where did the first air raid take place

The first bombs delivered to their targets by air were launched on unmanned balloons, carrying a single bomb, by the Austrians against Venice in 1849,[3] during the First Italian War of Independence.

Aerial bombing of cities

The aerial bombing of cities in warfare is an optional element of strategic bombing which became widespread during World War I. The bombing of cities grew to a vast scale in World War II, and is still practiced today. The development of aerial bombardment marked an increased capacity of armed forces to deliver ordnance from the air against combatants, military bases, and factories, with a greatly reduced risk to its ground forces. Civilian and non-combatant casualties in bombed cities have variously been a purposeful result of the bombings, or unavoidable collateral damage depending on intent and technology. A number of multilateral efforts have been made to restrict the use of aerial bombardment so as to protect non-combatants.[2]

The first ever air raid was conducted during the Italo-Turkish War by Italian forces against the Ottoman province of Libya on November 1, 1911. Giulio Gavotti dropped 1.5 kg of bombs on Ain Zara, a village 8 km west of the capital Tripoli.[4]

Adrianople (presently Edirne) was bombed by Bulgaria in 1912 in the First Balkan War.[5] Historically, it was the first bombardment of a city from a heavier-than-air aircraft.[6] In the morning of 29 October 1912 at 9:30 a.m. the plane Albatros F-3 took off from an airfield near the village of Mustafa Pasha - present day Svilengrad, Bulgaria. The pilot was captain Radul Mikov with spotter and bombardier Prodan Tarakchiev. The airfield was specially created to carry out the take off and landing. According to the report weather conditions were perfect. The flight lasted for 1 hour and 20 minutes and the altitude was 500m. During the flight the crew flew over the city of Edirne, discovered hidden Ottoman forces in the nearby villages and flew towards to city railroad station, near the village of Karaagach. The plane was equipped with two bombs, which were released at 10:00 am over the station. The crew landed successfully at the airfield with 4 holes on the hull. A number of journalists and military attachés attended the site.

In May 1914, during the revolution of 1910–17, General Venustiano Carranza, later president, ordered a biplane to bomb Neveria Hill adjacent to the downtown area of Mazatlán in order to take the city. The bomb landed not on target but in a city street and in the process killed two citizens and wounded several others.[citation needed]

The first civilian target to be bombed from the air was the Belgian city of Antwerp. This city, at that moment the National Redoubt of Belgium, was bombed during the night of 24–25 August 1914. Instead of targeting the surrounding fortresses, the Zeppelin LZ 25's intention was to bomb the clearly distinguishable historical centre of the city. After dropping approximately ten bombs, ten people were killed and forty injured. The British Royal Naval Air Service (RNAS) undertook the first Entente strategic bombing missions on 22 September 1914 and 8 October, when it bombed the Zeppelin bases in Cologne and Düsseldorf. The aeroplanes carried twenty-pound bombs, and at least one airship was destroyed.[7][8] On 19 January 1915 two German Zeppelins dropped 24 fifty-kilogram (110 lb) high-explosive bombs and ineffective three-kilogram incendiaries on the English towns of Great Yarmouth, Sheringham, King's Lynn, and the surrounding villages; in all, four people were killed, 16 injured, and monetary damage was estimated at £7,740.[9]

London was bombed for the first time on 30 May 1915. In July 1916, the German government allowed directed raids against urban centers, sparking 23 airship raids in 1916 in which 125 tons of ordnance were dropped, killing 293 people and injuring 691. Gradually British air defenses improved and the Germans also introduced large bomber aircraft for bombing Britain. In 1917 and 1918 there were only eleven Zeppelin raids against England, and the final raid occurred on 5 August 1918, which resulted in the death of KK Peter Strasser, commander of the German Naval Airship Department. By the end of the war, 51 raids had been undertaken, in which 5,806 bombs were dropped, killing 557 people and injuring 1,358[citation needed]. In the course of the Zeppelin raids the Germans lost more than half their airships and 40% of their crew. It has been argued that the raids were effective far beyond material damage inflicted, in diverting and hampering wartime production, and diverting twelve squadrons and over 10,000 men to air defenses.[citation needed] The British developed an Independent Force of long-range bombers that could bomb Berlin, but the war ended before these raids began.

