertrophy without the presence of any other form of heart disease ordinarily leading to increased work of the left ventricle.

They write: “Rosenburg and Deenstra 17 have demonstrated the admixture of oxygenated blood in the smaller pulmonary arteries in patients with chronic lung disease, particularly those with bronchiectasis, indicating an extensive collateral circulation from the bronchial arteries.

From the standpoint of the left ventricle this mixing represents an arteriovenous shunt and may be responsible for the left ventricular disease.”Another stipulation which was to serve as an explanation for generalized cardiac hypertrophy is the concept of increased myocardial work at certain degrees of low oxygen tensions.

In animal experiments this was achieved by Vacek 18 in 1926. The overstretching of the myocardial fibres has been incriminated as a factor possibly leading to their overgrowth (Best and Taylor). 19Cardiac overwork in terms of accelerated heart rate may also be cited among the hypothetical causes for ventricular hypertrophy. From the point of view of the Bainbridge 20 reflex the sequence of the following events is conceivable: a rise of venous pressure in the right atrium, increase of diastolic distention of the cardiac chambers and reflex stimulation resulting in acceleration of the cardiac rate. The author has seen many patients whose chronic pulmonary insufficiency was associated with myocardial hypertrophy and who did not have sustained tachycardia or any tachycardia prior to sudden or perhaps belatedly identified cardiac decompensation. Among the twenty-seven patients without digitalis therapy the electrocardiograms showed a heart rate ranging from eighty-eight to one hundred fifteen for nineteen patients.

The whole group includes a substantial number of persons who have had non-cardiac asthma and concomitant tachycardia periodically during numerous consecutive years. Therefore, tachycardia cannot be dismissed as one of the possible mechanisms contributing to cardiac overwork in chronic pulmonary disease.

It seems to be an established opinion that long lasting and severe pulmonary disease may cause a concentric thickening of the wall of the right ventricle and presumably because this chamber must pump against an increased resistance due to infringement upon the capillary bed. Among the theoretical considerations for the cause of an associated left ventricular hypertrophy the role of a possible diastolic suction may be stipulated as a hypothesis which merits investigation.

Rushmer 21 writes: “Greater diastolic distension without a corresponding increase in filling pressure may follow administration of epinephrine.”In summing up, the causation of bilateral ventricular hypertrophy in certain patients with chronic pulmonary disease is still an unsolved question.

SUMMARYA series of 32 necropsy cases with bilateral ventricular hypertrophy due to chronic, severe pulmonary diseases is analyzed. Three individuals had bilateral atrial hypertrophy, and three right atrial hypertrophy only. The thickness of the right ventricular wall ranged from 3 to 5 millimeters in the mildest case of cor pulmonale and from 10 to 15 millimeters in the severest case.

The thickness of the left ventricular wall ranged from 10 to 15 millimeters in the mildest case of cor pulmonale and also from 10 to 15 millimeters in the severest case. However, in several intermediate cases the left ventricular wall measured from 10 to 20 millimeters in thickness. An arrangement of the cases according to increasing thickness of the right ventricular wall did not disclose a parallel quantitative progression in the left ventricular hypertrophy.

This is substantiated by ratios as well as by the percentage increases above normal values, computed for the maximal widths of both ventricles.

For the whole series the hypertrophy was much greater in the right than the left ventricle. For the thickness of the right ventricular wall the percentage increase above normal amounted to 400 per cent in the severest case. For the left ventricle the maximum percentage increase above normal amounted to 66 per cent. However, with the exception of one single case, the absolute thickness of the right ventricular wall was considerably less than the absolute thickness of the left ventricular wall.

The right ventricular hypertrophy was reflected in the electrocardiogram by right axis deviation. Seven cases with a hypertrophied christa supraventricularis did not show an rs R' pattern in leads V 1 or V 2.

Such a pattern with a delayed onset of the intrinsicoid deflection could be demonstrated for a contrast case without right ventricular hypertrophy but with left ventricular hypertrophy. RESUMENSe estudia una serie de 32 necropsias de casos con hipertrofia ventricular bilateral debida a enfermedad crónica esvera pulmonar.

Tres individuos tenian hipertrofia bilateral atrial y tres sólo hipertrofia atrial derecha. El espesor de la pared ventricular derecha varió de 3 a 5 mm. en el caso mas leve de cor pulmonale y de lo a 15 mm. en el caso mas grave. El espesor de la pared ventricular izquierda tuvo un promedio de lo a 15 mm.

en el caso mas leve de cor pulmonale y tambien de lo a 15 mm. en el caso mas severo. Sin embargo, varios casos intermedios mostraron que la pared ventricular izquierda medía de 15 a 20 mm.

de espesor. Un arreglo de los casos de acverdo con el aumento de espesor de la pared ventricular derecha no condujo a un aumento cuantitativo parelelo de la hipertrofia ventricular izquierda. Esto es apoyado por las relaciones así como por el porcentaje de aumenot sobre lo normal, estimado por los máximos espesores de ambos ventrículos. Para todo la serie la hipertrofia fué mucho mayor en el ventriculo del lado derecho que del izquierdo.

Siendo el porcentaje de auemnto del espesor de la pared ventricular derecha de 400 por ciento sobre normal en el caso mas severo. Para el ventriculo izquierdo el porcentaje máximo de aumento sobre lo normal fué de 63 por ciento.

Con la excepcion de un solo caso, el espesor absoluto de la pared ventricular derecha fué considerablemente menor que el espesor absoluto de la pared del ventriculo izquierdo. La hipertrofia ventricular derecha se manifestó en el electrocardiogarma por una desviación derecha axial.

Siete casos con hipertrofia de la cresta supraventricularis no mostraron un forma rs R' en la V 1 ó V 2. Tal cuadro, con un principio retardado de la deflexión intrinsicoide podría ser demostrado por un caso de contraste sin hipertrofia ventricular derecha, pero con hipertrofia ventricular izquierda.

RESUMÉL'auteur analyse une série de 32 autopsies de malades atteints d'hypertrophie ventriculaire bilatérale consécutives à de graves affections pulmonaires chroniques. Trois individus avaient une hypertrophie bilatérale de l'oreillette et trois n'avaient qu'une hypertrophie de l'oreillette droite.

L'épaisseur de la paroi ventriculaire droite variait de 3 à 5 millimètres dans le cas le plus discret de coeur pulmonaire et de 10 à 15 millimètres dans le cas le plus sévère. Cependant, dans plusieurs cas intermédiaires, la paroi ventriculaire gauche mesurait de 15 à 20 millimètres d'épaisseur.

Une classification des cas selon l'augmentation dépaisseur de la paroi ventriculaire droite n'a pas fait découvrir de progression quantitative parallèle de l'hypertrophie du ventricule gauche.

En ce qui concerne la série totale, l'hypertrophie fut beaucoup plus importante pour le ventricule droit que pour le gauche. Pour l'épaisseur de la paroi ventriculaire droite, l'augmentation au-dessus de la normale atteignit jusqu'à 400% dans le cas le plus grave. Pour le ventricule gauche, l'augmentation maximale au-dessus de la normale atteignit jusqu'à 66%. Cependant, à l'exception d'un seul cas, l'épaisseur absolue de la paroi ventriculaire droite fut considérablement moindre que l'épaisseur absolue de la paroi ventriculaire gauche. L'hypertrophie ventriculaire droite se reflétait dans l'électrocardiogramme par une déviation de l'axe droit.

Dans sept cas comportant une hypertrophie de la crête supra-ventriculaire, il n'y avait pas l'aspect rs R' dans les dérivations V 1 ou V 2.

Un tel aspect avec un retard de la déflection intrinsécoîde pourrait être demonstré comme un cas sans hypertrophie ventriculaire droite mais avec hypertrophie ventriculaire gauche. ZUSAMMENFASSUNGEine Serie von 32 Sektionsfällen mit beiderseitiger Ventrikel-Hypertrophie als Folge chronischer schwerer Lungenkrankheit wird ausgewertet. Drei Fälle hatten eine bilaterale Vorhof-Hypertrophie und 3 eine solche des rechten Vorhofes allein.

Die Dicke der rechten Kammerwand schwankte zwischen 3 und 5 mm bei den leichtesten Fällen von Cor pulmonale und zwischen 10 und 15 mm bei den schwersten Fällen.

Die Dicke der linken Kammerwand lag zwischen 10 und 15 mm bei den leichtesten Fällen von Cor pulmonale und ebenfalls zwischen 10 und 15 mm bei den schwersten Fällen. Es maß jedoch bei verschiedenen dazwischen gelegenen Fällen die linke Ventrikelwand zwischen 15 und 20 mm. Eine Anordnung der Fälle nach zunehmender Dicke der Wand der rechten Kammer offenbarte keine parallele quantitative Progression der Hypertrophie der linken Kammer. Es wird dies erkenntlich sowohl durch die Verhältniszahl, als auch durch den prozentuale Anstieg über die Normalwerte, errechnet für die maximale Wandlicke beider Ventrikel.

In der ganzen Reihe war die Hypertrophie viel größer am rechten als am linken Ventrikel. Was die Dicke der Wand der rechten Kammer angeht, so erreichte der prozentuate Anstieg über die Normalwerte bis zu 400% bei den schwersten Fällen.

Beim linken Ventrikel kam es zu einem maximalen prozentualen Anstieg über die Normalwerte bis zu 66%. Mit Ausnahme eines einzigen Falles war jedoch die absolute Dicke der rechten Kammerwand beträchtlich geringer als die absolute Dicke der linken Kammerwand.

Die Hypertrophie des rechten Ventrikels äusserte sich im EKG in einer Abweichung der rechten Achse. Fälle mit einer hypertrophierten christa supraventricularis zeigten bei den Ableitungen V 1 oder V 2 keine rs R 1 Zeichen.

Ein solcher Ablauf mit verzögertem Beginn der wesentlichen Zacke konnte in einem Kontrastfall ohne Hypertrophie der rechten Kammer-aber mit Hypertrophie der linken Kammernachgewiesen werden. ACKNOWLEDGEMENTI wish to express my gratitude to Dr. Albert S. Hyman, Consultant Cardiologist, whose gift of penetrating inquiry stimulated me in my research. REFERENCESSaphir, O.in: Gould S. E. (Ed.) Pathology of the Heart. 1953. Charles C. Thomas, Publisher,; 1946:973–1068View in Article | Google Scholar Graybiel, Ashton, Malt, Ronald A., Colehour, James K., Barlow, George, and Spurr, Gerald.

Comparison of the Cardiovascular Dynamics and the Size and Fat Content of the Heart in Lean and Fat Dogs. Am. Jour. Cardiology. 1959 ; 3: 647View in Article | Abstract | Full Text PDF | Pub Med | Google Scholar Anderson, W. A. D. Pathology. C. V. Mosby Company,; 1953: 486View in Article | Google Scholar Michelson, Nicholas. P-Pulmonale in the Precordial Leads and a Review of the Mutability of the P-Waves in Chronic Cor Pulmonale.

Dis. Chest. 1956 ; 29: 187View in Article | Crossref | Google Scholar Groedel, Franz M. and Miller, Max. The U Wave in the Chest Leads. Exp. Med. and Surg. 1950; 8: 187View in Article | Google Scholar Kounitz, W. B., Alexander, H. L., and Prinzmetal, M. The Heart in Emphysema. Am. Heart Jour. 1936; 11: 163View in Article | Abstract | Full Text PDF | Scopus (17) | Google Scholar Hermann, G. R. and Wilson, F. N. Experimental Heart Disease.

Am. Heart Jour. 1925; 1: 213View in Article | Abstract | Full Text PDF | Google Scholar Parker, Robert L. Pulmonary Emphysema. Ann. Int. Med. 1940; 14: 795View in Article | Crossref | Google Scholar Harvey, Réjane M., Ferrer, M., Irené, Richards Jr., Dickinson, W., and Cournard, André.

Influence of Chronic Pulmonary Disease on the Heart and Circulation. Am. Jour. Med. 1951 ; 10: 730View in Article | Abstract | Full Text PDF | Scopus (41) | Google Scholar Zimmerman, Henry A. and Ryan, Joe M. Cor Pulmonale. Dis. Chest. 1951; 20: 286View in Article | Crossref | Pub Med | Google Scholar Scott, R. W. and Garvin, C. F. Cor Pulmonale. Am. Heart Jour. 1941; 22: 56View in Article | Abstract | Full Text PDF | Scopus (19) | Google Scholar Mc Michael, J. and Sharpey-Shaffer, E. P. The Action of Intravenous Digoxin in Man. Quart. J. Med.1944 ; 13: 123View in Article | Google Scholar Boettner, Juan Max, Serna, Gil Dami, and Maas, Luis Carlos. Cor Pulmonale en Tuberculosis. Tórax, Montevideo, Uruguay. 1957 ; 6: 241View in Article | Google Scholar Shepers, G. W. H. The Pathology of Cor Pulmonale. Transactions of the American College of Cardiology. 1957 ; 7: 49View in Article | Google Scholar Spain, D. M. and Handler, B. J. Chronic Cor Pulmonale. Sixty Cases Studied at Necropsy. Arch. Int. Med. 1946 ; 77: 37View in Article | Crossref | Pub Med | Scopus (9) | Google Scholar Armen, Robert N., Kantor, Milton, and Weiser, Nelson J. Pulmonary Heart Disease. Circulation. 1958; 17: 164View in Article | Crossref | Pub Med | Scopus (5) | Google Scholar Rosenburg, G. E. and Deenstra, H. Bronchial-Pulmonary Vascular Shunts in Chronic Pulmonary Affections. Dis. Chest. 1954 ; 26: 664View in Article | Crossref | Google Scholar Vacek, T. Functional Adaption of the Heart in Mice Living under Insufficient Oxygen Supply. Arch. F. D. Ges. Physiol. 1926 ; 212: 357View in Article | Crossref | Scopus (1) | Google Scholar Best, Charles Herbert and Taylor, Norman Burke. The Physiological Basis of Medical Practice. Sixth Edition. The William E. Wilkins Company ,; 1955: 258View in Article | Google Scholar Bainbridge, F. A. The Influence of Venous Filling Upon the Rate of the Heart. J. Physiol. 1915; 50: 65View in Article | Crossref | Pub Med | Scopus (178) | Google Scholar Rushmer, Robert F. Work of the Heart. Modern Concepts of Cardiovascular Disease. 1958; 27: 474View in Article | Google Scholar© 1960 The American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.

. What Is Mild Cardiomegaly? This condition is marked by a minor increase in size of the heart. Mild cases of this disorder generally arise due to diseases like General Hypertrophy Hypertrophy is a condition that arises when an organ of the body suffers enlargement. Left Ventricular Hypertrophy Hypertrophy affects only the left lower cardiac chamber.

Cardiomegaly (Enlarged Heart)

Home Heart, Blood and Circulation Cardiomegaly (Enlarged Heart)Cardiomegaly (Enlarged Heart)Hx Benefit Editorial Team June 6, 2011 Heart, Blood and Circulation Table Of Content: [ hide]How to Define Cardiomegaly? Cardiomegaly Causes Cardiomegaly Meaning How Is Cardiomegaly Pronounced? Cardiomegaly (Enlarged Heart) Symptoms Cardiomegaly Diagnosis Cardiomegaly Treatment Cardiomegaly Prevention Cardiomegaly Natural Remedies Cardiomegaly Management Cardiomegaly Pathophysiology What Is Mild Cardiomegaly?

Most people ignore mild abnormalities in heart beats and dizziness until they turn worse. If you are suffering from similar symptoms, do not ignore them for you may be having a case of Cardiomegaly. Read and know what is Cardiomegaly, its causes, symptoms, diagnosis and treatment. How to Define Cardiomegaly?

Cardiomegaly definition is given as an unusual cardiac condition in which the human heart grows larger in size and becomes bigger than it usually is. The disease is also known as “Enlarged Heart”. Cardiomegaly Image Source: Wikimedia Cardiomegaly Causes Cardiomegaly may arise due to a number of ailments and abnormal health conditions. Some of the main causes of Cardiomegaly are High Blood Pressure Congestive Heart Failure Hypertensive Heart Disease Connective Tissue Disease The condition may also be caused due to excessive workouts and long-time suffering from Anemia.

Lack of exercise may also cause this disorder. Usually, heart is enlarged when the organ has to work more than usual and pump more blood. Cardiomegaly Meaning The term Cardiomegaly means an enlarged heart. How Is Cardiomegaly Pronounced?

Cardiomegaly pronunciation is given as “Kar – Dee – o – meg – a – lee”. Cardiomegaly (Enlarged Heart) Symptoms Some people affected with Cardiomegaly are usually asymptomatic, meaning they do not suffer from any symptoms. However, many people suffer from difficulties due to this medical condition which shows that their heart is being gradually compromised.

Some of the most common Cardiomegaly symptoms are Respiratory difficulties Shortness of breath Dizziness In some cases, affected people may suddenly suffer from Cardiac arrhythmia, or an unnatural cardiac muscle contraction. Some other signs include a persistent cough and inflammation of lower limbs. Cardiomegaly Diagnosis The diagnosis of this condition usually involves a series of medical tests. In Cardiomegaly X Rays, Magnetic Resonance Imaging (MRI), Computerized Tomography (CT) Scans and blood tests.

Blood tests help assess the level of hemoglobin and check platelet and blood cell count. Imaging helps assess the condition of the heart. An electrocardiogram test may also be carried out to check the electrical impulses in the heart. Cardiomegaly Treatment Treatment of Cardiomegaly aims at treating the underlying conditions behind the disease and reducing undue stress on cardiac muscles.

If Cardiomegaly is caused by high blood pressure, beta blockers, angiotensin-converting enzyme (ACE) inhibitors and diuretics may be used to reduce pressure level. These medicines also cure problems like water retention and inflammation and improve functioning of heart. If a damaged valve is the cause of the heart enlargement, surgery may be needed to correct the condition.

The faulty valve is replaced with a donated valve or an artificial valve. Cardiac arrhythmia can be cured by implanting a pacemaker or Cardioverter-defibrillator (ICD). If all medications and treatment methods fail to bring about an improvement, a total heart replacement may become the only solution. Cardiomegaly Prevention This heart disease can be prevented by regular exercise and by making a few dietary and lifestyle modifications.

Balanced Diet A well-balanced diet can boost your immune system and also prevent heart ailments. It is best to avoid fatty foods altogether or keep them to a minimum. Fat increases your cholesterol levels and makes you vulnerable to heart disorders. Avoid Smoking and Drinking Smoking and alcohol intake puts unnecessary stress on your heart and reduces oxygen intake.

Avoidance of nicotine and alcohol can be highly beneficial for your cardiovascular system. Regular Exercise Moderate exercising on a regular basis increases oxygen intake and improves heart functioning. Cardiomegaly Natural Remedies For treatment of Cardiomegaly natural treatment is as necessary as medications. Natural cure is possible by foods as well as workouts. Apples – The humble apple, which is said to keep the doctor away if taken daily, can also help your heart from getting enlarged.

It is a rich source of Vitamin C, which regulates cholesterol levels in blood and defends the capillary walls.

Honey – Honey has always been regarded for its ability to improve blood circulation, reduce irregularities in heart beats and makes heart muscles stronger. Asparagus Mixture – Make a 2:1 mixture with asparagus juice and honey. Consuming this daily can help reduce enlargement of heart. Carrot Juice – Mix one-third alfalfa juice with two-third carrot juice. Daily consumption of this mixture can benefit cure heart enlargement.

Onion Juice – Having a spoonful of onion juice in the morning on an empty stomach helps normalize blood cholesterol levels and oxidizes extra cholesterol. Cardiomegaly Management The disease needs to be managed with medications and lifestyle modifications.

It is important to follow drug prescriptions correctly and take medicines properly. Performing light exercises such as brisk walking and stretching for a short time everyday can help the heart function better and restore normalcy in the body. Cardiomegaly Pathophysiology Pathophysiology refers to the functional changes resulting from a disease or an injury. Pathophysiology of Cardiomegaly involves enlargement of heart and its abnormal functioning. The cardiac muscles start working much harder. The heart muscles pump at an increased rate leading to physical discomforts and respiratory difficulties

Abnormalities in the cardiac chamber causes increased flow of blood through the heart valves. Heart Attack A heart attack leads to a blood clot which cuts of blood flow to cardiac muscles.

The cardiac muscle suffers damage or even dies due to this deprivation resulting in heart expansion. Congestive Heart Failure This condition arises when high blood pressure, cardiac infection and narrowed arteries reduces blood flow making the heart function harder than usual and grow bigger in size.

However dietary changes and medications help restore heart to its normal size. Cardiomyopathy This disease leads to cardiac muscle inflammation due to viral infection or other heart ailments. Cardiomegaly is a completely curable medical condition. If you are suffering from symptoms similar to this disease, visit your doctor and start treatment immediately. Early medical care will help you avoid all future complications and get back to health in no time.

Referenceshttp://www.wrongdiagnosis.com/c/cardiomegaly/basics.htmhttp://en.wikipedia.org/wiki/Cardiomegalyhttp://www.wisegeek.com/what-is-cardiomegaly.htm Image source 123rf.com: Olga Sadovnikova Related Posts Budd-Chiari Syndrome Renal Artery Stenosis Megaloblastic Anemia About The Author Hx Benefit Editorial Team

Chronic hypertension is the most common cause of diastolic dysfunction and failure. It leads to left ventricular hypertrophy and increased connective tissue content, both of which decrease cardiac compliance.

Diastolic Heart Failure: Challenges of Diagnosis and Treatment

Diastolic Heart Failure: Challenges of Diagnosis and Treatment PDF PRINT COMMENTSSHAREA more recent article on heart failure is available.

CECILIA GUTIERREZ, M. D, and DANIEL G. BLANCHARD, M. D., University of California, San Diego, School of Medicine, La Jolla, California Am Fam Physician. 2004 Jun 1;69 (11):2609-2617. This article exemplifies the AAFP 2004 Annual Clinical Focus on caring for America's aging population.

Diastolic heart failure, a major cause of morbidity and mortality, is defined as symptoms of heart failure in a patient with preserved left ventricular function. It is characterized by a stiff left ventricle with decreased compliance and impaired relaxation, which leads to increased end diastolic pressure. Signs and symptoms are similar to those of heart failure with systolic dysfunction.

The diagnosis of diastolic heart failure is best made with Doppler echocardiography. Based on current knowledge, pharmacologic treatment of diastolic heart failure should focus on normalizing blood pressure, promoting regression of left ventricular hypertrophy, avoiding tachycardia, treating symptoms of congestion, and maintaining normal atrial contraction when possible.

Diuretic therapy is the mainstay of treatment for preventing pulmonary congestion, while beta blockers appear to be useful in preventing tachycardia and thereby prolonging left ventricular diastolic filling time. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers may be beneficial in patients with diastolic dysfunction, especially those with hypertension.

Evidence from adequately powered randomized controlled trials, however, is not available yet. The outcomes of ongoing clinical trials may provide much-needed information to move from intuitive treatment to therapy based on evidence that matters: decreased morbidity and mortality and improved quality of life.

Heart failure affects approximately 4.8 million persons in the United States, with about 500,000 new cases diagnosed each year.

1, 2 It is the leading cause of hospitalization in patients older than 65 years. 3 In spite of significant advances in the treatment of heart failure, mortality rates remain high: 30 to 40 percent of patients with advanced disease and 5 to 10 percent of patients with mild symptoms die within five to 10 years. 4Heart failure can arise from any condition that compromises the contractility of the heart (systolic heart failure) or that interferes with the heart's ability to relax (diastolic heart failure).

Hospital- and community-based reports indicate that about one fourth to one half of patients with heart failure have normal left ventricular systolic function. 5, 6 Observational studies 5 – 7 indicate that diastolic heart failure is more common in women and elderly persons. Although patients with diastolic heart failure have a lower annual mortality rate than patients with systolic heart failure, they have a higher rate than the general population.

They also have hospitalization rates similar to those of patients with systolic heart failure. These observations emphasize diastolic heart failure as an important contributor to morbidity, mortality, and health care costs, and highlight the need for further research and clinical trials examining this condition. Pathophysiology Diastole is the process by which the heart returns to its relaxed state; it is also the time for cardiac perfusion.

During diastole, drastic changes in cardiac pressure-volume relationships occur. The relaxation process has four identifiable phases: isovolumetric relaxation from the time of aortic valve closure to mitral valve opening; early rapid filling after mitral valve opening; diastasis, a period of low flow during mid-diastole; and late filling of the ventricles from atrial contraction ( Figure 1 ).

In patients with isolated diastolic heart failure, the heart often is able to meet the body's metabolic needs, but at higher diastolic pressures.

The left ventricle is stiff, with decreased compliance and impaired relaxation. Transmission of the higher end-diastolic left ventricular pressure to the pulmonary circulation may lead to pulmonary congestion, dyspnea, and other symptoms of heart failure. 8, 9Diastole is a complex process that is affected by a number of factors, including ischemia, heart rate, velocity of relaxation, cardiac compliance (i.e., elastic recoil and stiffness), hypertrophy, and segmental wall coordination of the heart muscle. View/Print Figure FIGURE 1. Cardiac cycle, showing changes in left atrial pressure, left ventricular pressure, aortic pressure, and ventricular volume; the electrocardiogram (ECG); and the phonocardiogram. HYPERTENSION

Left ventricular hypertrophy may cause or facilitate many cardiac complications of hypertension, including congestive heart failure, ventricular arrhythmias, myocardial ischemia, and sudden death. Left ventricular diastolic dysfunction, which may present with all of the symptoms and signs of congestive heart failure, is common in patients with long-standing hypertension.

Complications of Untreated Hypertension

Systemic Hypertension |Complications of Untreated Hypertension Jul 20, 2007 Viewed: 1184Complications of hypertension are related either to sustained elevations of blood pressure, with consequent changes in the vasculature and heart, or to atherosclerosis that accompanies and is accelerated by long-standing hypertension.

Most of the adverse outcomes in hypertension are associated with thrombosis rather than bleeding, and there is evidence that increased vascular shear stress converts the normally anticoagulant endothelium to a prothrombotic state.

The excess morbidity and mortality related to hypertension are progressive over the whole range of systolic and diastolic blood pressures; the risk approximately doubles for each 6 mm Hg increase in diastolic blood pressure. However, target-organ damage varies markedly between individuals with similar levels of office hypertension.

Ambulatory pressures are superior to office readings in the prediction of end-organ damage. A. HYPERTENSIVE CARDIOVASCULAR DISEASE Cardiac complications are the major causes of morbidity and mortality in primary (essential) hypertension, and preventing them is a major goal of therapy. Electrocardiographic evidence of left ventricular hypertrophy is found in up to 15% of persons with chronic hypertension. For any level of blood pressure, its presence is associated with incremental cardiovascular risk. Echocardiographic left ventricular hypertrophy is a powerful predictor of prognosis.

The occurrence of heart failure is reduced by 50% with antihypertensive therapy. Hypertensive left ventricular hypertrophy regresses with therapy and is most closely related to the degree of systolic blood pressure reduction. Diuretics have produced equal or greater reductions of left ventricular mass when compared with other drug classes.

β-Blockers are less effective in reducing left ventricular hypertrophy but play a specific role in patients with established coronary artery disease or impaired left ventricular function.

B. HYPERTENSIVE CEREBROVASCULAR DISEASE AND DEMENTIA Hypertension is the major predisposing cause of hemorrhagic and ischemic stroke. Cerebrovascular complications are more closely correlated with systolic than diastolic blood pressure. The incidence of these complications is markedly reduced by antihypertensive therapy. Preceding hypertension is associated with a higher incidence of subsequent dementia of both vascular and Alzheimer types.

Effective blood pressure control may modify the risk or rate of progression of cognitive dysfunction. C. HYPERTENSIVE RENAL DISEASE Chronic hypertension leads to nephrosclerosis, a common cause of renal insufficiency; aggressive blood pressure control attenuates the process. In patients with hypertensive nephropathy, the blood pressure should be 130/80 mm Hg or lower, especially when proteinuria is present.

Secondary renal disease is more common in blacks, particularly when accompanied by diabetes mellitus. Hypertension also plays an important role in accelerating the progression of other forms of renal disease, most commonly diabetic nephropathy. ACE inhibitors are particularly effective in preventing the latter complication, but these agents also appear to prevent the progression of other forms of nephropathy.

D. AORTIC DISSECTION Hypertension is a contributing factor in many patients with dissection of the aorta. E. ATHEROSCLEROTIC COMPLICATIONS Most Americans with hypertension die of complications of atherosclerosis, but the linkage between hypertension and atherosclerotic cardiovascular disease is not as clear as that with the previously discussed complications.

Effective antihypertensive therapy is thus less successful in preventing complications of coronary heart disease. Bibliography Dielis AW et al: The prothrombotic paradox of hypertension: role of the renin-angiotensin and kallikrein-kinin systems. Hypertension 2005;46:1236. [PMID: 16286563] Forette F et al: The prevention of dementia with antihypertensive treatment. Arch Intern Med 2002;162:2046. [PMID: 12374512] Izzo JL et al: Mechanisms and management of hypertensive heart disease: from left ventricular hypertrophy to heart failure.

Med Clin North Am 2004;88:1257. [PMID: 15331316] Lapu-Bula R et al: Diastolic heart failure: the forgotten manifestation of hypertensive heart disease. Curr Hypertens Rep 2004; 6:164. [PMID: 15128466] Luft FC: Hypertensive nephrosclerosis: update. Curr Opin Nephrol Hypertens 2004;13:147. [PMID: 15202608] Manolio TA et al: Hypertension and cognitive function: pathophysiologic effects of hypertension on the brain. Curr Hypertens Rep 2003;5:255. [PMID: 12724059] Persu A et al: Recent insights in the development of organ damage caused by hypertension. Acta Cardiol 2004;59:369. [PMID: 15368798]Provided by Arm Med Media

ata]Left ventricular hypertrophy ( LVH) is thickening of the heart muscle of the left ventricle of the heart, that is, left-sided ventricular hypertrophy.

Left ventricular hypertrophy

"Left ventricular hypertrophy From Wikipedia, the free encyclopedianavigation search""LVH"" redirects here. For the Las Vegas hotel, see LVH – Las Vegas Hotel and Casino. For French schools abbreviated ""LVH"", see Lycée Victor Hugo.

Left ventricular hypertrophy A heart with left ventricular hypertrophy in short-axis view Classification and external resources Specialty Cardiology ICD - 10 I51.7ICD - 9-CM 429.3Diseases DB 7659Me SH D017379 [ edit on Wikid

Contents [ hide ]1 Causes2 Diagnosis2.1 Echocardiography2.2 ECG criteria3 Treatment4 See also5 References Causes [ edit]While ventricular hypertrophy occurs naturally as a reaction to aerobic exercise and strength training, it is most frequently referred to as a pathological reaction to cardiovascular disease, or high blood pressure. [1] It is one aspect of ventricular remodeling. While LVH itself is not a disease, it is usually a marker for disease involving the heart.

[2] Disease processes that can cause LVH include any disease that increases the afterload that the heart has to contract against, and some primary diseases of the muscle of the heart. Causes of increased afterload that can cause LVH include aortic stenosis, aortic insufficiency and hypertension.

Primary disease of the muscle of the heart that cause LVH are known as hypertrophic cardiomyopathies, which can lead into heart failure. Long-standing mitral insufficiency also leads to LVH as a compensatory mechanism. Associated genes include OGN, osteoglycin.

[ citation needed]Diagnosis [ edit]The principal method to diagnose LVH is echocardiography, with which the thickness of the muscle of the heart can be measured.

The electrocardiogram (ECG) often shows signs of increased voltage from the heart in individuals with LVH, so this is often used as a screening test to determine who should undergo further testing. Echocardiography [ edit]Two dimensional echocardiography can produce images of the left ventricle. The thickness of the left ventricle as visualized on echocardiography correlates with its actual mass.

Normal thickness of the left ventricular myocardium is from 0.6 to 1.1 cm (as measured at the very end of diastole. If the myocardium is more than 1.1 cm thick, the diagnosis of LVH can be made. ECG criteria [ edit]Left ventricular hypertrophy with secondary repolarization abnormalities as seen on ECGThere are several sets of criteria used to diagnose LVH via electrocardiography.

[3] None of them are perfect, though by using multiple criteria sets, the sensitivity and specificity are increased.

The Sokolow-Lyon index: [4] [5]S in V 1 + R in V 5 or V 6 (whichever is larger) ≥ 35 mm (≥ 7 large squares)R in a VL ≥ 11 mm The Cornell voltage criteria [6] for the ECG diagnosis of LVH involve measurement of the sum of the R wave in lead a VL and the S wave in lead V 3.

The Cornell criteria for LVH are: S in V 3 + R in a VL > 28 mm (men)S in V 3 + R in a VL > 20 mm (women)The Romhilt-Estes point score system (""diagnostic"" >5 points; ""probable"" 4 points): ECG Criteria Points Voltage Criteria (any of): R or S in limb leads ≥20 mm S in V 1 or V 2 ≥30 mm R in V 5 or V 6 ≥30 mm3ST-T Abnormalities: ST-T vector opposite to QRS without digitalis ST-T vector opposite to QRS with digitalis3 1Negative terminal P mode in V 1 1 mm in depth and 0.04 sec in duration (indicates left atrial enlargement) 3Left axis deviation (QRS of -30° or more) 2QRS duration ≥0.09 sec 1Delayed intrinsicoid deflection in V 5 or V 6 (>0.05 sec) 1Other voltage-based criteria for LVH include: Lead I: R wave > 14 mm Lead a VR: S wave > 15 mm Lead a VL: R wave > 12 mm Lead a VF: R wave > 21 mm Lead V 5: R wave > 26 mm Lead V 6: R wave > 20 mm Treatment [ edit]The enlargement is not permanent in all cases, and in some cases the growth can regress with the reduction of blood pressure.

[7]LVH may be a factor in determining treatment or diagnosis for other conditions. For example, LVH causes a patient to have an irregular ECG. Patients with LVH may have to participate in more complicated and precise diagnostic procedures, such as imaging, in situations in which a physician could otherwise give advice based on an ECG. [8] [9]See also [ edit]Cardiomegaly Ventricular hypertrophy Primary hyperparathyroidism References [ edit]^ ""Ask the doctor: Left Ventricular Hypertrophy"". Retrieved 2007-12-07.^ Meijs MF, Bots ML, Vonken EJ, et al. (2007). ""Rationale and design of the SMART Heart study: A prediction model for left ventricular hypertrophy in hypertension"".

Neth Heart J. 15 (9): 295–8. doi: 10.1007/BF03086003. PMC 1995099. PMID 18030317.^ ""Lesson VIII - Ventricular Hypertrophy"". Retrieved 2009-01-07.^ Sokolow M, Lyon TP. The ventricular complex in left ventricular hypertrophy as obtained by unipolar precordial and limb leads.

Am Heart J. 1949;37:161–186.^ ""Time-Voltage QRS Area of the 12-Lead Electrocardiogram : Detection of Left Ventricular Hypertrophy -- Okin et al. 31 (4): 937 -- Hypertension"". Retrieved 2007-12-07.^ Casale PN, Devereux RB, Alonso DR, Campo E, Kligfield P (1987).

""Improved sex-specific criteria of left ventricular hypertrophy for clinical and computer interpretation of electrocardiograms: validation with autopsy findings"". Circulation. 75 (3): 565–72. doi: 10.1161/01. CIR.75.3.565. PMID 2949887.^ Gradman AH, Alfayoumi F (2006). ""From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease"".

Prog Cardiovasc Dis. 48 (5): 326–41. doi: 10.1016/j.pcad.2006.02.001. PMID 16627048.^ American Society of Nuclear Cardiology, ""Five Things Physicians and Patients Should Question"" (PDF), Choosing Wisely: an initiative of the ABIM Foundation, American Society of Nuclear Cardiology, archived from the original (PDF) on April 16, 2012, retrieved August 17, 2012^ Anderson, J. L.; Adams, C. D.; Antman, E. M.; Bridges, C. R.; Califf, R. M.; Casey, D. E.; Chavey, W. E.; Fesmire, F. M.; Hochman, J. S.; Levin, T. N.; Lincoff, A. M.; Peterson, E. D.; Theroux, P.; Wenger, N. K.; Wright, R. S. (2007). ""ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction): Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons: Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine"". Circulation. 116 (7): 803. doi: 10.1161/CIRCULATIONAHA.107.185752. [ show]v t e Cardiovascular disease (heart) ( I00–I52, 390–429)Categories: Cardiomegaly "

The most common ventricular hypertrophy occurs on the left side, but a recent study published in the journal Circulation found that right ventricular hypertrophy (RVH) is associated with an increased risk of heart failure and cardiovascular death in patients without clinically diagnosed heart disease at the start of the study.

Right Ventricular Hypertrophy Can Often Be Prevented

Features November 2012 Issue Story Tools E-Mail to a friend E-Mail to the editor Printer Friendly Right Ventricular Hypertrophy Can Often Be Prevented Untreated, RVH can lead to a weakened heart or even heart failure When the muscle thickens around one of the heart’s lower chambers, it is a condition known as ventricular hypertrophy.

The thicker heart muscle loses elasticity over time, causing the heart to work harder to effectively pump blood to the lungs, brain and the rest of the body. And eventually, the result can be heart failure (HF), as a weakened heart can no longer meet the demands of the body.

Those with RVH had double the risk of heart failure or death, compared to those subjects with normal right ventricle size. Researchers also determined that about one in 10 heart failure events and cardiovascular deaths may be attributed to thickening of the right ventricle. Cleveland Clinic cardiologist Corinne Bott-Silverman, MD, notes that any abnormality with the right ventricle can be a sign of health problems ahead.