After the war, bombers' increasing sophistication led to the general belief that aerial bombing would both destroy cities and be impossible to stop; as Stanley Baldwin stated in a 1932 speech, "The bomber will always get through".

After World War I, there were protests in Iraq against continued British rule. Many Iraqis across a wide spectrum of opinion opposed the British Mandate for Iraq. The Iraqi revolt against the British began, with peaceful demonstrations in May 1920. Initial demands were rejected by the British administration, and fighting broke out in June 1920. This was suppressed, with many deaths, and at very high costs to the Empire. A policy of 'aerial policing', an invention of Winston Churchill's was brought in. This amounted to bombing restive civilians, followed up by pacification by ground troops. This continued up to the mid 1920s.[10] The aerial campaign included Sir Arthur Harris, 1st Baronet, who commanded a Vickers Vernon squadron engaged in the bombing and strafing of recalcitrant civilians.[11] Harris felt that the Arab civilians required this kind of "heavy hand" treatment.[12]

Following the end of World War I, the British stepped up their efforts in their war against the Somali Dervish state, led by the so-called "Mad Mullah", whom they had been fighting for the control the area formerly known as British Somaliland. However, they had been unable to defeat the Dervish state for nearly 25 years. In January 1920, the British launched a combined aerial and land attack, bombarding Taleeh, the capital of the Dervish State.[13] The Somaliland Campaign has been described as one of the bloodiest and longest-running conflicts in the history of sub-Saharan Africa and the Somali forces are noted for concurrently repelling the invading British, Italian and Abyssinian forces for a period of 25 years.[14]

During the Cristero War in Mexico in 1929, Irish pilot and mercenary Patrick Murphy mistakenly dropped several improvised "suitcase bombs" on the border town of Naco, Arizona, while bombing government forces in the adjacent town of Naco, Sonora, for the Cristero revolutionaries. The bombing, which caused damage to many buildings and injured several bystanders on the American side of the international border, became the first aerial bombardment of the Continental United States by a foreign power in American history.[15][16]

The Italians used aircraft against the Ethiopian cities in the Second Italo-Abyssinian War. For example, in February 1936, the Italian invasion forces in the south prepared for a major thrust towards the city of Harar. On 22 March, the Regia Aeronautica bombed Harar and Jijiga as a prelude. Both cities were reduced to ruins even though Harar had been declared an "open city".[17]

During the Spanish Civil War, the Nationalists under Francisco Franco made extensive use of aerial bombing on civilian targets. Nazi Germany gave aircraft to Franco to support the overthrow of the Spanish Republican government. The first major example of this came in November 1936, when German and Spanish aircraft bombed Republican-held Madrid; this bombardment was sustained throughout the Siege of Madrid. Barcelona and Valencia were also targeted in this way. On 26 April 1937, the German Luftwaffe (Condor Legion) bombed the Spanish city of Guernica carrying out the most high-profile aerial attack of the war. This act caused worldwide revulsion and was the subject of a famous painting by Picasso, but by the standards of bombings during World War II, casualties were fairly minor (estimates ranging from 500 to 1,500).[citation needed]

Shortly after, the front-page headlines of the Diario de Almeria, dated June 3, 1937, referred to the press in London and Paris carrying the news of the "criminal bombardment of Almeria by German planes".[18]

Barcelona was bombarded for three days beginning on 16 March 1938, at the height of the Spanish Civil War. Under the command of the Italian dictator Benito Mussolini, Italian aircraft stationed on the island of Majorca attacked 13 times dropping 44 tons of bombs, aimed at the civil population. These attacks were at the request of General Franco as retribution against the Catalan population.[citation needed][dubious – discuss] The medieval Cathedral of Barcelona suffered bomb damage and more than one thousand people died, including many children. The number of people injured is estimated to be in the thousands.[19] Many others Spanish towns and cities were bombed by the German Legion Condor and the Italian Aviazione Legionaria among them Jaen, Durango, Granollers and Alicante.

During the Manchurian Incident of 1931, the Japanese widely used airplanes to indiscriminately bomb key targets and cities, such as Mukden. After the Marco Polo Bridge Incident, the Imperial Japanese Army Air Service, in conjunction with the Imperial Japanese Navy Air Service, began relentlessly bombing Shanghai, Beijing (Peking), Tianjin (Tientsin) and several cities on the Chinese coast from the beginning of the Second Sino-Japanese War in 1937.