She explains that RVH usually stems from one of three causes: congenital heart conditions, such as Tetralogy of Fallot or ventricular septal defects; pulmonary arterial hypertension; or pulmonary venous hypertension.

Pulmonary venous hypertension, which is high blood pressure related to the inability to effectively carry blood away from the lungs, can usually be traced to problems with the heart’s left side.

Pulmonary arterial hypertension, which occurs when the arteries in the lungs contrict abnormally, is associated with chronic lung diseases and conditions such as obstructive sleep apnea (OSA).“Almost anything that can cause right ventricular hypertrophy can be treated if you’re aware of that underlying cause,” Dr. Bott-Silverman says. “I don’t know that there’s anything that can reverse it, but you can keep it from getting worse. It’s kind of the end result of a lot of different insults to the heart.

The risk you run is that if the insult isn’t taken care of, the muscle weakens over time.”Identifying Causes Typically, RVH isn’t identified until the condition is causing you to have symptoms, such as shortness of breath or swelling (edema), due to fluid build-up.

But these are also early signs of heart failure, and Dr. Bott-Silverman urges anyone with HF risk factors to start to address them promptly. The most obvious first step you can take is to quit smoking, if you currently smoke, and to seek out smoking cessation aids and other forms of assistance from your physician.

Maintaining good respiratory health is a key to preserving right ventricular health. But among the most common, yet largely under-identified risk factors is sleep apnea. Anyone can have OSA, but carrying extra weight, especially around the neck, does raise your risk of the condition.

The most obvious signs are snoring and gasping for breath while sleeping—characteristics only a partner may notice. In addition, if you often get tired during the day, you may have OSA.“If you’re obese with sleep apnea, and you don’t take care of it, you can get right heart failure,” Dr. Bott-Silverman says.

In addition, if you have been diagnosed with left ventricular hypertrophy, there is a chance the condition can eventually lead to a thickening on the other side. The left ventricle has received the most attention in clinical research, largely because it is easier to image and it’s more strongly associated with common conditions like hypertension, according to the study’s author, Steve Kawut, MD, of the University of Pennsylvania.“These findings run counter to the traditional belief that for otherwise-healthy adults, the right ventricle plays a limited role in heart failure,” he says.

So if you have LVH, and have questions about RVH or other prospects related to your heart, share your concerns with your physician. Diagnosis and Treatment Swelling of the right ventricle can be seen in an electrocardiogram or echocardiogram, Dr. Bott-Silverman says.

But magnetic resonance imaging (MRI) is the most reliable, she adds. As she noted earlier, treating RVH usually involves treating the causes of the ventricular abnormality. Blood pressure medications and a heart-healthy lifestyle are important, but certain other drugs are specifically aimed at treating pulmonary hypertension.

If that’s the problem, your doctor may prescribe blood vessel dilators or vasodilators, such as epoprostenol (Flolan). Research has also shown that common erectile dysfunction drugs such as sildenafil (Viagra) and tadalafil (Cialis) can also be effective at opening up the pulmonary arteries. Read More on These Topics Meds Management Heart Failure Valves and Vessels Diet, Exercise and Supplements

. Losartan is also used to decrease the risk of stroke in people who have high blood pressure and a heart condition called left ventricular hypertrophy – or enlargement of the walls of the left side of the heart, says the National Institutes of Health.

What Is Losartan Potassium?

What Is Losartan Potassium? Be first to comment RATECurrently 3/5 Stars. 1 2 3 4 5Print PREVIOUS NEXTWhat is losartan potassium used for? It’s an antihypertensive drug prescribed to treat high blood pressure – either alone or in combination with other medications

Another reason losartan is prescribed is for the treatment of kidney disease in people with type 2 diabetes.

Losartan side effects include leg, knee or back pain; muscle cramps or weakness; diarrhea; heartburn and a decreased sensitivity to touch. Tell your doctor if you experience any of these side effects and they’re severe or don’t go away.

lve.hypertrophic subaortic stenosis ( idiopathic hypertrophic subaortic stenosis) a cardiomyopathy of unknown cause, in which the left ventricle is hypertrophied and the cavity is small; it is marked by obstruction to left ventricular outflow.

stenosis

Correct all you're your grammar errors instantly. Try it now.stenosis Also found in: Dictionary, Thesaurus, Legal, Financial, Encyclopedia, Wikipedia. Related to stenosis: pyloric stenosis, mitral stenosis, aortic stenosis, Spinal stenosis, Cervical stenosisstenosis [ stĕ-no´sis] (pl.

steno´ses) an abnormal narrowing or contraction of a body passage or opening; called also arctation, coarctation, and stricture.aortic stenosis obstruction to the outflow of blood from the left ventricle into the aorta; in themajority of adult cases the etiology is degenerative calcific disease of the va

mitral stenosis a narrowing of the left atrioventricular orifice ( mitral valve) due to inflammationand scarring; the cause is almost always rheumatic heart disease. Normally the leaflets openwith each pulsation of the heart, allowing blood to flow from the left atrium into the left ventricle,and close as the ventricle fills again so that they prevent a backward flow of blood.

In mitralstenosis there is a resultant increase of pressure in the pulmonary artery and hypertrophy of theleft ventricle. The usual treatment is surgical replacement of the valve.pulmonary stenosis (PS) narrowing of the opening between the pulmonary artery and the rightventricle.pyloric stenosis see pyloric stenosis.renal artery stenosis narrowing of one or both renal arteries by atherosclerosis or by fibrousdysplasia or hyperplasia, so that renal function is impaired (see ischemic nephropathy ).

Increased renin release by the affected kidney causes renovascular hypertension, and bilateralstenosis may result in chronic renal failure.spinal stenosis narrowing of the vertebral canal, nerve root canals, or intervertebral foramina of the lumbar spine, caused by encroachment of bone upon the space; symptoms are caused by compression of the cauda equina and include pain, paresthesias, and neurogenic claudication.

The condition may be either congenital or due to spinal degeneration.subaortic stenosis aortic stenosis due to an obstructive lesion in the left ventricle below theaortic valve, causing a pressure gradient across the obstruction within the ventricle.

See alsoidiopathic hypertrophic subaortic stenosis.subglottic stenosis stenosis of the trachea below the glottis. A congenital form results in neonatal stridor or laryngotracheitis, often requiring tracheotomy but resolving with age. An acquired form is caused by repeated intubations.tracheal stenosis scarring of the trachea with narrowing, usually as a result of injury from an artificial airway or trauma.tricuspid stenosis (TS) narrowing or stricture of the tricuspid orifice of the heart, a conditionoften seen in patients with severe congestive heart failure, usually the result of volume overloadand pulmonary hypertension with right ventricular and tricuspid annular dilation.

Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition.

© 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.ste·no·sis, pl.ste·no·ses ( ste-nō'sis, -sēz ), Do not confuse this word with atresia or occlusion. A stricture of any canal or orifice. [G. stenōsis, a narrowing]Farlex Partner Medical Dictionary © Farlex 2012stenosis/ste·no·sis/ ( stĕ-no´sis) pl.

steno´ses [Gr.] stricture; an abnormal narrowing or contraction of a duct or canal.aortic stenosis (AS) a narrowing of the aortic orifice of the heart or of the aorta near the valve.hypertrophic pyloric stenosis narrowing of the pyloric canal due to muscular hypertrophy andmucosal edema, usually in infants.hypertrophic subaortic stenosis , idiopathic hypertrophic subaortic stenosis (IHSS) a form of hypertrophic cardiomyopathy in which the left ventricle is hypertrophied and the cavity is small; it is marked by obstruction to left ventricular outflow.infantile hypertrophic gastric stenosis congenital hypertrophy and hyperplasia of themusculature of the pyloric sphincter, leading to partial obstruction of the gastric outlet.mitral stenosis a narrowing of the left atrioventricular orifice.pulmonary stenosis (PS) narrowing of the opening between the pulmonary artery and the rightventricle, usually at the level of the valve leaflets.pyloric stenosis obstruction of the pyloric orifice of the stomach; it may be congenital or acquired.renal artery stenosis narrowing of one or both renal arteries, so that renal function is impaired,resulting in renal hypertension and, if stenosis is bilateral, chronic renal failure.subaortic stenosis aortic stenosis due to an obstructive lesion in the left ventricle below theaortic valve, causing a pressure gradient across the obstruction within the ventricle.tricuspid stenosis (TS) narrowing or stricture of the tricuspid orifice of the heart.

Dorland's Medical Dictionary for Health Consumers. © 2007 by Saunders, an imprint of Elsevier, Inc. All rights reserved.stenosis (stə-nō′sĭs)n. pl. steno·ses (-sēz)A constriction or narrowing of a duct or passage; a stricture.ste·not′ic (-nŏt′ĭk) adj.

The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.stenosis [stinō′sis]Etymology: Gk, stenos, narrow, osis, conditionan abnormal condition characterized by the constriction or narrowing of an opening or passageway in a body structure. The term is commonly used to describe heart valve and vesselabnormalities as well as narrowing of joint spaces, as in cervical stenosis.

Kinds of stenosisinclude aortic stenosis and pyloric stenosis. stenotic, adj. Mosby's Medical Dictionary, 9th edition. © 2009, Elsevier.stenosis An abnormal ↓ in the diameter of a lumen, in particular of an artery or heart valve–eg, in ASHD with plaque buildup on the inner wall of an artery. See Aortic stenosis, Carotid stenosis, Cervical stenosis, Fishmouth stenosis, Hypertrophic pyloric stenosis, Meatal stenosis, Mitral stenosis, Occlusion, Pulmonary stenosis, Restenosis, Supravalvular aortic stenosis, Subvalvular pulmonary stenosis, Supravalvular pulmonary stenosis. Cf Regurgitation. Mc Graw-Hill Concise Dictionary of Modern Medicine. © 2002 by The Mc Graw-Hill Companies, Inc.ste·no·sis, pl.

stenoses ( stĕ-nō'sis, -sēz) A stricture of any canal, especially a narrowing of one of the cardiac valves. [G. stenōsis, a narrowing]Medical Dictionary for the Health Professions and Nursing © Farlex 2012stenosis (ste-no'sis) [Gr. stenosis, a narrowing]The constriction or narrowing of a passage or orifice. stenosed stenotic (ste-nost', ste-nozd',) (ste-not'ik), adjective Etiology Stenosis may result from embryonic maldevelopment, hypertrophy and thickening of a sphinctermuscle, inflammatory disorders, or excessive development of fibrous tissue.

It may involve almostany tube or duct.aortic stenosis Stenosis of blood flow from the left ventricle to the aorta due to aortic valve disease or obstructionsjust above or below the valve.

The stenosis may be congenital or secondary to diseases of adolescence or adulthood, e.g., rheumatic fever or fibrocalcific degeneration of the valve. It is themost common cardiac valve dysfunction in the U. S. Synonym: aortostenosis Symptoms Many patients with mild or moderate aortic stenosis, e.g., with a valve area that is more than 1 cm 2 or a valve gradient that is less than 50 mm Hg, have no symptoms and are unaware of theircondition.

A heart murmur is usually heard on physical examination of the patient. This murmur is best heard at the right second intercostal space during systole.

Palpation of the arteries in severeaortic stenosis may reveal a delayed and weakened pulse, e.g., at the carotids. The heart's apicalimpulse may be laterally and inferiorly displaced as a result of left ventricular hypertrophy.

Alarmingsymptoms include anginal chest pain, syncope, and dyspnea on exertion. When these occur,surgery to repair or replace the diseased valve are necessary. Physical Findings Transthoracic echocardiography (TTE) diagnoses aortic stenosis and helps to evaluate its severity,determine left ventricular size and function, and detect other valvular disease. Treatment If the aortic valve area is significantly narrowed, i.e., < 0.8 cm 2, or if the patient has experiencedsymptoms of heart failure or syncope, percutaneous balloon aortic valvuloplasty or aortic valvereplacement may be necessary.

Patient care A history of related cardiac disorders is obtained. Cardiopulmonary function is assessed regularly by monitoring vital signs and weight, intake, and output for signs of fluid overload.

The patient is monitored for chest pain, which may indicate cardiac ischemia, and the electrocardiogram is evaluated for ischemic changes. Activity tolerance and fatigue are assessed. After cardiac catheterization, the insertion site is checked according to protocol (often every 15 minfor 6 hr) for signs of bleeding; the patient is assessed for chest pain, and vital signs, heart rhythm,and peripheral pulses distal to the insertion site are monitored.

Problems are reported to thecardiologist. Desired outcomes for all aortic valve surgeries include adequate cardiopulmonary tissue perfusionand cardiac output, reduced fatigue with exertion, absence of fluid volume excess, and ability to manage the treatment regimen.

Patients with aortic stenosis (with or without surgical repair) requireprophylactic antibiotics before invasive procedures (including dental extractions, cleanings) because of the risk they pose for bacteremia and infective endocarditis.cicatricial stenosis Stenosis due to a contracted scar.coronary artery stenosis A physical obstruction to the flow of blood through the epicardial arteries, usually due to atherosclerotic plaque.diaphyseal medullary stenosis Hardcastle syndrome.infantile hypertrophic pyloric stenosis Pyloric stenosis.lumbar spinal stenosis Stenosis of the spinal canal due to degenerative or traumatic changes at the level of the lumbarvertebrae.

This condition causes back pain, often associated with pain that radiates into the legs,esp. when the patient is standing. Sitting often relieves the pain. The diagnosis is performed by spinal imaging, e.g., computed tomography or magnetic resonance imaging scanning. Treatmentsinclude physical therapy, braces, analgesic agents, and spinal surgery.mitral stenosis Abbreviation: MSStenosis of the mitral valve orifice with obstruction of blood flow from the left atrium to the leftventricle.

In most adults, previous bouts of rheumatic carditis are responsible for the lesion. Lessoften, MS may be present at birth (Lutembacher's disease), or it may develop as the mitral valvecalcifies during aging.

The abnormality of the valve may predispose patients to infective endocarditis; to left atrialenlargement and atrial arrhythmias; or to left ventricular failure.pulmonary stenosis Stenosis of the opening into the pulmonary artery from the right cardiac ventricle.pyloric stenosis Stenosis of the pyloric orifice.

In infants, excessive thickening of the pyloric sphincter or hypertrophyand hyperplasia of the mucosa and submucosa of the pylorus are usually responsible. Treatment In infants, treatment may involve open or laparoscopic division of the muscles of the pylorus. Infantile pyloric stenosis is usually diagnosed in the first 6 months of life when babies have troublewith vomiting after eating, sometimes with projectile vomiting and consequent dehydration.

Thedisease occurs in 2 to 3 infants per 1000 births and is more common in boys than girls. In adults,endoscopic stents may be placed to open malignant obstructions. Synonym: infantile hypertrophic pyloric stenosis; pyloristenosis RENAL ARTERY STENOSIS: (A) Renal arterystenosis (before angioplasty); (B) Renal arterystenosis (after angioplasty) (Courtesy of Arnold Klein, M. D., Northwest Permanente, P. C.)RENAL ARTERY STENOSIS: (A) Renal arterystenosis (before angioplasty); (B) Renal arterystenosis (after angioplasty) (Courtesy of Arnold Klein, M. D., Northwest Permanente, P. C.)renal artery stenosis Stenosis in one or both arteries that supply thekidneys; a relatively uncommon cause of hypertension.

In young women the cause is usually fibromuscular dysplasia of one or botharteries. In older people the cause is usuallyatherosclerosis. Treatment Patients may be treated medically with standardantihypertensive drugs, or, in some cases, withrenal artery angioplasty or bypass surgery. See: illustrationsubaortic stenosis A congenital stenosis of the aortic tract below the aortic valves.

See: hypertrophic cardiomyopathytricuspid stenosis Stenosis of the opening to the tricuspid valve. Medical Dictionary, © 2009 Farlex and Partnersstenosis Narrowing of a duct, orifice or tubular organ such as the intestinal canal or a bloodvessel.

Collins Dictionary of Medicine © Robert M. Youngson 2004, 2005Stenosis The narrowing of an opening or passage-way in the body. In arteries, stenosis is caused by a build-up of atherosclerotic plaque, disease, or other disorder. Mentioned in: Anesthesia, General, Balloon Valvuloplasty, Cervical Spondylosis, Congenital Heart Disease, Heart Surgery for Congenital Defects, Heart Valve Repair, Hydrocephalus, Pulmonary Valve Stenosis, Pyloric Stenosis, Spinal Stenosis, Transient Ischemic Attack, Trigger Finger, Valvular Heart Disease Gale Encyclopedia of Medicine.

Copyright 2008 The Gale Group, Inc. All rights reserved.stenosisnarrowing/constriction of a hollow structure Illustrated Dictionary of Podiatry and Foot Science by Jean Mooney © 2009 Elsevier Limited.

All rights reserved.stenosis (st ·nōˑ·sis),n a decrease in the size of a channel, passageway, or opening within a structure, such as pyloric stenosis or aortic stenosis. Stenosis. Jonas: Mosby's Dictionary of Complementary and Alternative Medicine. (c) 2005, Elsevier.ste·no·sis, pl. stenoses ( stĕ-nō'sis, -sēz) Stricture of any canal or orifice. [G. stenōsis, a narrowing]Medical Dictionary for the Dental Professions © Farlex 2012stenosis (stenō´sis),n narrowing or stricture of a duct, canal, or vessel.

Mosby's Dental Dictionary, 2nd edition. © 2008 Elsevier, Inc. All rights reserved.stenosisnarrowing or contraction of a body passage or opening. See also specific anatomical sites.aortic stenosisobstruction to the outflow of blood from the left ventricle into the aorta.

May be due to an anomaly of the valves (valvular), an obstruction in the ascending aorta (supravalvular), or an obstruction in the left ventricular outflow tract (subvalvular). See also aortic subvalvularstenosis, aortic valvular disease.esophageal stenosisa common cause of esophageal obstruction, caused commonly by esophageal trauma;congenital stenosis often associated with tracheoesophageal fistula.left atrioventricular stenosissee mitral stenosis (below), valvular stenosis.mesonephric duct stenosisoccurs as stenosis of the ductus deferens or epididymis; may be associated with renalaplasia.mitral stenosisa narrowing of the left atrioventricular orifice.

See also mitral commissurotomy.nasopharyngeal stenosisan acquired disorder in cats, usually following chronic upper respiratory infection, whichcauses upper airway obstruction with mucopurulent nasal discharge and a wheezingrespiration, which is relieved with open mouth breathing.paramesonephric duct stenosisfocal defects in the duct lead to segmental aplasia or stenosis of the uterine tube or horn.pulmonary artery stenosisthe commonest cardiac defect in dogs; it is a narrowing of the pulmonary outflow tract andmay occur in any one of a number of common sites including infundibular, valvular andsubvalvular.rectovaginal stenosissee rectovaginal constriction.right atrioventricular stenosissee tricuspid stenosis (below).subepiglottic stenosishas the effect of reducing air flow into and out of the lungs.tricuspid stenosisnarrowing or stricture of the tricuspid orifice of the heart.valvular stenosissee aortic, pulmonary, atrioventricular.

Saunders Comprehensive Veterinary Dictionary, 3 ed. © 2007 Elsevier, Inc. All rights reserved Patient discussion about stenosis Q. Why does Aortic stenosis causes an enlarged heart? My father was recently diagnosed as suffering from enlarged heart due to his Aortic stenosis.

what is the connection between those to conditions? As far as I understand that aortic stenosis mean that the aortic valve is too small nottoo large... A. there are several explanations for the enlargement of the heart that occurs due to Aorticstenosis.

the most reasonable is that the mechanical power that the heart uses makes it bigger. it easy to see it here: http://www.marvistavet.com/assets/images/aortic_stenosis.gifthis is called Left Ventricular Hypertrophy or LVH in abbreviations.this is a classic LVH E. C. G.http://www.frca.co.uk/images_main/resources/ECG/ECGresource39.jpg Q.

How does alcohol affect someone who has been diagnosed with aortic valve stenosis? My brother has been diagnosed with aortic valve stenosis and also is a smoker and does drinkalcohol on the weekends. He knows that he should stop smoking but what about the effects of alcohol? Does this also contribute to his stenosis?

A. Alcohol changes blood pressure and speed of the heart- that is not a good idea if you have an Aortic stenosis. Could probably makes things worst. I would avoid alcohol… but he should ask GP. Q. what does c4-5 mild central disk bulging impinging upon cervical cord without spinalstenosis or distortion of the cord.

mild righ neural foraminal narrowing from uncovertebral jointhypertropy mean A. Well this basically means there is a very small narrowing of the cervical (your neck area)spinal canal (where the spinal cord is), however the narrowing does not cause any damage to thespinal cord, therefore probably does not cause any major symptoms involving the nerves.

The c4-5 bulging part refers to the part in between the two cervical vertebras c4 and c5, in which the disc (a part in the spinal cord) is sliding a bit side-ways, but again, it does not seem to be causingany trouble.

More discussions about stenosis This content is provided by i Medix and is subject to i Medix Terms. The Questions and Answers are not endorsed or recommended and are made available by patients, not doctors. Want to thank TFD for its existence? Tell a friend about us, add a link to this page, or visit the webmaster's page for free fun content . Link to this page: Facebook Twitter Finally, Farlex brings you all the rules of English grammar, all in one place, explained in simple terms. The Farlex Grammar Bookis available now in paperback and e Book formats.

. In patients with hypertension and especially in those with left ventricular hypertrophy (LVH), there is an upward shift of the coronary perfusion pressure to 70 mm Hg for hypertensive patients and 80–90 mm Hg for those with hypertension and LVH, compared with normotensive controls of 60 mm Hg.

Hypertension and the J-curve phenomenon: implications for tight blood pressure control

Altmetric: 0 Citations: 7More detail Commentary Hypertension and the J-curve phenomenon: implications for tight blood pressure control Fabio Angeli, Gianpaolo Reboldi & Paolo Verdecchia The term J-curve is used in several fields of science to refer to a variety of J-shaped diagrams where a curve initially falls, but then rises to higher levels.

In cardiovascular (CV) medicine, the J-curve phenomenon arises when a risk factor becomes inversely related to risk below a certain point, whereas the more widely accepted positive risk association exists across most of the observed risk factor distribution. In simpler terms, when elevated blood pressure (BP) is lowered, the risk of CV events decreases, but lowering BP below a critical ‘nadir’ is no longer beneficial and possibly deleterious, thus shaping a J-curve.

This phenomenon was originally described for diastolic BP by Stewart 1 in 169 well-matched hypertensive patients treated and followed for 6.25 years. At the end of the study, the incidence of myocardial infarction (MI) was five times higher in the patients with achieved diastolic BP<90 mm Hg, compared with those who reached a diastolic BP of 100–109 mm Hg ( P <0.01).

Similar observations have been reported later by Cruickshank et al. 2 on 902 hypertensive patients treated with atenolol in combination with other drugs and followed for a mean of 6.1 years.

They observed a J-curve relationship between diastolic BP, and MI and death in patients with coronary artery disease (CAD). More recently, some post-hoc analyses of randomized clinical trials documented a J-shaped relationship between systolic BP and the risk of CV events ( Figure 1, left panel) and cast doubts to what level the systolic BP should be lowered to optimize treatment. 3Figure 1Clinical trials demonstrating a J-curve effect for cardiovascular events (left panel) and clinical studies without clear evidence of the J-curve phenomenon (right panel).

Data from references 3, 4, 5. Data from The International Verapamil-Trandopril Study (INVEST), Valsartan Antihypertensive Long-Term Use Evaluation (VALUE) trial, Ongoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial (ONTARGET), Physicians’ Health Study (PHS) and Women’s Health Study (WHS) and Cardiovascular Heart Study (CHS).

Full size image On the contrary, there are some studies where such an effect has not been clearly demonstrated 3, 4, 5 ( Figure 1, right panel). For example, in the physicians and women’s studies by Glynn et al., 4 no J-curve effect for CV disease was noted in both women and men.

In the Cardiovascular Health Study, 5 after adjustment for potential confounders, systolic and diastolic BP were directly associated with the risk of incident MI and stroke. In the adjusted model for MI, a 1-standard deviation (s.d.) change in systolic and diastolic BP was associated with hazard ratios (HRs) of 1.24 (95% confidence interval (CI): 1.15–1.35) and 1.13 (95% CI: 1.04–1.22), respectively.

For stroke, the HRs were 1.34 (95% CI: 1.21–1.47) with systolic BP and 1.29 (95% CI: 1.17–1.42) with diastolic BP. The associations between systolic and diastolic BP levels and CV disease risk were generally linear; specifically, there was no evidence of a J-shaped relationship.

The same study also showed any increase in CV complications with decrease in pulse pressure (PP). Specifically, in multivariable models a 1-SD change in PP was associated with HR of 1.21 (95% CI: 1.12–1.31) for both MI or stroke. Mechanisms of J-curve The question is at what pathophysiologic BP range the J-curve may occur. Although the underlying mechanisms which may explain a J-curve association between CV risk and systolic BP are still elusive, some possible explanations have been proposed to link low diastolic BP levels and coronary complications. As coronary artery perfusion occurs predominantly during diastole, an association could be expected between diastolic BP and coronary artery perfusion

Below these pressures the coronary blood flow decreases and the oxygen extraction increases. In addition, low perfusion pressure is associated to severely impaired coronary autoregulation especially in presence of coronary epicardial stenosis and predisposes to severe ischemia of the subendocardial myocardium or MI 1, 2 ( Figure 2 ).

Figure 2Possible mechanisms that increase the risk of manifesting a J-curve effect with low diastolic blood pressure in patients with coronary artery disease, hypertension and left ventricular hypertrophy.

In patients with coronary stenosis, the autoregulation of coronary blood flow is compromised and a fall in diastolic blood pressure might lower the perfusion pressure distal to the epicardial artery stenosis below a critical level at which the autoregulation is no longer functional and the fractional flow reserve is compromised and may lead to myocardial ischemia and myocardial infarction.

This is further aggravated with the coexistence of hypertension and left ventricular hypertrophy. Full size image In contrast to the coronary circulation, the cerebral circulation depends mostly on systolic BP. In particular, cerebral blood flow is not seriously affected by low diastolic BP and could explain the lack of a J-curve effect regarding strokes at low diastolic BP in contrast with CV and coronary complications.

5New insights For more 30 years there has been controversy regarding the clinical significance of the J-curve, especially in individuals receiving antihypertensive therapy and with a history of known CAD.

Recently, some effect modifiers in influencing the presence or absence of a J-curve in predicting CV disease risk have been investigated. The results of the study by Yamazaki et al. 6 published in the current issue of the Journal add new data in this intriguing area.

Briefly, this prospective survey with central registry was designed to investigate drug use among 28 536 hypertensive subjects treated with valsartan. The primary end point was defined as cerebrovascular or cardiac events. The relationship between end points and BP measured at the last visit or before the occurrence of events was performed post hoc.

During a median follow-up of 2.93 years, 550 patients developed a cerebrovascular event and 576 a cardiac event.

Higher BP achieved during treatment (systolic BP ⩾ 140 mm Hg and diastolic BP ⩾ 90 mm Hg) were stronger risk factors for the incidence of both cerebrovascular and cardiac events and the risks of developing these events were increased in an age-dependent manner. A weak, but significant, systolic J-curve phenomenon was only observed in elderly patients ( ⩾ 75 years) for cardiac events: subjects with achieved systolic BP<120 mm Hg showed an HR for cardiac events of 1.90 (95% CI: 1.18–2.99, P =0.008) when compared with hypertensive patients with achieved systolic BP ranging from 130 to 140 mm Hg.

Although intriguing, these findings are open to some observations and should be cautiously interpreted. First, the results show that aging has an important role as potential effect modifier in influencing the manifestation of a J-curve paradox in hypertension. Notably, elderly patients are more likely to have isolated systolic hypertension (ISH; that is, increased PP), especially in association with CAD and hemodynamically significant coronary artery stenosis.

Importantly, PP has been shown to be a marker of increased large artery stiffness and an independent predictor of increased CV disease risk. In the context of this study, low values of systolic BP did not exclude high levels of PP for the coexistence of very low diastolic BP.

Second, antihypertensive therapy in the elderly person with ISH preferentially decreases systolic over diastolic BP, lowers PP, decreases arterial stiffness, and therefore, may improve the coronary oxygen supply/demand ratio of the left ventricle (thereby protecting it from ischemia). In addition, orthostatic hypotension is relatively common in elderly patients and may be intensified by antihypertensive drugs.

Notably, the presence of orthostatic hypotension has been associated with a 3.5-fold increase in the risk of CAD. 7Taken together, these observations suggest that the systolic BP J-curve documented in this study is more compatible with reverse causality than with antihypertensive drug overtreatment. Reverse causality occurs when a disease event causes reduction in the primary risk factor (in our case BP), making the event rate appear higher than it should be at lower risk levels.

In other words, low systolic BP might be only an epiphenomenon related to an underlying chronic debilitating illness and/or cardiac dysfunction. Finally, a J-curve for diastolic BP in elderly hypertensives was not observed by the Authors 6 of the study and, consequently, the effect of low diastolic BP on the exacerbation of treatment-induced coronary ischemia is not supported.

Comparison of different BP targets Only few trials have directly compared BP goals to test the hypothesis that attained BPs below the usual goal of less than 140/90 mm Hg improve outcomes.

In a recent Japanese (JATOS) Study, 8 4418 older hypertensive patients were randomized to either a systolic BP reduction to <140 mm Hg or to ⩾ 140 mm Hg and followed for 2 years.

At the end of the study, there was no difference in the primary end point of CV disease or renal failure between the two groups.

Similar observations were also reported from the Action to Control Cardiovascular Risk in Diabetes study, 9 in which there was no difference between the intensively (systolic BP<120 mm Hg) and less intensively (systolic BP<140 mm Hg) treated groups with respect to a composite of CV events. However, the incidence of stroke, a pre-specified secondary end point, was significantly lower in the tight control group. Conversely, the Studio Italiano Sugli Effetti Cardiovascolari del Controllo della Pressione Arteriosa Sistolica (Cardio-Sis) 10 clearly demonstrated that a tight BP control in non-diabetic patients with hypertension is associated to an improved CV prognosis.

In particular, the composite pool of pre-specified CV events and death occurred less frequently in the tight (<130 mm Hg) than in the usual (<140 mm Hg) control group (HR: 0.50;CI: 0.31–0.79; P =0.003). 10Recommendations in clinical practice Antihypertensive treatment reduces the risk of all CV events across all age and BP strata to a similar extent, and the absolute benefit of treatment increased with age.

The standard goal of antihypertensive therapy (that is, <140/90 mm Hg) is well established and should be maintained in all hypertensive patients. Despite their obvious limitations, post-hoc analyses of trial data indicate a progressive reduction in the incidence of CV events with progressive lowering of systolic BP down to about 120 mm Hg, and diastolic BP down to about 75 mm Hg, although the additional benefit at low BP values becomes rather small.

A J-curve phenomenon is unlikely to occur until lower values are reached, except perhaps in patients with advanced CAD. In these patients, the optimal BP target remains undefined. References1. Stewart IM. Relation of reduction in pressure to first myocardial infarction in patients receiving treatment for severe hypertension. Lancet 1979; 1: 861–865. Show context CAS Pub Med Article2. Cruickshank JM, Thorp JM, Zacharias FJ. Benefits and potential harm of lowering high blood pressure. Lancet 1987; 1: 581–584. Show context CAS Pub Med Article3.

Verdecchia P, Angeli F, Cavallini C, Mazzotta G, Garofoli M, Martire P, Reboldi G. The optimal blood pressure target for patients with coronary artery disease. Curr Cardiol Rep 2010; 12: 302–306. Show context Pub Med Article4. Glynn RJ, L’Italien GJ, Sesso HD, Jackson EA, Buring JE.

Development of predictive models for long-term cardiovascular risk associated with systolic and diastolic blood pressure. Hypertension 2002; 39: 105–110. Show context CAS Pub Med Article5. Psaty BM, Furberg CD, Kuller LH, Cushman M, Savage PJ, Levine D, O'Leary DH, Bryan RN, Anderson M, Lumley T. Association between blood pressure level and the risk of myocardial infarction, stroke, and total mortality: the cardiovascular health study.

Arch Intern Med 2001; 161: 1183–1192. Show context CAS Pub Med Article6. Yamazaki T, Kohro T, Chujo M, Ishigaki M, Hashimoto T. The occurrence rate of cerebrovascular and cardiac events in patients receiving antihypertensive therapy from the post-marketing surveillance data for valsartan in Japan (J-VALID). Hypertens Res 2013; 36: 140–150. Show context Pub Med Article7. Rose KM, Tyroler HA, Nardo CJ, Arnett DK, Light KC, Rosamond W, Sharrett AR, Szklo M. Orthostatic hypotension and the incidence of coronary heart disease: the atherosclerosis risk in communities study.

Am J Hypertens 2000; 13: 571–578. Show context CAS Pub Med Article8. JATOS Study Group. Principal results of the Japanese trial to assess optimal systolic blood pressure in elderly hypertensive patients (jatos). Hypertens Res 2008; 31: 2115–2127. Show context Pub Med Article9. Cushman WC, Evans GW, Byington RP, Goff DC, Grimm RH, Cutler JA, Simons-Morton DG, Basile JN, Corson MA, Probstfield JL, Katz L, Peterson KA, Friedewald WT, Buse JB, Bigger JT, Gerstein HC, Ismail-Beigi F. Effects of intensive blood-pressure control in type 2 diabetes mellitus.

N Engl J Med 2010; 362: 1575–1585. Show context CAS Pub Med Article10. Verdecchia P, Staessen JA, Angeli F, de Simone G, Achilli A, Ganau A, Mureddu G, Pede S, Maggioni AP, Lucci D, Reboldi G. Usual versus tight control of systolic blood pressure in non-diabetic patients with hypertension (cardio-sis): an open-label randomised trial. Lancet 2009; 374: 525–533. Show context Pub Med Article Download references Author information Affiliations Section of Cardiology, Hospital Media Valle del Tevere, Perugia, Italy Fabio Angeli Department of Internal Medicine, University of Perugia, Perugia, Italy Gianpaolo Reboldi Department of Internal Medicine, Hospital of Assisi, Assisi, Italy. Paolo Verdecchia Corresponding author Correspondence to Fabio Angeli.

Left ventricular hypertrophy is more common in people who have uncontrolled high blood pressure. But no matter what your blood pressure is, developing left ventricular hypertrophy puts you at higher risk for a heart attack and stroke. Treating high blood pressure can help ease your symptoms and may reverse left ventricular hypertrophy.

Overview

Overview Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some factor — such as high blood pressure or a heart condition — that causes the left ventricle to work harder.

As the workload increases, the muscle tissue in the chamber wall thickens, and sometimes the size of the chamber itself also increases. The enlarged heart muscle loses elasticity and eventually may fail to pump with as much force as needed.

Symptoms Left ventricular hypertrophy usually develops gradually. You may experience no signs or symptoms, especially during the early stages of the condition. As left ventricular hypertrophy progresses, you may experience: Shortness of breath Fatigue Chest pain, often after exercising Sensation of rapid, fluttering or pounding heartbeats (palpitations)Dizziness or fainting When to see a doctor Seek emergency care if: You feel chest pain that lasts more than a few minutes You have severe difficulty breathing You have severe, recurring lightheadedness or lose consciousness If you experience mild shortness of breath or other symptoms, such as palpitations, see your doctor.

If you have high blood pressure or another condition that increases your risk of left ventricular hypertrophy, your doctor is likely to recommend regular appointments to monitor your heart.

Even if you feel well, you need to have your blood pressure checked annually, or more often if you: Smoke Are overweight Have other conditions that increase the risk of high blood pressure Request an Appointment at Mayo Clinic Causes Left ventricular hypertrophy can occur when some factor makes your heart work harder than normal to pump blood to your body. Factors that can cause your heart to work harder include: High blood pressure (hypertension). This is the most common cause of left ventricular hypertrophy.

More than one-third of people show evidence of left ventricular hypertrophy at the time of their diagnosis with hypertension. Aortic valve stenosis. This disease is a narrowing of the tissue flap (aortic valve) that separates the left ventricle from the large blood vessel leaving your heart (aorta). The narrowing of the aortic valve requires the left ventricle to work harder to pump blood into the aorta.

Hypertrophic cardiomyopathy. This genetic disease occurs when the heart muscle becomes abnormally thick, making it harder for the heart to pump blood. Athletic training. Intense, prolonged endurance and strength training can cause the heart to adapt to handle the extra workload.

It's unclear whether this athletic type of left ventricle hypertrophy can lead to stiffening of the heart muscle and disease. Risk factors In addition to hypertension and aortic valve stenosis, factors that increase your risk for left ventricular hypertrophy include: Age. Left ventricular hypertrophy is more common in older people. Weight. Being overweight increases your risk of high blood pressure and left ventricular hypertrophy.

Family history. Certain genetic conditions are associated with developing hypertrophy. Diabetes. Race. African-Americans are at higher risk of left ventricular hypertrophy than are white people with similar blood pressure measurements.

Sex. Women with hypertension are at higher risk of left ventricular hypertrophy than are men with similar blood pressure measurements.

Complications Left ventricular hypertrophy changes the structure and working of the heart. The enlarged left ventricle can: Weaken Stiffen and lose elasticity, preventing the chamber from filling properly and increasing pressure in the heart Compress the chamber's blood vessels (coronary arteries) and restrict its supply of blood As a result of these changes, complications of left ventricular hypertrophy include: Interruption of blood supply to the heart Inability of the heart to pump enough blood to your body (heart failure)Abnormal heart rhythm (arrhythmia)Irregular, often rapid heartbeat (atrial fibrillation) that decreases blood flow to the body Insufficient supply of oxygen to the heart (ischemic heart disease)Enlargement of a section of the aorta (aortic root dilation)Stroke Sudden, unexpected loss of heart function, breathing and consciousness (sudden cardiac arrest)Prevention The best way to prevent left ventricular hypertrophy is to maintain healthy blood pressure.