The bombing campaigns on Nanking and Canton which started in September 1937 evoked protests from the Western powers culminating in a resolution by the Far Eastern Advisory Committee of the League of Nations. An example of the many expressions of indignation came from Lord Cranborne, the British Under-Secretary of State For Foreign Affairs:

Words cannot express the feelings of profound horror with which the news of these raids had been received by the whole civilized world. They are often directed against places far from the actual area of hostilities. The military objective, where it exists, seems to take a completely second place. The main object seems to be to inspire terror by the indiscriminate slaughter of civiliansÂ ...[20]

At the beginning of World War II, bombing of cities prior to invasion was an integral part of Nazi Germany's strategy. In the first stages of war, the Germans carried out many bombings of towns and cities in Poland (1939), including the capital Warsaw (also bombed in 1944), with Wieluń being the first city destroyed by 75%. The Soviet Union also attempted strategic bombing against Poland and Finland, bombing Helsinki.[citation needed]

The British bombed the German city of Monchengladbach on 11 May 1940.[21] While Germany had refrained from aerial bombing of British cities after the British declaration of war on Germany in September 1939, Britain started aerial bombing of Germany, officially focusing on military and industrial targets, on the night of 15/16 May with 78 bombers against oil targets, 9 against steelworks and 9 against marshaling yards.[22] Oil remained the main British objective until the summer of 1941, although German cities and towns were regularly bombed from May 1940.

After the Fall of France, the Luftwaffe turned its attention to the United Kingdom. The scale of the attack increased greatly in July 1940, with 258 civilians killed, and again in August with 1,075 dead.[23] During the night of 25 August, British bombers raided targets in and around Greater Berlin for the first time, in response to the accidental bombing of Oxford Street and the West End by the Luftwaffe while it was bombing the London docks.[24] On 4 September 1940 Hitler, frustrated by the RAF's superiority over the Luftwaffe and enraged by its bombing of German cities, decided to retaliate by bombing London and other cities in the UK.[25] On 7 September the Luftwaffe began massed attacks on London. The bombing campaign was known in the UK as "the Blitz", and ran from September 1940 through to May 1941. The Coventry Blitz and the Belfast Blitz were two of the heaviest of all bombings by the Luftwaffe, killing 568-1,000 civilians of Coventry, killing over 1,100 civilians in Belfast, and destroying much of both city centres.

British bombing policy evolved during the war. In the beginning, the RAF was forbidden to attack targets in Germany due to the risk of accidental civilian casualties.[26] Following a German attack on military targets in the Orkney Islands on 16 March 1940 that killed a civilian, the RAF mounted its first attack against a German land target, the seaplane base on the island of Sylt.[27] The RAF began attacking transport targets west of the Rhine on the night of 10 May following the German invasion of the Low Countries, and military targets in the rest of Germany after the bombing of Rotterdam.[28] On 9 September 1940 RAF crews were instructed that due to the "indiscriminate" nature of German bombing, if they failed to find their assigned targets they were to attack targets of opportunity rather than bring their bombs home.[29] On the 15/16 December the RAF carried out its first area bombing attack (destroying 45% of the city of Mannheim), officially in response to the raid on Coventry.[30] The bombing of Mannheim has often been described as the first deliberate "terror bombing" of the war.[31]

In 1942, the goals of the British attacks were defined: the primary goal was the so-called "morale bombing", to weaken the will of the civil population to resist. Following this directive intensive bombing of highly populated city centers and working class quarters started. On 30 May 1942, the RAF Bomber Command launched the first "1,000 bomber raid" when 1,046 aircraft bombed Cologne in Operation Millennium, dropping over 2,000 tons of high explosive and incendiaries on the medieval town and burning it from end to end. 411 civilians and 85 combatants were killed, more than 130,000 had to leave the city.[citation needed]

Two further 1,000 bomber raids were executed over Essen and Bremen, but to less effect than the destruction at Cologne. The effects of the massive raids using a combination of blockbuster bombs and incendiaries created firestorms in some cites. The most extreme examples were caused by the bombing of Hamburg in Operation Gomorrah (45,000 dead), and the bombings of Kassel (10,000 dead), Darmstadt (12,500 dead), Pforzheim (21,200 dead), Swinemuende (23,000 dead), and Dresden (25,000 dead[32]).[citation needed]