To better manage your blood pressure: Monitor high blood pressure. Purchase a home blood pressure measuring device and check your blood pressure frequently. Schedule regular checkups with your doctor. Make time for exercise. Regular exercise helps to lower blood pressure and keep it at normal levels.

Aim for 30 minutes of moderate activity most days of the week. Watch your diet. Avoid foods that are high in fat and salt, and eat more fruits and vegetables. Avoid alcoholic beverages or drink them in moderation. Quit smoking. Giving up smoking improves your blood pressure and overall health.

By Mayo Clinic Staff Request an Appointment at Mayo Clinic Diagnosis & treatment June 06, 2015Share on: Facebook Twitter References Related Dizziness Shortness of breath Left ventricular hypertrophy Symptoms & causes Diagnosis & treatment Advertisement Mayo Clinic does not endorse companies or products.

Advertising revenue supports our not-for-profit mission. Advertising & Sponsorship Policy Opportunities Ad Choices Mayo Clinic Marketplace Check out these best-sellers and special offers on books and newsletters from Mayo Clinic. FREE TRIAL – Mayo Clinic Health Letter Best Treatment Strategies for Arthritis Mayo Clinic on Digestive Health Effective Home Remedies from Mayo Clinic The Mayo Clinic Diet Online CON-20374296Patient Care & Health Information Diseases & Conditions Left ventricular hypertrophy

High blood pressure forces your heart to work harder than necessary in order to pump blood to the rest of your body. This causes the left ventricle to thicken or stiffen (left ventricular hypertrophy). These changes limit the ventricle's ability to pump blood to your body.

High blood pressure dangers: Hypertension's effects on your body

High blood pressure dangers: Hypertension's effects on your body High blood pressure is a risk factor for more than heart disease. Discover what complications high blood pressure can cause. By Mayo Clinic Staff High blood pressure complications High blood pressure (hypertension) can quietly damage your body for years before symptoms develop.

Left uncontrolled, you may wind up with a disability, a poor quality of life or even a fatal heart attack. Roughly half the people with untreated hypertension die of heart disease related to poor blood flow (ischemic heart disease) and another third die of stroke.

Treatment and lifestyle changes can help control your high blood pressure to reduce your risk of life-threatening complications. Here's a look at the complications high blood pressure can cause when it's not effectively controlled.

Damage to your arteries Healthy arteries are flexible, strong and elastic. Their inner lining is smooth so that blood flows freely, supplying vital organs and tissues with nutrients and oxygen. Hypertension gradually increases the pressure of blood flowing through your arteries. As a result, you might experience: Damaged and narrowed arteries. High blood pressure can damage the cells of your arteries' inner lining. When fats from your diet enter your bloodstream, they can collect in the damaged arteries.

Eventually, your artery walls become less elastic, limiting blood flow throughout your body. Aneurysm. Over time, the constant pressure of blood moving through a weakened artery can cause a section of its wall to enlarge and form a bulge (aneurysm). An aneurysm can potentially rupture and cause life-threatening internal bleeding. Aneurysms can form in any artery throughout your body, but they're most common in your body's largest artery (aorta).

Damage to your heart Your heart pumps blood to your entire body. Uncontrolled high blood pressure can damage your heart in a number of ways, such as: Coronary artery disease.

Coronary artery disease affects the arteries that supply blood to your heart muscle. Arteries narrowed by coronary artery disease don't allow blood to flow freely through your arteries. When blood can't flow freely to your heart, you can experience chest pain, a heart attack or irregular heart rhythms (arrhythmias). Enlarged left heart.

This condition increases your risk of heart attack, heart failure and sudden cardiac death. Heart failure. Over time, the strain on your heart caused by high blood pressure can cause your heart muscle to weaken and work less efficiently. Eventually, your overwhelmed heart simply begins to wear out and fail. Damage from heart attacks adds to this problem.

Damage to your brain Just like your heart, your brain depends on a nourishing blood supply to work properly and survive. But high blood pressure can cause several problems, including: Transient ischemic attack (TIA). Sometimes called a ministroke, a transient ischemic (is-KEE-mik) attack is a brief, temporary disruption of blood supply to your brain. It's often caused by atherosclerosis or a blood clot — both of which can arise from high blood pressure.

A transient ischemic attack is often a warning that you're at risk of a full-blown stroke. Stroke. A stroke occurs when part of your brain is deprived of oxygen and nutrients, causing brain cells to die. Uncontrolled high blood pressure can lead to stroke by damaging and weakening your brain's blood vessels, causing them to narrow, rupture or leak. High blood pressure can also cause blood clots to form in the arteries leading to your brain, blocking blood flow and potentially causing a stroke.

Dementia. Dementia is a brain disease resulting in problems with thinking, speaking, reasoning, memory, vision and movement. There are a number of causes of dementia. One cause, vascular dementia, can result from narrowing and blockage of the arteries that supply blood to the brain.

It can also result from strokes caused by an interruption of blood flow to the brain. In either case, high blood pressure may be the culprit. Mild cognitive impairment. Mild cognitive impairment is a transition stage between the changes in understanding and memory that come with aging and the more-serious problems caused by Alzheimer's disease.

Like dementia, it can result from blocked blood flow to the brain when high blood pressure damages arteries. Damage to your kidneys Your kidneys filter excess fluid and waste from your blood — a process that depends on healthy blood vessels. High blood pressure can injure both the blood vessels in and leading to your kidneys, causing several types of kidney disease (nephropathy). Having diabetes in addition to high blood pressure can worsen the damage.

Kidney failure. High blood pressure is one of the most common causes of kidney failure. That's because it can damage both the large arteries leading to your kidneys and the tiny blood vessels (glomeruli) within the kidneys. Damage to either makes it so your kidneys can't effectively filter waste from your blood.

In this condition, the walls of the left and/or right ventricles of the heart become thin and stretched. The result is an enlarged heart. In the other types of cardiomegaly, the heart's large muscular left ventricle becomes abnormally thick. Hypertrophy is usually what causes left ventricular enlargement.

Cardiomegaly

"From Wikipedia, the free encyclopedianavigation search Cardiomegaly Cardiomegaly on chest X-ray and a pacemaker Classification and external resources Specialty cardiology ICD - 10 I51.7ICD - 9-CM 429.3Diseases DB 30769Me SH D006332 [ edit on Wikidata]Cardiomegaly is a medical condition in which the heart is enlarged

. It is more commonly referred to as an enlarged heart. The causes of cardiomegaly may vary. Many times this condition results from high blood pressure ( hypertension) or coronary artery disease. An enlarged heart may not pump blood effectively, resulting in congestive heart failure. Cardiomegaly may improve over time, but many people with an enlarged heart need lifelong treatment with medications.

[1] Having an immediate family member who has or had cardiomegaly may indicate that a person is more susceptible to getting this condition. [2] Cardiomegaly is not a disease but rather a condition that can result from a host of other diseases such as obesity or coronary artery disease. Recent studies suggest that cardiomegaly is associated with a higher risk of sudden cardiac death (SCD).

[3]Contents [ hide ]1 Mechanism2 Signs and symptoms3 Diagnosis4 Cause and prevention5 Treatment and prognosis6 Recent research7 See also8 References9 External links Mechanism [ edit]Cardiomegaly is a condition affecting the cardiovascular system, specifically the heart. This condition is strongly associated with congestive heart failure. [2] Within the heart, the working fibers of the myocardial tissue increase in size.

As the heart works harder the actin and myosin filaments experience less overlap which increases the size of the myocardial fibers.

If there is less overlap of the protein filaments actin and myosin within the sarcomeres of muscle fibers, they will not be able to effectively pull on one another. If the heart tissue (walls of left and right ventricle) gets too big and stretches too far, then those filaments cannot effectively pull on one another to shorten the muscle fibers, thus impacting the heart's sliding filament mechanism.

If fibers cannot shorten properly, and the heart cannot contract properly, then blood cannot be effectively pumped to the lungs to be re-oxygenated and to the body to deliver oxygen to the working tissues of the body. Signs and symptoms [ edit]For many people cardiomegaly is asymptomatic. For others, if the enlarged heart begins to affect the body's ability to pump blood effectively, then symptoms associated with congestive heart failure may arise. [2]Heart palpitations – irregular beating of the heart, usually associated with a valve issue inside the heart.

Severe shortness of breath (especially when physically active) – irregularly unable to catch one's breath. Chest pain Fatigue Swelling in legs Increased abdominal girth Weight gain Edema – swelling Fainting [2]Diagnosis [ edit]There are two main types of cardiomegaly: Dilated cardiomyopathy is the most common type of cardiomegaly.

Losartan is used alone or in combination with other medications to treat high blood pressure. Losartan is also used to decrease the risk of stroke in people who have high blood pressure and a heart condition called left ventricular hypertrophy (enlargement of the walls of the left side of the heart).

Losartan

Losartanpronounced as (loe sar' tan)Why is this medication prescribed? How should this medicine be used?

Other uses for this medicine What special precautions should I follow? What special dietary instructions should I follow? What should I do if I forget a dose? What side effects can this medication cause? What should I know about storage and disposal of this medication?

In case of emergency/overdose What other information should I know? Brand names Brand names of combination products IMPORTANT WARNING: Tell your doctor if you are pregnant or plan to become pregnant.

Do not take losartan if you are pregnant. If you become pregnant while you are taking losartan, stop taking losartan and call your doctor immediately. Losartan may cause death or serious injury to the fetus when taken in the last 6 months of pregnancy. Why is this medication prescribed?

Losartan may not decrease the risk of stroke in African Americans who have these conditions. This medication is also used to treat kidney disease in people who have type 2 diabetes (condition in which the body does not use insulin normally and therefore cannot control the amount of sugar in the blood) and high blood pressure.

Losartan is in a class of medications called angiotensin II receptor antagonists. It works by blocking the action of certain natural substances that tighten the blood vessels, allowing the blood to flow more smoothly and the heart to pump more efficiently. High blood pressure is a common condition, and when not treated it can cause damage to the brain, heart, blood vessels, kidneys, and other parts of the body. Damage to these organs may cause heart disease, a heart attack, heart failure, stroke, kidney failure, loss of vision, and other problems.

In addition to taking medication, making lifestyle changes will also help to control your blood pressure. These changes include eating a diet that is low in fat and salt, maintaining a healthy weight, exercising at least 30 minutes most days, not smoking, and using alcohol in moderation.

How should this medicine be used? Losartan comes as a tablet to take by mouth. It is usually taken once or twice a day with or without food.

To help you remember to take losartan, take it at around the same time (s) every day. Follow the directions on your prescription label carefully, and ask your doctor or pharmacist to explain any part you do not understand. Take losartan exactly as directed. Do not take more or less of it or take it more often than prescribed by your doctor.

Your doctor will probably start you on a low dose of losartan and gradually increase your dose. If your child can not swallow a tablet, talk to your doctor or pharmacist.

The pharmacist can prepare a liquid form of this medication for your child. Losartan controls high blood pressure but does not cure it. Your blood pressure may decrease during the first week of your treatment, but it may take 3 to 6 weeks for you to notice the full benefit of losartan. Continue to take losartan even if you feel well. Do not stop taking losartan without talking to your doctor.

Ask your pharmacist or doctor for a copy of the manufacturer's information for the patient. Other uses for this medicine Losartan is also sometimes used to treat heart failure (condition in which the heart is unable to pump enough blood to the rest of the body).

Talk to your doctor about the possible risks of using this medication for your condition. This medication may be prescribed for other uses; ask your doctor or pharmacist for more information. What special precautions should I follow? Before taking losartan,tell your doctor and pharmacist if you are allergic to losartan, any other medications, or any of the ingredients in losartan tablets.

Ask your pharmacist for a list of the ingredients.tell your doctor if you have diabetes (high blood sugar) and you are taking aliskiren (Tekturna, in Amturnide, Tekamlo, Tekturna HCT).

Your doctor will probably tell you not to take losartan if you have diabetes and you are also taking aliskiren.tell your doctor and pharmacist what other prescription and nonprescription medications, vitamins, nutritional supplements, and herbal products you are taking or plan to take.

Be sure to mention any of the following: angiotensin-converting enzyme (ACE) inhibitors such as benazepril (Lotensin, in Lotrel), captopril (Capoten, in Capozide), enalapril (Vasotec), fosinopril, lisinopril (in Prinzide, in Zestoretic), moexipril (Univasc, in Uniretic), perindopril (Aceon), quinapril (Accupril, in Accuretic, in Quinaretic), ramipril (Altace), and trandolapril (Mavik, in Tarka); aspirin and other nonsteroidal anti-inflammatory medications (NSAIDs) such as ibuprofen (Advil, Motrin) and naproxen (Aleve, Naprosyn), and selective COX-2 inhibitors such as celecoxib (Celebrex); diuretics ('water pills') including potassium-sparing diuretics such as amiloride (Midamor), spironolactone (Aldactone, in Aldactazide), and triamterene (Dyrenium, in Dyazide, in Maxzide); fluconazole (Diflucan); lithium ( Lithobid); phenobarbital; potassium supplements; and rifampin (Rifadin, Rimactane, in Rifamate, in Rifater).

Your doctor may need to change the doses of your medications or monitor you carefully for side effects.tell your doctor if you have or have ever had heart failure or kidney or liver disease.tell your doctor if you are breastfeeding.you should know that losartan may cause dizziness, lightheadedness, and fainting when you get up too quickly from a lying position.

This is more common when you first start taking losartan. To help avoid this problem, get out of bed slowly, resting your feet on the floor for a few minutes before standing up.you should know that diarrhea, vomiting, not drinking enough fluids, and sweating a lot can cause a drop in blood pressure, which may cause lightheadedness and fainting.

Tell your doctor if you have any of these problems or develop them during your treatment. What special dietary instructions should I follow? Do not use salt substitutes containing potassium without talking to your doctor. If your doctor prescribes a low-salt or low-sodium diet, follow these directions carefully.

What should I do if I forget a dose? Take the missed dose as soon as you remember it. However, if it is almost time for the next dose, skip the missed dose and continue your regular dosing schedule.

Do not take a double dose to make up for a missed one. What side effects can this medication cause? Losartan may cause side effects. Tell your doctor if any of these symptoms are severe or do not go away:leg, knee, or back painmuscle cramps or weaknessdiarrheaheartburndecreased sensitivity to touch Some side effects can be serious.

If you experience any of these symptoms or those listed in the SPECIAL PRECAUTIONS section, call your doctor immediately:swelling of the face, throat, tongue, lips, eyes, hands, feet, ankles, or lower legshoarsenessdifficulty breathing or swallowingchest pain Losartan may cause other side effects. Call your doctor if you have any unusual problems while taking this medication. If you experience a serious side effect, you or your doctor may send a report to the Food and Drug Administration's (FDA) Med Watch Adverse Event Reporting program online ( http://www.fda.gov/Safety/Med Watch) or by phone (1-800-332-1088).

What should I know about storage and disposal of this medication? Keep this medication in the container it came in, tightly closed, and out of reach of children. Store it at room temperature and away from excess heat, light, and moisture (not in the bathroom).

It is important to keep all medication out of sight and reach of children as many containers (such as weekly pill minders and those for eye drops, creams, patches, and inhalers) are not child-resistant and young children can open them easily. To protect young children from poisoning, always lock safety caps and immediately place the medication in a safe location – one that is up and away and out of their sight and reach.

http://www.upandaway.org Unneeded medications should be disposed of in special ways to ensure that pets, children, and other people cannot consume them. However, you should not flush this medication down the toilet. Instead, the best way to dispose of your medication is through a medicine take-back program. Talk to your pharmacist or contact your local garbage/recycling department to learn about take-back programs in your community.

See the FDA's Safe Disposal of Medicines website ( http://goo.gl/c4Rm4p) for more information if you do not have access to a take-back program. In case of emergency/overdose In case of overdose, call the poison control helpline at 1-800-222-1222. Information is also available online at https://www.poisonhelp.org/help. If the victim has collapsed, had a seizure, has trouble breathing, or can't be awakened, immediately call emergency services at 911.

Symptoms of overdose may include the following:dizzinessfaintingfast or slow heartbeat What other information should I know? Keep all appointments with your doctor and the laboratory. Your blood pressure should be checked regularly to determine your response to losartan.

Do not let anyone else take your medication. Ask your pharmacist any questions you have about refilling your prescription. It is important for you to keep a written list of all of the prescription and nonprescription (over-the-counter) medicines you are taking, as well as any products such as vitamins, minerals, or other dietary supplements.

You should bring this list with you each time you visit a doctor or if you are admitted to a hospital. It is also important information to carry with you in case of emergencies. Brand names Cozaar ®Brand names of combination products Hyzaar ® (containing Hydrochlorothiazide, Losartan)Last Revised - 02/15/2018Browse Drugs and Medicines

However, there are other conditions in which elevated T-waves can present such as myocardial infarction (heart attack), or a condition known as ""left ventricular hypertrophy"" in which the chamber of the heart responsible for pumping your blood to the rest of your body becomes enlarged (probably due to being overworked).

What causes elevated T waves?

"Answers.com ® Wiki Answers ® Categories Uncategorized What causes elevated T waves? Flag What causes elevated T waves? Answer by ER Nobody Confidence votes 74Elevated T-waves are usually indicative of a hyperkalemic state, which basically means too much potassium in the body.

9 people found this useful Was this answer useful? Yes Somewhat No What causes waves and wave movement?

The moon. If something gets pulled by Earth, it pulls back. However, the only thing that the moon can pull is water, so it pulls the water, causing waves. Invigilator - 007 94,836 Contributions SENIOR SUPERVISOR - SENIOR MENTORWhat are waves are caused by? Waves are caused by wind hitting the surface of the water. They are caused by earthquakes too. BJ SINGLETON 16 Contributions What causes waves?

The MOON cause waves on the surface of the ocean (and on lakes). The MOON transfers some of its energy to the water, throughfriction between the air molecules and the water mol …Livvilolli 3 Contributions What causes a wave?

ENERGY!Snappychan 18 Contributions How are waves caused?waves are caused when it is windy or win like something big hits the water Tucker98 135 Contributions What are the causes of waves?wind is one of the main cause of waves Oneal'ryan Torres 1 Contribution What causes wave?

Wave is cause by a vibration by an object . What is a wave caused by? A wave is caused by WIND!!!!!! !curt weinstein 1,459 Contributions I am the elder Weinstein, Weinstein the lesser. What cause waves? Best guess: a change in matter density. What is the cause of waves? The cause of waves depends on the strength of the wind. The stronger the wind the bigger the wave. What illnesses cause elevated esr and t cell lymphocyte counts?

Hep BWhat was the cause of the elevator? The elevator was invested and made because of disabled people, the cause: disabled people among many other reasons. Brittanny Marie 5 Contributions Answered In Science Experiments What are waves caused by? Waves are caused by vibrating objects Julien Redfern 340 Contributions Answered In Oceans and Seas What is the cause of wave?

The cause of a wave is simply the wind blowing the water. Ask 'what is the cause of the wind' or 'what is the cause of tides. 'Ivesita Bermudez Galvez 1 Contribution Answered In EMGIn an ECG pattern the T wave is caused by? Repolarization of ventricular muscle fibers. Answered In Uncategorized What causes peaked t waves?too much calcium Answered In Uncategorized What type of wave causes your skin t burn?uv rays "

Sound waves produce live-action images of your heart. Echocardiogram can reveal thickened muscle tissue in the left ventricle, blood flow through the heart with each beat, and heart abnormalities related to left ventricular hypertrophy, such as aortic valve stenosis. MRI. Images of your heart can be used to diagnose left ventricular hypertrophy.

Diagnosis

Print Diagnosis Your doctor will start with a health history, family history and thorough physical examination including checking your blood pressure and heart function.

Your doctor might then recommend screening tests: Electrocardiogram (ECG or EKG). Electrical signals are recorded as they travel through your heart. Your doctor can look for patterns that indicate abnormal heart function and increased left ventricle muscle tissue. Echocardiogram.

Treatment

Treatment for left ventricular hypertrophy depends on the underlying cause, and may involve medication or surgery. Treating high blood pressure Your doctor is likely to recommend lifestyle changes, including:

Regular exercise Low-sodium, low-fat diet Smoking cessation Blood pressure medication might also help prevent further enlargement of the left ventricle and even shrink your hypertrophic muscles. Your doctor might recommend: Angiotensin-converting enzyme (ACE) inhibitors. These medications widen blood vessels to lower blood pressure, improve blood flow and decrease the heart's workload.

Examples include Captopril, Enalapril and Lisinopril. Side effects might include an irritating dry cough. Angiotensin II receptor blockers (ARBs). Medications such as losartan (Cozaar) have benefits similar to ACE inhibitors but don't cause a persistent cough. Beta blockers. Medications such as atenolol (Tenormin) can lower your heart rate, reduce blood pressure and prevent some of the harmful effects of stress hormones.

Beta blockers aren't usually given as an initial treatment for hypertension. Your doctor might recommend adding a beta blocker if another type of medication isn't effective alone.

Calcium channel blockers. These medications prevent calcium from entering cells of the heart and blood vessel walls, resulting in lower blood pressure. Examples include amlodipine (Norvasc) and diltiazem (Cardizem). Diuretics. Medications known as thiazide-type diuretics can facilitate blood flow, lowering hypertension.

Examples include chlorthalidone and hydrochlorothiazide. Treating sleep apnea If you've already been diagnosed with sleep apnea, treating this sleep disorder can lower your blood pressure and help reverse left ventricular hypertrophy. If you haven't been diagnosed with sleep apnea, but your partner tells you that you snore or that you stop breathing momentarily while you sleep, talk with your doctor about getting tested for sleep apnea.

Sleep apnea treatment involves using a machine that provides continuous positive airway pressure (CPAP) while you sleep. CPAP keeps your airways open, allowing you to get the oxygen you need to keep your blood pressure at a normal level. Aortic valve repair or replacement

Left ventricular hypertrophy that is caused by aortic valve stenosis might require surgery to repair the narrow valve or to replace it with an artificial or tissue valve. Request an Appointment at Mayo Clinic

Lifestyle and home remedies

Lifestyle changes can help lower your blood pressure and improve left ventricular hypertrophy signs. Consider: Weight loss. Left ventricular hypertrophy is often found in obese people regardless of blood pressure. Losing weight has been shown to reverse left ventricular hypertrophy. Limiting salt in your diet.

Diagnosis

Treatment

Lifestyle and home remedies

Diagnosis

Treatment

Lifestyle and home remedies

Diagnosis

Treatment

Lifestyle and home remedies

. The enlarged left ventricle can: Weaken Stiffen and lose elasticity, preventing the chamber from filling properly and increasing pressure in the heart Compress the chamber's blood vessels (coronary arteries) and restrict its supply of blood As a result of these changes, complications of left ventricular hypertrophy include:

Overview

Overview Left ventricular hypertrophy is enlargement and thickening (hypertrophy) of the walls of your heart's main pumping chamber (left ventricle). Left ventricular hypertrophy can develop in response to some factor — such as high blood pressure or a heart condition — that causes the left ventricle to work harder. As the workload increases, the muscle tissue in the chamber wall thickens, and sometimes the size of the chamber itself also increases.

The enlarged heart muscle loses elasticity and eventually may fail to pump with as much force as needed. Left ventricular hypertrophy is more common in people who have uncontrolled high blood pressure. But no matter what your blood pressure is, developing left ventricular hypertrophy puts you at higher risk for a heart attack and stroke.

Treating high blood pressure can help ease your symptoms and may reverse left ventricular hypertrophy. Symptoms Left ventricular hypertrophy usually develops gradually. You may experience no signs or symptoms, especially during the early stages of the condition.

As left ventricular hypertrophy progresses, you may experience: Shortness of breath Fatigue Chest pain, often after exercising Sensation of rapid, fluttering or pounding heartbeats (palpitations)Dizziness or fainting When to see a doctor Seek emergency care if: You feel chest pain that lasts more than a few minutes You have severe difficulty breathing You have severe, recurring lightheadedness or lose consciousness If you experience mild shortness of breath or other symptoms, such as palpitations, see your doctor.

If you have high blood pressure or another condition that increases your risk of left ventricular hypertrophy, your doctor is likely to recommend regular appointments to monitor your heart.

Even if you feel well, you need to have your blood pressure checked annually, or more often if you: Smoke Are overweight Have other conditions that increase the risk of high blood pressure Request an Appointment at Mayo Clinic Causes Left ventricular hypertrophy can occur when some factor makes your heart work harder than normal to pump blood to your body. Factors that can cause your heart to work harder include: High blood pressure (hypertension). This is the most common cause of left ventricular hypertrophy.

More than one-third of people show evidence of left ventricular hypertrophy at the time of their diagnosis with hypertension. Aortic valve stenosis. This disease is a narrowing of the tissue flap (aortic valve) that separates the left ventricle from the large blood vessel leaving your heart (aorta). The narrowing of the aortic valve requires the left ventricle to work harder to pump blood into the aorta.

Hypertrophic cardiomyopathy. This genetic disease occurs when the heart muscle becomes abnormally thick, making it harder for the heart to pump blood. Athletic training. Intense, prolonged endurance and strength training can cause the heart to adapt to handle the extra workload.

It's unclear whether this athletic type of left ventricle hypertrophy can lead to stiffening of the heart muscle and disease. Risk factors In addition to hypertension and aortic valve stenosis, factors that increase your risk for left ventricular hypertrophy include: Age. Left ventricular hypertrophy is more common in older people. Weight. Being overweight increases your risk of high blood pressure and left ventricular hypertrophy.

Family history. Certain genetic conditions are associated with developing hypertrophy. Diabetes. Race. African-Americans are at higher risk of left ventricular hypertrophy than are white people with similar blood pressure measurements. Sex. Women with hypertension are at higher risk of left ventricular hypertrophy than are men with similar blood pressure measurements. Complications Left ventricular hypertrophy changes the structure and working of the heart

To better manage your blood pressure: Monitor high blood pressure. Purchase a home blood pressure measuring device and check your blood pressure frequently. Schedule regular checkups with your doctor. Make time for exercise. Regular exercise helps to lower blood pressure and keep it at normal levels.

Aim for 30 minutes of moderate activity most days of the week. Watch your diet. Avoid foods that are high in fat and salt, and eat more fruits and vegetables.

Avoid alcoholic beverages or drink them in moderation. Quit smoking. Giving up smoking improves your blood pressure and overall health. By Mayo Clinic Staff Request an Appointment at Mayo Clinic Diagnosis & treatment June 06, 2015Share on: Facebook Twitter References Related Dizziness Shortness of breath Left ventricular hypertrophy Symptoms & causes Diagnosis & treatment Advertisement Mayo Clinic does not endorse companies or products.

Advertising revenue supports our not-for-profit mission. Advertising & Sponsorship Policy Opportunities Ad Choices Mayo Clinic Marketplace Check out these best-sellers and special offers on books and newsletters from Mayo Clinic. FREE TRIAL – Mayo Clinic Health Letter Best Treatment Strategies for Arthritis Mayo Clinic on Digestive Health Effective Home Remedies from Mayo Clinic The Mayo Clinic Diet Online CON-20374296Patient Care & Health Information Diseases & Conditions Left ventricular hypertrophy

To determine the frequency of right ventricular hypertrophy and its relation to increased left ventricular wall thickness in patients with left ventricular pressure overload, right ventricular wall thickness was measured using M-mode echocardiography with two-dimensional echocardiographic guidance in 65 patients with left ventricular pressure overload; 49 patients had essential hypertension and 16 had aortic valve stenosis.

"Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the ""nonstressed"" ventricle."

"1. J Am Coll Cardiol. 1985 Sep;6 (3):550-5. Increased right ventricular wall thickness in left ventricular pressure overload: echocardiographic determination of hypertrophic response of the ""nonstressed"" ventricle.

Gottdiener JS, Gay JA, Maron BJ, Fletcher RD. Left ventricular hypertrophy in left ventricular pressure overload occurs in response to excessive work load imposed on the left ventricle by increased impedance to ejection. Right ventricular hypertrophy may occur in patients with these findings, but has been considered to be secondary to pulmonary hypertension.

These measurements were compared with data from 13 patients with ""thin-walled"" dilated cardiomyopathy and 20 normal subjects.

Average right ventricular wall thickness in hypertensive patients (7 +/- 2 mm) and patients with aortic stenosis (6 +/- 2 mm) was significantly greater than that in normal subjects (4 +/- 1 mm) and patients with dilated cardiomyopathy (4 +/- 1 mm) who had normal left ventricular wall thickness, even though left ventricular mass was increased in all patient groups.

Increased right ventricular wall thickness was present in 40 (80%) of 49 patients with hypertension and 10 (63%) of 16 patients with aortic stenosis. The magnitude of increase in right ventricular wall thickness was linearly correlated (r = 0.76, p less than 0.005) with left ventricular wall thickness, but was not associated with pulmonary hypertension. It is concluded that increased right ventricular wall thickness is common in patients with left ventricular pressure overload, is directly related to increases in left ventricular wall thickness, and is independent of right ventricular hypertension.

(ABSTRACT TRUNCATED AT 250 WORDS)PMID:3161925 [Pub Med - indexed for MEDLINE]Publication Types: Research Support, U. S. Gov't, Non-P. H. S. Me SH Terms Adult Aged Aortic Valve Stenosis/physiopathology*Cardiomegaly/etiology Cardiomegaly/physiopathology*Cardiomyopathy, Dilated/physiopathology*Echocardiography*Female Heart Failure/physiopathology*Humans Hypertension/physiopathology*Male Middle Aged Myocardial Contraction*Pressure Stress, Physiological/physiopathology "

Left ventricular hypertrophy (LVH) occurs when the muscle tissue in the heart’s main pumping chamber becomes enlarged. LVH is often caused by high blood pressure or other heart problems and can lead to serious complications, such as heart disease , heart attack and heart failure.

Conditions

Conditions Find answers to frequently asked questions about a variety of health conditions, like heart attack, high blood pressure and atrial fibrillation.1 2 3 4 5 Next >> 1 - 25 of 517What is fatigue? Fatigue is often described as extreme tiredness and can affect either physical health, mental health, or both. Most often, fatigue is caused by a number of factors such diet or lack of sleep and exercise. In some cases, however, fatigue may be a sign of underlying conditions, such as depression, sleep apnea, heart disease and diabetes.

It’s important to discuss feelings of fatigue with a doctor to help identify the cause and relieve symptoms. What is dementia? Dementia includes a group of symptoms that affect memory, thinking and social skills and that interfere with normal daily functioning.

Common symptoms include memory loss, difficulty finding words, personality changes and inability to reason. It’s important to see a doctor if you or a loved one experiences symptoms, as some causes can be treated. What is an arrhythmia? An arrhythmia is an abnormal heart rhythm that causes the heart to beat too quickly, too slowly or irregularly.

There are many types of arrhythmias, some of which are harmless. However, treatment may be required depending on the type and severity of arrhythmia a patient has. What is vasovagal syncope? Vasovagal syncope is the most common cause of fainting. It occurs when heart rate and blood pressure suddenly drop, causing a brief loss of consciousness.

Vasovagal syncope is often triggered by stressful events, such as seeing blood or getting a shot. Although fainting is generally not serious, it’s important to see a doctor if it happens often or is associated with other symptoms like shortness of breath or chest pain.

Is it hard to conceive when taking normalol and tambocor for supraventricular tachycardia Answer goes here What is chronic obstructive pulmonary disease (COPD)? COPD is a chronic disease that makes it hard to breathe. COPD is often caused by smoking and can cause symptoms like difficulty breathing, coughing and wheezing.

Although COPD worsens over time, proper treatment and management helps improve outcomes and quality of life. What is microvascular disease? Microvascular disease, or non-obstructive heart disease, occurs when the heart’s small blood vessels are damaged, decreasing blood flow to the heart.

Women develop non-obstructive heart disease more often than men. Diagnosing this condition can be a challenge, since standard tests are not designed to detect this microvascular disease. What is familial hypercholesterolemia? Familial hypercholesterolemia (or FH) is a genetic condition that causes high cholesterol levels beginning at birth. FH happens when the body is unable to remove the low density lipoprotein (“bad”) cholesterol from the blood.

When the body can’t eliminate bad cholesterol, it builds up in the arteries and can cause heart disease earlier in life than normal. Left undiagnosed and untreated, individuals with FH are at significantly increased risk for heart disease, heart attack, stroke and other serious complications. What is cardiomyopathy? Cardiomyopathy refers to diseases of the heart muscle, which cause the heart to become weaker and can lead to serious complications such as heart failure, abnormal heart rhythm or heart valve problems.

Cardiomyopathy can vary in severity, as some patients can have no symptoms while others have debilitating symptoms that require immediate treatment. However, cardiomyopathy often worsens over time, weakening the heart and making it difficult for the heart to pump enough blood to the rest of the body.

How is cardiomyopathy treated? Treatment depends on which major type of cardiomyopathy a patient has. However, goals of treatment are usually to minimize symptoms, reduce risk of complications and prevent the condition from worsening.

Treatment options may include medication, surgery, and/or medical devices. What is peripartum cardiomyopathy? Peripartum cardiomyopathy is a rare disorder in which a pregnant woman’s heart becomes weakened and enlarged. This condition typically develops during the last month of pregnancy or within the first five months after the baby is born.

How can I help prevent a second heart attack? Patients with a history of heart attack have significantly increased risk of a second heart event.

Participating in a cardiac rehabilitation program can help patients regain strength after a heart attack and teach individuals how to prevent a second heart attack, like by quitting smoking, reducing blood pressure, staying active, eating healthy, and adhering to therapies advised by the doctor. Is it safe to have sex after a heart attack? Although many people are afraid to resume sexual activity after a heart attack, the risk of having a heart attack during sex is low for most patients.

However, it’s important to discuss resuming both physical activity and sex after a heart attack to reduce risk of a second event. What is atherosclerosis? Atherosclerosis is the hardening of the arteries caused by the build-up of fat and cholesterol on the artery walls. Atherosclerosis can lead to serious health problems, such as heart attack , stroke and even death. How is atherosclerosis treated? Treatment for atherosclerosis may include lifestyle changes, medication and/or medical procedures, depending on the severity of plaque build-up in the arteries.

Lifestyle changes like eating healthy, staying active , quitting smoking and reducing stress can help reduce risk of complications from atherosclerosis. Certain medications like cholesterol and blood pressure-lowering drugs may also be prescribed to slow the progress of plaque build-up. If atherosclerosis is severe, certain procedures may also be recommended to open blocked or narrowed arteries. What is an aortic dissection? Aortic dissection occurs when there is a tear in the wall of the heart’s major artery, called the aorta.

As the tear extends, it can cause bleeding and if not treated promptly, can be fatal. Aortic dissection is relatively uncommon and risk increases with age. What is a thoracic aortic aneurysm? A thoracic aortic aneurysm occurs when the upper part of the aorta is weakened. A thoracic aneurysm can eventually lead to a life-threatening tear in the aorta, called an aortic dissection.

When a thoracic aortic aneurysm is detected, doctors may watch the growth rate of the aneurysm to determine the best possible treatment. What is ejection fraction? Ejection fraction is a test used to measure the amount of blood leaving the heart each time it contracts. Doctors typically measure ejection fraction when a patient shows signs of or is diagnosed with heart failure.

Ejection fraction tells a doctor how well the heart pumps with each beat, which is used to determine the best possible treatment options to improve outcomes and quality of life. How common are congenital heart defects? Congenital heart defects are the most common type of birth defect, affecting roughly 1% of all births in the United States.

Thanks to advancements in treatments, it’s estimated that 1 million adults are now living with a congenital heart defect. What are congenital heart defects? Congenital heart defects refer to a number of different conditions that can occur when a baby’s heart is forming or at birth. Although most defects are found during pregnancy or in early childhood, some defects aren’t discovered until adulthood. Survival rates depend on the severity of the heart defect, but most individuals with congenital heart defects live long and healthy lives. What is left ventricular hypertrophy?

Left ventricular hypertrophy (LVH) occurs when the muscle tissue in the heart’s main pumping chamber becomes enlarged. LVH is often caused by high blood pressure or other heart problems and can lead to serious complications, such as heart disease , heart attack and heart failure.

The good news is that LVH can often be treated by addressing the underlying cause of the condition. How is atrial fibrillation treated? In general, the goals of atrial fibrillation treatment are to promote a regular heart rhythm or rate and prevent blood clots, which can cause stroke.

However, treatment strategies depend on the unique needs of each patient. Treatment options may include antiarrhythmic medication, blood thinners, and a variety of procedures that can help control atrial fibrillation. How can I help prevent a heart attack? Healthy lifestyle choices can go a long way in preventing heart attack, like by avoiding smoking, eating a heart-healthy diet , staying active and managing stress levels.

Controlling cholesterol and blood pressure are also key to heart attack prevention, as well as managing conditions like diabetes, which increase cardiovascular risk. Certain patients may benefit from taking daily aspirin to further reduce heart attack risk. At what age should I worry about heart disease?

Risk factors that lead to heart disease often develop slowly over time and can take decades to develop. That’s why it’s important to make healthy lifestyle choices like eating healthy , staying active and maintaining a healthy weight, at all stages in life.

As an adult, it’s especially important to work closely with your doctor to monitor key risk factors and address any risk factors to reduce risk for heart disease. At what age should I worry about my cholesterol? More than one-third of Americans have high cholesterol and risk for high cholesterol increases with age.