The Allies also bombed urban areas in the other countries, including occupied France (Caen) and the major industrial cities of northern Italy, like Milan and Turin. Some cities were bombed at the different times by the Luftwaffe and the Allies, for example Belgrade in Yugoslavia and Bucharest in Romania.[citation needed]

The Luftwaffe also bombed cities in the Soviet Union, destroying Stalingrad in a massive air raid at the start of the Battle of Stalingrad and bombing Leningrad during the siege of the city of 1941â€“1943. The Soviet bombing of the German cities was limited in comparison with the RAF bombing (destruction caused by the Soviet army was mainly due to the land artillery). The Soviet Air Force also bombed Budapest in Hungary.[citation needed]

In the Pacific theater, Japan continued to bomb Chinese cities as well as other Asian cities such as Singapore, Rangoon, and Mandalay. In the first few months of the war with the Western Powers, Japan projected its airpower on cities as distant as Colombo and Darwin.

The U.S. firebombed Tokyo on the night of March 9–10, 1945, and killed more than 100,000 people in the deadliest conventional bombing in history, known to the United States Army Air Forces (USAAF) as Operation Meetinghouse.[33] In a few hours, 100,000 people who were in Tokyo including civilians died either by the bombing or the conflagration that followed the bombing by 325 U.S. B-29's night attacks. The fleet included 279 bombers. The bombing was meant to burn wooden buildings and indeed the bombing caused fire that created a 50 m/s wind that is comparable to tornadoes. A total of 381,300 bombs amounting to 1783 tons, were used in the bombing.

After the successful Operation Meetinghouse raid, the USAAF then went on to attack other Japanese cities with incendiary and high-explosives bombs in effort to pulverize the enemy's war industry and shatter the enemy's civilian morale to contribute to the war effort. From March to August 1945, the U.S. firebombing of 66 other Japanese cities had killed 350,000 civilians. In addition, the atomic bombings of Hiroshima and Nagasaki killed 120,000 non-combatants, most of them civilians, and combatants.[34]

During the Korean War of 1950â€“1953, U.S.-led UN air forces heavily bombed the cities in North Korea and the North-occupied South Korea, including their respective capital cities.[35] There were also plans to use nuclear weapons against North Korea and the People's Republic of China.[36]

From 1965 to 1968, during the Vietnam War, the United States Air Force conducted an aerial campaign known as Operation Rolling Thunder. The campaign began with interdiction of supply lines in rural areas of southern North Vietnam but incrementally spread northward throughout the country. In 1966, restrictions against bombing the capital city of Hanoi and the country's largest port, Haiphong, were lifted, and they were bombed by the USAF and Navy.[37] The bombing of the city centers continued to be prohibited.[38] However, the South Vietnamese cities seized by the communists were bombed, including the former capital of Huế during the 1968 Tet Offensive.[citation needed]

The Republic of Vietnam Air Force bombed contested cities in South Vietnam in 1968, 1972 and 1975, while the Vietnam People's Air Force attacked Southern cities (including the capital city of Saigon) in 1975.[citation needed]

The Lebanese capital of Beirut was attacked by the Israeli aircraft during the Siege of Beirut in 1982, and during the 2006 Lebanon War (using guided munitions). Israeli cities were bombed by Egyptian, Syrian and Jordanian aircraft during the 1948 Arab-Israeli war and the Six day war. The bombing included attacks on some of Israel's largest cities, such as Tel Aviv, Jerusalem and Haifa. Israel also conducted air strikes targeting Palestinian targets during the Second Intifada, including against Hamas in Gaza.[citation needed]

In March 1979, in response to an uprising, the Khalq-control army of Democratic Republic of Afghanistan carpet-bombed the Afghan third-largest city of Herat, causing massive destruction[39] and some 5,000 to 25,000 deaths.[40] Herat was also repeatedly bombed during the following Soviet involvement in the Afghan civil war.

Following the September 11, 2001 attacks, the U.S.-led coalition attacked the urban targets in Afghanistan using mainly precision-guided munitions (or "smart bombs"). The United States government maintains that it has a policy of striking only significant combatant targets while doing all possible to avoid what it terms "collateral damage" to civilians and non-combatants during the U.S.-led war in Afghanistan.

Saddam Hussein's Iraq attacked civilian targets in Iranian cities in the "War of the Cities" during the Iran–Iraq War in the 1980s, with Iranians retaliating in kind (both sides soon switched to ballistic missile attacks).[citation needed] Iraqi aircraft also bombed the Iraqi Kurdistan city of Halabja with conventional and chemical weapons in 1988, killing more than 5,000 people in the largest aerial poison gas attack in history.

In 1988 Somali Air Force aircraft conducted intense aerial bombardment of major Isaaq cities targeting civilian Isaaqs during its campaign against Somali National Movement in the north of the country. Civilians were also strafed by Somali Air Force aircraft as they were fleeing the aerial bombardment.[42] The artillery shelling and aerial bombardment caused the deaths of estimated 50,000 - 200,000 Isaaq civilians, as well as the complete destruction of Somalia's second and third largest cities.[43] It also caused up to 500,000[44][45] Somalis (primarily of the Isaaq clan)[46] to flee and cross the border into Hartasheikh in Ethiopia as refugees in what was described as "one of the fastest and largest forced movements of people recorded in Africa",[47] and resulted in the creation of the world's largest refugee camp then (1988),[48] with another 400,000 being internally displaced.[49][50][51] The scale of destruction led to Hargeisa being known as the 'Dresden of Africa'.[52]

The Iraqi Air Force attacked Kuwait City in 1990 and bombed their own cities during the 1991 uprisings in Iraq, targeting civilians with the use of bomb-carrying helicopters (use of airplanes was banned by the Coalition as part of the ceasefire agreement that ended hostilities of the Gulf War but not the war itself).

UN-led coalition aircraft attacked targets in Iraqi cities, including in the capital Baghdad and the largest southern city of Basra during Operation Desert Storm in 1991.[citation needed]

At the beginning of the Yugoslav Wars, in Croatia (1991), the Yugoslav People's Army (JNA) carried out aerial bombing of Dubrovnik and Vukovar.[53]

NATO's aerial bombing of FR Yugoslavia in 1999, an answer to the conflict in Kosovo, included aerial bombing throughout Serbia, notably of Belgrade, Novi Sad and Niš. There were civilian casualties. Despite that the NATO campaign indeed being a violation of NATO's own charter,[54] the UNSC rebutted the case on March 24 and March 26 1999.[55] NATO hit civilian economic infrastructure, the integrated national power grid (leaving many cities in the dark), schools, hospitals, water purification plants, dams, oil refineries fertilizer factories, a petrochemical plant, national parks and marketplaces, and also nearly hit nuclear reactors and waste facilities.[56] The 78-day bombing campaign is assessed as having been an 'economic catastrophe', cutting the Yugoslav economy in half.[56]

Post-Soviet Russia heavily bombed the Chechen capital of Grozny from the air with mostly unguided munitions (including fuel-air explosives) as well as bombarding it with a massive artillery barrages (1994–1995, 1996 and 1999–2000), killing thousands of people (some estimates say 27,000 civilians were killed during the 1994-1995 siege alone[57]) including civilians during the First and Second Chechen Wars. Although the Russian pilots and soldiers were ordered to attack designated targets only, such as the Presidential Palace, due to their inexperience and lack of training, Russian soldiers and pilots bombed and shelled random targets inside the city. In 2003, the UN still called Grozny the most destroyed city on earth.[58]

In 2003 Invasion of Iraq, the U.S.-led coalition aircraft again bombed Iraq, including the Shock and Awe campaign of precision bombing[citation needed] of government targets in the city centers. Since then, coalition aircraft attack Iraqi insurgent targets, including in urban locations like Najaf, Fallujah, Basra and Baghdad.[citation needed] There are frequent reports of civilian casualties, though it is often hard to distinguish guerrillas and civilians.