However, high cholesterol can be a problem at any age. It’s estimated that 22% of adults in their 20s have high cholesterol and 62% of adults in their 50s have high cholesterol. It’s important to have cholesterol checked regularly and make healthy lifestyle choices like eating healthy and staying active, which help control cholesterol levels.1 2 3 4 5 Next >> 1 - 25 of 517

Patient Information Left Ventricular Hypertrophy on ECGLeft ventricular hypertrophy (LVH) means that the muscle of the left pumping chamber of the heart (left ventricle) is thickened. The left ventricle's job is to pump blood to the body, and conditions that increase the work the left ventricle has to do can lead to thickening of the muscle.

High blood pressure, tight valves, certain malformations of the heart (hypertrophic cardiomyopathy) and some medications (such as certain steroids) can lead to LVH, but in many cases the cause is not known.

LVH can also be normal in people who are very athletically conditioned. In addition, very often the EKG suggests LVH when in fact the heart muscle is normal - this is a weakness of EKGs as a test.

If there is any concern about whether a child with LVH on ECG actually has a heart problem, the usual next step would be to consider a consultation with a pediatric cardiac specialist and usually an ultrasound of the heart (echocardiogram).

Left ventricular hypertrophy (LVH) is serious when the muscle is very thick (max thickness >3 cm), or if the increased muscle mass is impeding blood flow through the heart (defined as increased outflow pressure gradient).

How serious is left ventricular hypertrophy?

"Liang-Hai Sie, Retired general internist, former intensive care physician. Answered May 26, 2016 · Author has 24.7k answers and 48.4m answer views See the Mayo Clinic webpage Left ventricular hypertrophy (LVH).

It’s the thickening of the muscle of the left ventricle, usually because pumping against a higher resistance (hypertension, aortic valve defects) or as part of a hereditary heart muscle disease (hypertrophic cardiomyopathy). It’s correlated with more heart failure, more heart attacks, more deaths. In hypertension we preferably chose meds that will revert this LVH (angiotensin converting enzyme inhibitors, angiotensin receptor blockers and the old fashioned methyldopa).12k Views · View Upvoters · Answer requested by Tonya Olsen Related Questions More Answers Below What does it mean when the ECG indicates that you have Borderline Left Ventricular Hypertrophy?

What are some notable diets/food items to reduce heart problems (left ventricular hypertrophy)? What is left ventricular hypertrophy?

Can left ventricular hypertrophy cause edema in legs and feet? What are the symptoms of left ventricular dysfunction? Ask New Question James Kneller, Cardiac Electrophysiologist Updated Oct 22, 2015 · Upvoted by Liang-Hai Sie · Author has 167 answers and 134.4k answer views

When an outflow gradient is excessively high, the affected individual will likely experienced related symptoms, such as decreased exercise tolerance, lightheadedness, or fainting. In these cases, medication or surgical treatment may be required to relieve the obstruction. Increased thickness predisposes to dangerous heart rhythms arising from the ventricles (ventricular tachycardia, ventricular fibrillation) which may be life threatening, and patients may qualify for an implantable cardioverter defibrillators (ICD).

The decision for an ICD is typically based on the presence of several risk factors, such as the degree of muscle thickening, history of faint, documentation of ventricular tachycardia, or a family history of sudden cardiac death due to LVH.6.1k Views · View Upvoters This answer is not a substitute for professional medical advic... (more)Your response is private.

Is this answer still relevant and up to date?promoted by Nikah Plan your wedding. Get married in style, plan your wedding. Learn More at planyourwedding.tk Mark Huth, Cardiologist, Southern Oregon Cardiology Answered Feb 8, 2012 · Upvoted by Liang-Hai Sie, Retired general internist, former intensive care physician.

Left ventricular hypertropy (thickening of the heart muscle) is a common finding in patients with hypertension. There is an association with increased cardiovascular risk. Note, that association does not mean that the hypertrophy causes the increased risk, just that there may be an increased risk. Hypertrophic cardiomyopathy is a genetic disease in which the walls of the heart thicken. Here, too, there may be an increased risk.

In the first situation, left ventricular hypertrophy, the walls thicken as a result of hypertension. In the second situation, they thicken as a result of genetics. In both the walls are thickened. In order to assess risk, the patient needs testing.

In general, we begin with an echocardiogram to assess how thickened the walls are, to see if there is valvular or other disease, and to estimate the function of the heart.

Depending on the findings, we may do more testing. How serious it is depends on what we find.11.6k Views · View Upvoters Your response is private. Is this answer still relevant and up to date? Quora User, Scientist, Entrepreneur Answered Jan 29, 2012 · Upvoted by Liang-Hai Sie, Retired general internist, former intensive care physician.

· Author has 295 answers and 1.1m answer views It can be serious, depending on the degree. Athletes and runners can show this as a positive trait after a lifetime of exercise. However, it can also occur if the individual has hypertension, for example. In this case the heart is pumping against increased resistance. So, the heart responds by increasing the size of the cardiac muscles (hypertrophy), which can lead to failure.

Friend or not, you can only know this following some rather serious cardiac testing. So, you or ""your friend"" really need to talk to your/their cardiologist about this.8.1k Views · View Upvoterspromoted by Lets Get Checked At home STD testing.

The same laboratory tests used by doctors or clinics, delivered to you. Learn More at letsgetchecked.com Deborah Weaver, Veteran Nurse and Life Learner Answered Feb 21, 2016 · Author has 680 answers and 596.4k answer views The left ventricle is the workhorse muscle of the heart. When it dosen't function to eject enough blood enough--it compensates by becoming bigger. Sounds good, but the muscle wall can become weaker, and the blood will still not be ejected in good time.

These changes can occur over time, especially with uncontrolled hypertension--the heart has to work harder to pump blood against a higher pressure.

This condition is relatively common, especially in our elderly, and if the weakened muscle becomes a problem, there are drugs to help.5.1k Views · View Upvoters · Answer requested by Lori Blanton Meeks Deborah Cobb, Professor Answered Oct 15, 2017Deadly. I lost my 37 yr old son to this disease. Three years ago my whole world changed. LVHT disease can cause death if undiagnosed. It doesn't discriminate against to any race, gender, color, female and male, adult or child, old young, etc.577 Views "

What is Left Ventricular Hypertrophy? Left ventricular hypertrophy is a disorder of the heart involving the enlargement or thickening of the wall of cardiac muscle situated in the chamber of the heart known as the left ventricle.

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy Written by Dr. Mary IN THIS ARTICLE: What is Left Ventricular Hypertrophy? Symptoms Causes Treatment Left Ventricular Hypertrophy in Children

The disease occurs as a result of several possible precipitating factors that prompt the heart to increase the amount of effort and power it exerts in order to supply blood to the entire body, such as heightened blood pressure. The left ventricle is the chief chamber of the heart that takes helm over the task of delivering blood to the majority of the body.

Although the heart is made up of four chambers in total, each one with its own designated areas that they are built to pump and supply blood to, the left atrium, the right atrium, and the right ventricle merely deliver blood to the lungs or to their adjacent chambers. The left ventricle, however, is easily distinguished as the chamber that puts forth the greatest amount of effort as it is responsible for pumping out oxygenated blood to nourish practically the entire human body as a whole.

Under certain circumstances, the heart may be required to work harder in order to steadily provide the needed amount of blood to the various organs in the body.

The myocardium, the specialized cardiac muscle designed to rhythmically pump the blood into and out of the heart, may thicken and enlarge in an attempt to adapt to the increased workload. In the process of enlargement, the muscle eventually loses its elasticity and subsequently, loses its ability to effectively pump – drastically impairing the circulation of blood within the body.

The condition can be life threatening if allowed to persist without prompt medical care. Symptoms Left ventricular hypertrophy will take a while to progress before it produces any observable symptoms. As the process is one that is gradual, the patient may not even experience any symptoms at all during the earlier stages of the disease as changes are too minor or miniscule to result in any obvious alterations in the body’s performance.

However, if the causative factors responsible for the heart’s struggle are not done away with, the muscles within the left ventricle will thicken and harden enough to produce apparent, and often debilitating, symptoms.

These include the following: Difficulty breathing Increased rate of respiration Patient is easily fatigued or tired out by normal physical activities Rapidly beating heart rhythm, otherwise known as palpitations Chest pain Light-headedness Episodes of spontaneously losing consciousness or fainting The last few items on the list of symptoms are cause for alarm and indicate the need for emergency medical assistance.

Should a patient experience any of the above signs, he or she should seek out prompt medical care before the condition is allowed to worsen.

Causes Left ventricular hypertrophy occurs as a result of the heart’s adaptive reaction to any factor that may be requiring the heart to work harder than usual.

In most instances of left ventricular hypertrophy, the disease develops due to an underlying condition of hypertension which brings about the need for the heart to hasten its pace in order to still effectively supply blood to the entire body despite the resistance of the heightened levels of blood pressure.

The myocardium or heart muscle within the left ventricle enlarges and thickens in order to still effectively perform its critically important task. Although the changes in the heart muscle is meant as an adaptive move, the hypertrophy or enlargement of the muscles eventually robs the heart of the elasticity it requires to pump blood in the constant rhythm needed. In the long run, the hypertrophy ends up as a liability to the heart’s performance, preventing the left ventricle from keeping up with the essential constant delivery of blood the body needs

. Several underlying conditions can contribute to or influence the enlargement of the heart muscle in the left ventricle. Hypertension is the most common cause, setting the stage for left ventricular hypertrophy once a person’s blood pressure exceeds the normal level of 140/90 mm Hg. Aside from hypertension, the condition known as aortic valve stenosis is also a common cause of the hypertrophic changes in the heart.

The disease involves the narrowing of the valve that comes between the left ventricle and the aorta, a major blood vessel in the body. Although the barrier may only exist within the aortic valve, the obstacle is enough to require the left ventricle to increase its efforts.

Advertisement Left ventricular hypertrophy can also result without succeeding an underlying disorder. The condition may occur in athletes who constantly undergo training in an attempt to improve their stamina.

Under such circumstances, the heart can still react by adapting in order to accommodate the additional amount of work. Treatment The treatment for left ventricular hypertrophy depends on the cause of the condition. Doctors will aim to eliminate the cause of the heart’s enlargement in order to normalize the heart’s efforts and prevent incapacitation of the heart muscles. If high blood pressure is determined as the root cause of the disease, doctors will usually devise a treatment regimen involving medications as well as lifestyle modifications.

The patient may be prescribed medications that promote the reduction of blood pressure. These include thiazide diuretics which help by reducing the amount of fluid constantly circulating in the body, the reduction of the blood’s volume thus decreases blood pressure. Another type of medication used is angiotensin-converting enzyme inhibitors. These act on the blood vessels in the body by promoting their dilation, allowing better passage of blood and reduced blood pressure. in addition to the aforementioned types of medications are beta blockers and calcium channel blockers which both contributed to reducing blood pressure.

Coupled with the use of drugs is the need for changes in the patient’s lifestyle. The patient will have to initiate a lifestyle and diet that improves heart function through engaging in regular physical exercise, avoiding smoking at all costs, and consuming a diet that is low in both sodium and fat as both types of food components take a toll on the heart’s performance.

In severe cases, the patient may have to undergo surgery in order to effectively restore proper heart function. An aortic valve repair or replacement is the surgical procedure carried out for patients with left ventricular hypertrophy resulting from aortic valve stenosis. Treatment is achieved through getting rid of the narrowed valve and substituting it with one that is healthy and wide enough to allow proper blood flow. Left Ventricular Hypertrophy in Children

Left ventricular hypertrophy can occur as an inborn disease in infants and children, due to an underlying condition known as hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy or HCM is a hereditary disease that involves an inborn abnormality of the cardiac muscles.

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy Written by Dr. Mary IN THIS ARTICLE: What is Left Ventricular Hypertrophy? Symptoms Causes Treatment Left Ventricular Hypertrophy in Children

What is Left Ventricular Hypertrophy? Left ventricular hypertrophy is a disorder of the heart involving the enlargement or thickening of the wall of cardiac muscle situated in the chamber of the heart known as the left ventricle.

The disease occurs as a result of several possible precipitating factors that prompt the heart to increase the amount of effort and power it exerts in order to supply blood to the entire body, such as heightened blood pressure. The left ventricle is the chief chamber of the heart that takes helm over the task of delivering blood to the majority of the body.

Although the heart is made up of four chambers in total, each one with its own designated areas that they are built to pump and supply blood to, the left atrium, the right atrium, and the right ventricle merely deliver blood to the lungs or to their adjacent chambers. The left ventricle, however, is easily distinguished as the chamber that puts forth the greatest amount of effort as it is responsible for pumping out oxygenated blood to nourish practically the entire human body as a whole.

Under certain circumstances, the heart may be required to work harder in order to steadily provide the needed amount of blood to the various organs in the body.

The myocardium, the specialized cardiac muscle designed to rhythmically pump the blood into and out of the heart, may thicken and enlarge in an attempt to adapt to the increased workload. In the process of enlargement, the muscle eventually loses its elasticity and subsequently, loses its ability to effectively pump – drastically impairing the circulation of blood within the body.

The condition can be life threatening if allowed to persist without prompt medical care. Symptoms Left ventricular hypertrophy will take a while to progress before it produces any observable symptoms. As the process is one that is gradual, the patient may not even experience any symptoms at all during the earlier stages of the disease as changes are too minor or miniscule to result in any obvious alterations in the body’s performance.

However, if the causative factors responsible for the heart’s struggle are not done away with, the muscles within the left ventricle will thicken and harden enough to produce apparent, and often debilitating, symptoms.

These include the following: Difficulty breathing Increased rate of respiration Patient is easily fatigued or tired out by normal physical activities Rapidly beating heart rhythm, otherwise known as palpitations Chest pain Light-headedness Episodes of spontaneously losing consciousness or fainting The last few items on the list of symptoms are cause for alarm and indicate the need for emergency medical assistance.

Should a patient experience any of the above signs, he or she should seek out prompt medical care before the condition is allowed to worsen.

Causes Left ventricular hypertrophy occurs as a result of the heart’s adaptive reaction to any factor that may be requiring the heart to work harder than usual.

In most instances of left ventricular hypertrophy, the disease develops due to an underlying condition of hypertension which brings about the need for the heart to hasten its pace in order to still effectively supply blood to the entire body despite the resistance of the heightened levels of blood pressure.

. Several underlying conditions can contribute to or influence the enlargement of the heart muscle in the left ventricle. Hypertension is the most common cause, setting the stage for left ventricular hypertrophy once a person’s blood pressure exceeds the normal level of 140/90 mm Hg. Aside from hypertension, the condition known as aortic valve stenosis is also a common cause of the hypertrophic changes in the heart.

The disease involves the narrowing of the valve that comes between the left ventricle and the aorta, a major blood vessel in the body. Although the barrier may only exist within the aortic valve, the obstacle is enough to require the left ventricle to increase its efforts.

Advertisement Left ventricular hypertrophy can also result without succeeding an underlying disorder. The condition may occur in athletes who constantly undergo training in an attempt to improve their stamina.

Under such circumstances, the heart can still react by adapting in order to accommodate the additional amount of work. Treatment The treatment for left ventricular hypertrophy depends on the cause of the condition. Doctors will aim to eliminate the cause of the heart’s enlargement in order to normalize the heart’s efforts and prevent incapacitation of the heart muscles. If high blood pressure is determined as the root cause of the disease, doctors will usually devise a treatment regimen involving medications as well as lifestyle modifications.

Coupled with the use of drugs is the need for changes in the patient’s lifestyle. The patient will have to initiate a lifestyle and diet that improves heart function through engaging in regular physical exercise, avoiding smoking at all costs, and consuming a diet that is low in both sodium and fat as both types of food components take a toll on the heart’s performance.

In severe cases, the patient may have to undergo surgery in order to effectively restore proper heart function. An aortic valve repair or replacement is the surgical procedure carried out for patients with left ventricular hypertrophy resulting from aortic valve stenosis. Treatment is achieved through getting rid of the narrowed valve and substituting it with one that is healthy and wide enough to allow proper blood flow. Left Ventricular Hypertrophy in Children

Left ventricular hypertrophy can occur as an inborn disease in infants and children, due to an underlying condition known as hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy or HCM is a hereditary disease that involves an inborn abnormality of the cardiac muscles.

Left Ventricular Hypertrophy

Left Ventricular Hypertrophy Written by Dr. Mary IN THIS ARTICLE: What is Left Ventricular Hypertrophy? Symptoms Causes Treatment Left Ventricular Hypertrophy in Children

What is Left Ventricular Hypertrophy? Left ventricular hypertrophy is a disorder of the heart involving the enlargement or thickening of the wall of cardiac muscle situated in the chamber of the heart known as the left ventricle.

The disease occurs as a result of several possible precipitating factors that prompt the heart to increase the amount of effort and power it exerts in order to supply blood to the entire body, such as heightened blood pressure. The left ventricle is the chief chamber of the heart that takes helm over the task of delivering blood to the majority of the body.

Although the heart is made up of four chambers in total, each one with its own designated areas that they are built to pump and supply blood to, the left atrium, the right atrium, and the right ventricle merely deliver blood to the lungs or to their adjacent chambers. The left ventricle, however, is easily distinguished as the chamber that puts forth the greatest amount of effort as it is responsible for pumping out oxygenated blood to nourish practically the entire human body as a whole.

Under certain circumstances, the heart may be required to work harder in order to steadily provide the needed amount of blood to the various organs in the body.

The myocardium, the specialized cardiac muscle designed to rhythmically pump the blood into and out of the heart, may thicken and enlarge in an attempt to adapt to the increased workload. In the process of enlargement, the muscle eventually loses its elasticity and subsequently, loses its ability to effectively pump – drastically impairing the circulation of blood within the body.

The condition can be life threatening if allowed to persist without prompt medical care. Symptoms Left ventricular hypertrophy will take a while to progress before it produces any observable symptoms. As the process is one that is gradual, the patient may not even experience any symptoms at all during the earlier stages of the disease as changes are too minor or miniscule to result in any obvious alterations in the body’s performance.

However, if the causative factors responsible for the heart’s struggle are not done away with, the muscles within the left ventricle will thicken and harden enough to produce apparent, and often debilitating, symptoms.

These include the following: Difficulty breathing Increased rate of respiration Patient is easily fatigued or tired out by normal physical activities Rapidly beating heart rhythm, otherwise known as palpitations Chest pain Light-headedness Episodes of spontaneously losing consciousness or fainting The last few items on the list of symptoms are cause for alarm and indicate the need for emergency medical assistance.

Should a patient experience any of the above signs, he or she should seek out prompt medical care before the condition is allowed to worsen.

Causes Left ventricular hypertrophy occurs as a result of the heart’s adaptive reaction to any factor that may be requiring the heart to work harder than usual.