Syrian MiG-23s bombed the city of Aleppo on 24 July 2012, the first use of aerial bombing in the Syrian civil war.[59][60][61]

Budapest was attacked by the Soviet air strikes in 1956 during the Hungarian Revolution.[citation needed] In 2008, the cities of Tskhinvali and Gori were hit by the Georgian and Russian aircraft during the war in Georgia.[62]

Air warfare, theoretically, must comply with laws and customs of war, including international humanitarian law by protecting the victims of the conflict and refraining from attacks on protected persons.[63]

These restraints on aerial warfare are covered by the general laws of war, because unlike war on land and at sea—which are specifically covered by rules such as the 1907 Hague Convention and Protocol I additional to the Geneva Conventions, which contain pertinent restrictions, prohibitions and guidelines— there are no treaties specific to aerial warfare.[63]

To be legal, aerial operations must comply with the principles of humanitarian law: military necessity, distinction, and proportionality:[63] An attack or action must be intended to help in the defeat of the enemy; it must be an attack on a legitimate military objective, and the harm caused to civilians or civilian property must be proportional and not excessive in relation to the concrete and direct military advantage anticipated.


why did the house of lords issue the practice statement in 1966

Until the year 1966, the House of Lords in the United Kingdom was bound to follow all of its previous decisions under the principle of stare decisis, even if this created "injustice" and "unduly restrict(s) the proper development of the law" (London Tramways Co. v London County Council [1898] AC 375). The Practice Statement 1966 is authority for the House of Lords to depart from their previous decisions. It does not affect the precedential value of cases in lower courts; all other courts that recognise the Supreme Court (formerly the House of Lords) as the court of last resort are still bound by Supreme Court decisions. Before this, the only way a binding precedent could be avoided was to create new legislation on the matter.

Practice Statement

The Practice Statement [1966] 3 All ER 77[1] was a statement made in the House of Lords by Lord Gardiner LC on July 26, 1966 on behalf of himself and the Lords of Appeal in ordinary, that they would depart from precedent in the Lords in order to achieve justice.

A germane example is the case of Anderton v Ryan (1985)[2] where the House of Lords interpreted the Criminal Attempts Act 1981 in such a way as to make the Act virtually ineffective. Only one year later in R v Shivpuri (1986)[3] Lord Bridge (a member of the erroneous majority in Anderton) acknowledged the error and said "the Practice Statement is an effective abandonment of our pretension to infallibility. If a serious error embodied in a decision of this House has been distorted by the law, the sooner it is corrected the better".[4]

By contrast, in Knuller v DPP,[5] Lord Reid, who had previously given a strong dissenting judgment in Shaw v DPP,[6] said while he still disagreed with the majority decision in that case, in the interests of certainty he would not overturn Shaw (even though the Practice Statement had given authority to do so).

This is the text of the Practice Statement:

Their Lordships nevertheless recognise that too rigid adherence to precedent may lead to injustice in a particular case and also unduly restrict the proper development of the law. They propose therefore, to modify their present practice and, while treating former decisions of this house as normally binding, to depart from a previous decision when it appears right to do so.

In this connection they will bear in mind the danger of disturbing retrospectively the basis on which contracts, settlement of property, and fiscal arrangements have been entered into and also the especial need for certainty as to the criminal law.

This announcement is not intended to affect the use of precedent elsewhere than in this House.


most common cause of death in acute myocardial infarction

Complications may occur immediately following the myocardial infarction or may take time to develop. Disturbances of heart rhythms, including atrial fibrillation, ventricular tachycardia and fibrillation and heart block can arise as a result of ischemia, cardiac scarring, and infarct location.[15][58] Stroke is also a risk, either as a result of clots transmitted from the heart during PCI, as a result of bleeding following anticoagulation, or as a result of disturbances in the heart's ability to pump effectively as a result of the infarction.[58] Regurgitation of blood through the mitral valve is possible, particularly if the infarction causes dysfunction of the papillary muscle.[58] Cardiogenic shock as a result of the heart being unable to adequately pump blood may develop, dependent on infarct size, and is most likely to occur within the days following an acute myocardial infarction. Cardiogenic shock is the largest cause of in-hospital mortality.[25][58] Rupture of the ventricular dividing wall or left ventricular wall may occur within the initial weeks.[58] Dressler's syndrome, a reaction following larger infarcts and a cause of pericarditis is also possible.[58]

Myocardial infarction

Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing damage to the heart muscle.[1] The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw.[1] Often it occurs in the center or left side of the chest and lasts for more than a few minutes.[1] The discomfort may occasionally feel like heartburn.[1] Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat, or feeling tired.[1] About 30% of people have atypical symptoms.[7] Women more often have atypical symptoms than men.[10] Among those over 75 years old, about 5% have had an MI with little or no history of symptoms.[11] An MI may cause heart failure, an irregular heartbeat, cardiogenic shock, or cardiac arrest.[2][3]

Most MIs occur due to coronary artery disease.[2] Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, and excessive alcohol intake, among others.[4][5] The complete blockage of a coronary artery caused by a rupture of an atherosclerotic plaque is usually the underlying mechanism of an MI.[2] MIs are less commonly caused by coronary artery spasms, which may be due to cocaine, significant emotional stress, and extreme cold, among others.[12][13] A number of tests are useful to help with diagnosis, including electrocardiograms (ECGs), blood tests, and coronary angiography.[6] An ECG, which is a recording of the heart's electrical activity, may confirm an ST elevation MI (STEMI) if ST elevation is present.[7][14] Commonly used blood tests include troponin and less often creatine kinase MB.[6]

Treatment of an MI is time critical.[15] Aspirin is an appropriate immediate treatment for a suspected MI.[8] Nitroglycerin or opioids may be used to help with chest pain; however, they do not improve overall outcomes.[7][8] Supplemental oxygen should be used in those with low oxygen levels or shortness of breath.[8] In a STEMI, treatments attempt to restore blood flow to the heart, and include percutaneous coronary intervention (PCI), where the arteries are pushed open and may be stented, or thrombolysis, where the blockage is removed using medications.[7] People who have a non-ST elevation myocardial infarction (NSTEMI) are often managed with the blood thinner heparin, with the additional use of PCI in those at high risk.[8] In people with blockages of multiple coronary arteries and diabetes, coronary artery bypass surgery (CABG) may be recommended rather than angioplasty.[16] After an MI, lifestyle modifications, along with long term treatment with aspirin, beta blockers, and statins, are typically recommended.[7]

Worldwide, about 15.9 million myocardial infarctions occurred in 2015.[9] More than 3 million people had an ST elevation MI and more than 4 million had an NSTEMI.[17] STEMIs occur about twice as often in men as women.[18] About one million people have an MI each year in the United States.[2] In the developed world the risk of death in those who have had an STEMI is about 10%.[7] Rates of MI for a given age have decreased globally between 1990 and 2010.[19] In 2011, AMI was one of the top five most expensive conditions during inpatient hospitalizations in the US, with a cost of about $11.5 billion for 612,000 hospital stays.[20]

Myocardial infarction (MI) refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart.[21] Unlike other causes of acute coronary syndromes, such as unstable angina, a myocardial infarction occurs when there is cell death, as measured by a blood test of cardiac enzymes such as troponin or CK-MB.[15] When there is evidence of an MI, it may be classified as an ST elevation myocardial infarction (STEMI) or Non-ST elevation myocardial infarction (NSTEMI) based on the results of an ECG.[22]

The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden cardiac death. An MI is different from—but can cause—cardiac arrest, where the heart is not contracting at all or so poorly that all vital organs cease to function, thus causing death. It is also distinct from heart failure, in which the pumping action of the heart is impaired. However, an MI may lead to heart failure.[23]

Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen.[24] The pain most suggestive of an acute MI, with the highest likelihood ratio, is pain radiating to the right arm and shoulder.[25] Similarly, chest pain similar to a previous heart attack is also suggestive.[26] The pain associated with MI is usually diffuse, does not change with position, and lasts for more than 20 minutes.[22] Levine's sign, in which a person localizes the chest pain by clenching one or both fists over their sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poor positive predictive value.[27] Pain that responds to nitroglycerin does not indicate the presence or absence of a myocardial infarction.[28]

Chest pain may be accompanied by sweating, nausea or vomiting, and fainting,[22][25] and these symptoms may also occur without any pain at all.[24] In women, the most common symptoms of myocardial infarction include shortness of breath, weakness, and fatigue.[29] Shortness of breath is a common, and sometimes the only symptom, occurring when damage to the heart limits the output of the left ventricle, with breathlessness arising either from low oxygen in the blood, or pulmonary edema.[24][30] Other less common symptoms include weakness, light-headedness, palpitations, and abnormalities in heart rate or blood pressure.[15] These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system, which occurs in response to pain and, where present, low blood pressure.[31] Loss of consciousness due to inadequate blood flow to the brain and cardiogenic shock, and sudden death, frequently due to the development of ventricular fibrillation, can occur in myocardial infarctions.[23] Cardiac arrest, and atypical symptoms such as palpitations, occur more frequently in women, the elderly, those with diabetes, in people who have just had surgery, and in critically ill patients.[22]