In most instances of left ventricular hypertrophy, the disease develops due to an underlying condition of hypertension which brings about the need for the heart to hasten its pace in order to still effectively supply blood to the entire body despite the resistance of the heightened levels of blood pressure.

The myocardium or heart muscle within the left ventricle enlarges and thickens in order to still effectively perform its critically important task. Although the changes in the heart muscle is meant as an adaptive move, the hypertrophy or enlargement of the muscles eventually robs the heart of the elasticity it requires to pump blood in the constant rhythm needed. In the long run, the hypertrophy ends up as a liability to the heart’s performance, preventing the left ventricle from keeping up with the essential constant delivery of blood the body needs

. Several underlying conditions can contribute to or influence the enlargement of the heart muscle in the left ventricle. Hypertension is the most common cause, setting the stage for left ventricular hypertrophy once a person’s blood pressure exceeds the normal level of 140/90 mm Hg. Aside from hypertension, the condition known as aortic valve stenosis is also a common cause of the hypertrophic changes in the heart.

The disease involves the narrowing of the valve that comes between the left ventricle and the aorta, a major blood vessel in the body. Although the barrier may only exist within the aortic valve, the obstacle is enough to require the left ventricle to increase its efforts.

Advertisement Left ventricular hypertrophy can also result without succeeding an underlying disorder. The condition may occur in athletes who constantly undergo training in an attempt to improve their stamina.

Under such circumstances, the heart can still react by adapting in order to accommodate the additional amount of work. Treatment The treatment for left ventricular hypertrophy depends on the cause of the condition. Doctors will aim to eliminate the cause of the heart’s enlargement in order to normalize the heart’s efforts and prevent incapacitation of the heart muscles. If high blood pressure is determined as the root cause of the disease, doctors will usually devise a treatment regimen involving medications as well as lifestyle modifications.

Coupled with the use of drugs is the need for changes in the patient’s lifestyle. The patient will have to initiate a lifestyle and diet that improves heart function through engaging in regular physical exercise, avoiding smoking at all costs, and consuming a diet that is low in both sodium and fat as both types of food components take a toll on the heart’s performance.

In severe cases, the patient may have to undergo surgery in order to effectively restore proper heart function. An aortic valve repair or replacement is the surgical procedure carried out for patients with left ventricular hypertrophy resulting from aortic valve stenosis. Treatment is achieved through getting rid of the narrowed valve and substituting it with one that is healthy and wide enough to allow proper blood flow. Left Ventricular Hypertrophy in Children

Left ventricular hypertrophy can occur as an inborn disease in infants and children, due to an underlying condition known as hypertrophic cardiomyopathy. Hypertrophic cardiomyopathy or HCM is a hereditary disease that involves an inborn abnormality of the cardiac muscles.

Hypertrophic cardiomyopathy is the most common genetic cardiac disease, and occurs when there is marked left ventricular hypertrophy in the absence of inciting factors, such as hypertension.

Hypertrophic cardiomyopathy (IHSS)

"Hypertrophic Cardiomyopathy I. What every physician needs to know.

It is caused by autosomal dominant mutations in one of 10 different genes coding for proteins needed to form the cardiac sarcomere, with more than 80% of these mutations occurring in the beta-myosin heavy chain, cardiac troponin T, and myosin-binding protein C. These mutations lead to a disorganized arrangement in cardiac myocytes resulting in hypertrophy.

This hypertrophy leads to the complex pathophysiology characteristic of hypertrophic cardiomyopathy which includes left ventricular outflow tract obstruction, diastolic dysfunction, mitral regurgitation, myocardial ischemia, and arrhythmias.

As more information has been gathered about this disease process it has been found to be increasingly heterogenic in its phenotypic expression. A large proportion of patients with hypertrophic cardiomyopathy are asymptomatic and can anticipate a normal life expectancy. Left ventricular outflow tract obstruction is not always present as one third of patients have no obstruction either at rest or with provocation.

It is important to distinguish between the obstructive and nonobstructive forms of this disease, however, as this will determine management. In truth, only a small subset of patients with this disease suffer from the more significant complications, which include symptomatic heart failure, atrial fibrillation, and sudden cardiac death due to ventricular tachyarrhythmias. Along with disorganized and hypertrophied myocytes, this disease process manifests with abnormal intramural coronary arteries.

They have thickened walls and are considered small vessels. This leads to a mismatch between cardiac muscle and perfusion leading to episodes of ischemia. This ischemia may be part of the driving force behind the arrhythmias seen in this disease process.

II. Diagnostic Confirmation: Are you sure your patient has hypertrophic cardiomyopathy? The diagnosis of hypertrophic cardiomyopathy is most commonly confirmed by 2D echocardiography and usually recognized as a left ventricular wall thickness > 15 mm. This imaging technique can not only unearth the presence and severity of hypertrophy but also that of left ventricular outflow obstruction.

Approximately, one quarter of all patients with hypertrophic cardiomyopathy will have a resting gradient (>30 millimeters mercury [mm Hg]). It is important to note that a left ventricular wall thickness > 30 mm and an outflow obstruction gradient > 30 mm Hg are both independently associated with a greater risk for sudden cardiac death.

In some cases, there is diffuse hypertrophy, but it is common to have only one area that exhibits evidence of wall thickening. A large proportion will have no gradient or only a gradient that manifests during maneuvers that simulate exertion. In these cases, evidence of left ventricular hypertrophy supports the diagnosis. When there is suspicion for hypertrophic cardiomyopathy but no evidence on echocardiography, magnetic resonance imaging of the heart can be useful in identifying the asymmetric areas of hypertrophy common in this disease.

A. History Part I: Pattern Recognition: Unfortunately, as researchers have gathered more information about hypertrophic cardiomyopathy, it has become increasingly clear that there is no ""typical"" presentation.

Over the course of their lives, patients can have varying presentations ranging from no pathology, to atrial fibrillation to congestive heart failure, to sudden cardiac death.

In general, the older a patient is with this diagnosis the more likely it is that the patient will not manifest the more malignant side effects of this disease process. Perhaps the most important identifying feature of this disease is recognizing when a patient has a family history of hypertrophic cardiomyopathy. This allows for testing of other relatives and periodic screening to identify disease progression. B. History Part 2: Prevalence: Hypertrophic cardiomyopathy is an autosomal dominant disease that has a prevalence of 1 in 500 adults.

C. History Part 3: Competing diagnoses that can mimic hypertrophic cardiomyopathy. When outflow obstruction is present, this disease process can sometimes be confused with aortic stenosis on physical exam. Furthermore, a focused history should be taken to determine if patients have an underlying cause for their ventricular hypertrophy, for example a history of systemic hypertension or reasons for infiltrative heart disease.

D. Physical Examination Findings. The most recognizable physical exam findings of hypertrophic cardiomyopathy are those correlated with outflow obstruction. When outflow obstruction is present, it is possible to hear a systolic crescendo-decrescendo murmur similar to that of aortic stenosis. but it is heard best at the left lower sternal border on auscultation. This murmur can be distinguished from aortic stenosis, however, in that it becomes less intense with maneuvers that increase venous return or vascular resistance as with squatting or hand grip, and becomes more prominent and harsh with maneuvers that decrease ventricular filling as with the Valsalva maneuver or standing up from a squatting position.

In these instances, the practitioner should listen for a murmur of aortic insufficiency since this can be present as well. When severe outflow obstruction is present, S2 may be paradoxically split due to the prolonged outflow time from the obstruction to flow. Other physical exam findings that are consistent with hypertrophic cardiomyopathy include a prominent jugular a wave due to hypertrophy and poor right ventricle compliance.

Due to hypertrophy, a heave may be present and the point of maximal impulse is often diffuse and displaced. Carotid pulsation has a classic bifid pattern which is a rapid upstroke followed by a second peak. It should be noted that there are patients with genotype positive hypertrophic cardiomyopathy that have no or minimal physiologic expression of their disease. These patients may have no abnormal physical exam findings although they do have the diagnosis of hypertrophic cardiomyopathy. E. What diagnostic tests should be performed? Since there are patients with this disease process that have no physical manifestations of the disease, there is not a physical exam finding that confirms the diagnosis.

Instead, exam findings of ventricular hypertrophy in the proper setting should lead a clinician to get imaging studies to aid in diagnosis. Please see the section on imaging studies for further information about tests that are useful to order.1.

What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted? Genetic testing may be useful to help identify patients that have mutations that portend a higher likelihood of sudden cardiac death.

For example, beta myosin heavy chain mutations and troponin T mutations may be associated with higher rates of sudden death. However, elderly patients identified with this disease often have minimal symptoms, even when outflow gradients are present.

These patients commonly have mutations in cardiac myosin binding protein C and troponin I genes. Once a patient with hypertrophic cardiomyopathy has been identified it is important to test their first degree relatives for this disease.2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Two dimensional echocardiography is the diagnostic modality of choice for this disease. It is widely available and efficient at diagnosing ventricular hypertrophy. Hypertrophic cardiomyopathy can present with just a genotype diagnosis and no initial evidence of hypertrophy on echocardiogram. In fact, hypertrophy is often first apparent during late adolescence. Patients also have varying degrees of hypertrophy ranging from mild (13-15mm) to massive (>30mm).

Hypertrophy can be diffuse or only be found in specific segments of the myocardium. If hypertrophy is present in only one area, it is found in decreasing order in the septum, apex, and the mid-ventricle respectively. When echocardiography does not identify hypertrophy, magnetic resonance imaging (MRI) can be useful in identifying specific segments of hypertrophy that may be missed with the aforementioned modality. Transthoracic echocardiography can also be used to diagnose left ventricular outflow tract obstruction which is defined as an outflow tract gradient > 30 mm Hg at rest or with provocation.

While electrocardiograms are often abnormal in patients with hypertrophic cardiomyopathy, there is no clear pattern that will aid in the diagnosis of this disease. In fact, there is no association between voltage on electrocardiogram and degree of hypertrophy on echocardiograph.

F. Over-utilized or “wasted” diagnostic tests associated with this diagnosis. N/AIII. Default Management. Management of hypertrophic cardiomyopathy is determined by symptom manifestation. In patients that are asymptomatic without concerning risk factors for sudden cardiac death there is no evidence that prophylactic therapy makes any difference in disease progression. In asymptomatic patients with very large (> 35mm) left ventricular hypertrophy, initiation of medical therapy may help delay the onset of symptoms. However, there is minimal data to support this assertion. The vast majority of patients do not have massive hypertrophy and management is targeted at control of symptoms of heart failure, ischemia, atrial fibrillation and prevention of sudden cardiac death.

Largely these are managed through medical therapy; however, in certain instances surgical intervention may be useful. A. Immediate management. Patients that present to the hospital with hypertrophic cardiomyopathy will likely be presenting due to a heart failure exacerbation. Since the majority of patients have diastolic heart failure, management is based on relieving outflow track obstruction (when present), controlling hypertension and relieving congestion.

Symptom management has been best described by use of beta-blockade as well as non-dihydropyridines (specifically Verapamil). These medications slow heart rate leading to a prolongation in diastole and increased ventricular filling time.

This in turn leads to greater cardiac output. In patients that are experiencing chest pain these medicines also decrease the cardiac muscle's demand for oxygen, leading to reduced ischemia. Diuresis with loop diuretics is advisable in patients that have evidence of volume overload, but they should be used cautiously as to not decrease preload too dramatically. These patients are also very sensitive to loss of their atrial kick, and may present with an exacerbation during an episode of atrial fibrillation.

Patients with hypertrophic cardiomyopathy are prone to episodes of atrial fibrillation. Due to wall hypertrophy and their dependence on ventricular filling to get adequate cardiac output, a rapid ventricular rate can make patients quite symptomatic. As in the general population, medical therapy to control the ventricular rate with beta-blockade or a non-dihydropyridine is the first line of therapy. If patients fail medical management and remain symptomatic atrioventricular (AV) node ablation and pacemaker implantation may be necessary to prevent episodes of tachycardia.

Unlike the general population, patient's with hypertrophic cardiomyopathy are more likely to develop thrombus with systemic embolization. Therefore, practitioners should have a very low threshold for initiating anticoagulation therapy. B.

Physical Examination Tips to Guide Management. Practitioners should pay close attention to signs of volume overload. They should monitor lung sounds for evidence of crackles indicating pulmonary edema. Furthermore, a thorough cardiac exam daily will help with management. Assessing degree of jugular venous distention and edema will help determine the extent of congestion that a patient is experiencing.

Furthermore, cardiac auscultation should be used to ensure a patient is in sinus rhythm, or rate controlled if they are experiencing atrial fibrillation.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management. As with congestive heart failure exacerbations in patients without hypertrophic cardiomyopathy, response to treatment can be monitored by symptom resolution and improvement in physical exam findings of venous congestion. There is no laboratory test or diagnostic study that needs to be followed on a regular basis to determine resolution of an exacerbation. However, in patients being treated with diuresis it may be wise to follow electrolyte levels and monitor kidney function to ensure patients are not pushed into a pre-renal state due to diuresis. D. Long-term management. Medical management of heart failure symptoms should be initiated as outlined in the immediate management section.

There is no evidence that beta-blockers or non dihydropyridines are more efficacious at treating symptoms. It is often based on physician preference and monitoring symptom control in patients. If these medications do not relieve symptoms of heart failure or chest pain then disopyramide, an antiarrhythmic agent, may be considered.

In patients with an outflow gradient, this medication may reduce and help relieve symptoms. Usually patients have evidence of diastolic heart failure, but there are those that progress to systolic dysfunction as well. In this small but important patient population the usual management of systolic heart failure should be initiated.

This includes the addition of angiotensin converter enzyme inhibitors, beta-blockade, and in certain instances aldosterone inhibitors and long acting nitrates in combination with hydralazine. In patients that have an outflow tract obstruction and remain symptomatic despite medical therapy, surgical intervention can be considered.

In patients with a gradient of over 50 mm Hg and severe heart failure symptoms, surgery can help reduce these symptoms. Myotomy-myectomy is a surgical procedure where a small amount of septal tissue is removed in order to reduce or abolish the outflow obstruction.

When performed by an experienced surgeon, it has a less than 2% mortality rate and can reduce or abolish symptoms in up to 90% of cases. In some cases, replacement of the mitral valve can be performed to help reduce the outflow tract obstruction. There are also percutaneous procedures that have been used to reduce outflow tract obstructions in patients that remain symptomatic on medical therapy.

Septal alcohol ablation is a technique used by cardiologist to reduce outflow gradients for symptom relief. In experienced centers the results can be as effective as myotomy-myectomy surgeries and can be considered for patients that have high surgical risk factors. Patients without outflow tract obstruction that remain symptomatic despite optimal medical management may need to be considered for heart transplantation.

The other subset of patients that require intervention are those patients that are at risk for ventricular arrhythmias, and possible sudden cardiac death. Sudden cardiac death is the most feared outcome of hypertrophic cardiomyopathy. It often occurs in younger patients during times of rest or minimal exertion. Amongst the general population of patients with hypertrophic cardiomyopathy the annual mortality rate is about 1%.

However, there is a subset of patients, compromising about 10% to 20%, that are at much higher risk for sudden cardiac death with an annual rate of up to 5%.

Genetic testing is beginning to reveal the mutations that are most commonly associated with sudden cardiac death which include: beta myosin heavy chain and troponin T. There are also clinical risk factors that convey a higher risk of sudden cardiac death.

In a patient with a diagnosis of hypertrophic cardiomyopathy, these high-risk factors include a prior cardiac arrest, family history of premature cardiac death, spontaneous sustained ventricular tachycardia or multiple episodes of nonsustained ventricular tachycardia on Holter monitor, multiple episodes of syncope or pre-syncope, extreme left ventricular hypertrophy (wall thickness >30 mm), or exercise induced hypotension.

It is in these high-risk patients that physicians should consider placement of implantable defibrillator devices or anti-arrhythmia therapy with amiodarone. A. Renal Insufficiency. Ensure to dose medications appropriately. B. Liver Insufficiency. No change in standard management. C. Systolic and Diastolic Heart Failure This disease leads to diastolic heart failure, and in rare instances progresses to systolic heart failure.

Please see the management section for discussion of the treatment of these diseases in the setting of hypertrophic cardiomyopathy. D. Coronary Artery Disease or Peripheral Vascular Disease Patients that are proceeding to surgery to treat symptomatic and refractory outflow tract obstruction should be evaluated for coronary artery disease prior to surgical intervention.

If necessary bypass surgery may need to be performed concurrently with myotomy-myomectomy. E. Diabetes or other Endocrine issues No change in standard management. F. Malignancy Patients that have manifestations of systolic heart failure due to hypertrophic cardiomyopathy may have limitations in the chemotherapeutic agents they can be administered.

G. Immunosuppression (HIV, chronic steroids, etc). No change in standard management. H. Primary Lung Disease (COPD, Asthma, ILD)Take into consideration the presence of lung disease if treatment for possible ventricular arrhythmias is being pursued, this may argue against using amiodarone. I. Gastrointestinal or Nutrition Issues No change in management. J. Hematologic or Coagulation Issues No change in management. K. Dementia or Psychiatric Illness/Treatment No change in management. A. Sign-out considerations While Hospitalized.

Patients with hypertrophic cardiomyopathy frequently experience atrial fibrillation. They are also more prone to clot formation leading to risk of thromboembolic events.

If a patient goes into atrial fibrillation while the patient is being cross covered, it may be prudent to have the patient started on therapeutic anticoagulation despite their CHADS2 (congestive heart failure, hypertension, age (75 years old, diabetes mellitus, stroke/transient ischemic attack) score. B. Anticipated Length of Stay. Length of stay will be largely determined by the manifestations of hypertrophic cardiomyopathy with which the patient presents. If patients are in decompensated heart failure then their length of stay should mimic those of other patients admitted for decompensated heart failure. C. When is the Patient Ready for Discharge. The patient is ready for discharge when they display a normal volume status with their baseline functional capacity.

Furthermore, they should be rate controlled and likely anticoagulated if they present with atrial fibrillation. D. Arranging for Clinic Follow-up Patients should follow with a primary care provider, and be seen by a cardiologist.1. When should clinic follow-up be arranged and with whom. Patients should follow with cardiology and general medicine.

There is no defined time for a patient to follow with these specialists after discharge. It will vary widely based on the symptoms they demonstrate related to their hypertrophic cardiomyopathy and their reason for admission.2. What tests should be conducted prior to discharge to enable best clinic first visit. N/A3. What tests should be ordered as an outpatient prior to, or on the day of, the clinic visit.

N/AE. Placement Considerations. Patients with hypertrophic cardiomyopathy will most likely live independently at home following hospitalization. F. Prognosis and Patient Counseling. Prognosis varies widely based on the patients' particular manifestations of hypertrophic cardiomyopathy. In general, the majority of patients with this disease have a very good prognosis with normal life expectancy and minimal symptoms. A. Core Indicator Standards and Documentation. Follow systolic heart failure core measures if the patient has progressed to systolic heart failure. B. Appropriate Prophylaxis and Other Measures to Prevent Readmission. N/A "