"Silent" myocardial infarctions can happen without any symptoms at all.[11] These cases can be discovered later on electrocardiograms, using blood enzyme tests, or at autopsy after a person has died. Such silent myocardial infarctions represent between 22 and 64% of all infarctions,[11] and are more common in the elderly,[11] in those with diabetes mellitus[15] and after heart transplantation. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.[32] In heart transplantation, the donor heart is not fully innervated by the nervous system of the recipient.[33]

The most prominent risk factors for myocardial infarction are older age, actively smoking, high blood pressure, diabetes mellitus, and total cholesterol and high-density lipoprotein levels.[18] Many risk factors of myocardial infarction are shared with coronary artery disease, the primary cause of myocardial infarction,[15] with other risk factors including male sex, low levels of physical activity, a past family history, obesity, and alcohol use.[15] Risk factors for myocardial disease are often included in risk factor stratification scores, such as the Framingham risk score.[18] At any given age, men are more at risk than women for the development of cardiovascular disease.[34] High levels of blood cholesterol is a known risk factor, particularly high low-density lipoprotein, low high-density lipoprotein, and high triglycerides.[35]

Many risk factors for myocardial infarction are potentially modifiable, with the most important being tobacco smoking (including secondhand smoke).[15] Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease.[36] Lack of physical activity has been linked to 7â€“12% of cases.[36][37] Less common causes include stress-related causes such as job stress, which accounts for about 3% of cases,[36] and chronic high stress levels.[38]

There is varying evidence about the importance of saturated fat in the development of myocardial infarctions. Eating polyunsaturated fat instead of saturated fats has been shown in studies to be associated with a decreased risk of myocardial infarction,[39] while other studies find little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake affects heart attack risk.[40][41] Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed.[42] Trans fats do appear to increase risk.[40] Acute and prolonged intake of high quantities of alcoholic drinks (3â€“4 or more) increases the risk of a heart attack.[43]

Family history of ischemic heart disease or MI, particularly if one has a male first-degree relative (father, brother) who had a myocardial infarction before age 55 years, or a female first-degree relative (mother, sister) less than age 65 increases a person's risk of MI.[34]

Genome-wide association studies have found 27 genetic variants that are associated with an increased risk of myocardial infarction.[44] The strongest association of MI has been found with chromosome 9 on the short arm p at locus 21, which contains genes CDKN2A and 2B, although the single nucleotide polymorphisms that are implicated are within a non-coding region.[44] The majority of these variants are in regions that have not been previously implicated in coronary artery disease. The following genes have an association with MI: PCSK9, SORT1, MIA3, WDR12, MRAS, PHACTR1, LPA, TCF21, MTHFDSL, ZC3HC1, CDKN2A, 2B, ABO, PDGF0, APOA5, MNF1ASM283, COL4A1, HHIPC1, SMAD3, ADAMTS7, RAS1, SMG6, SNF8, LDLR, SLC5A3, MRPS6, KCNE2.[44]

The risk of having a myocardial infarction increases with older age, low physical activity, and low socioeconomic status.[34] Heart attacks appear to occur more commonly in the morning hours, especially between 6AM and noon.[45] Evidence suggests that heart attacks are at least three times more likely to occur in the morning than in the late evening.[46] Shift work is also associated with a higher risk of MI.[47]

Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors.[48] The use of non-steroidal anti inflammatory drugs (NSAIDs), even for as short as a week, increases risk.[49]

Endometriosis in women under the age of 40 is an identified risk factor.[50]

Short-term exposure to air pollution such as carbon monoxide, nitrogen dioxide, and sulfur dioxide (but not ozone) have been associated with MI.[51]

A number of acute and chronic infections including Chlamydophila pneumoniae, influenza, Helicobacter pylori, and Porphyromonas gingivalis among others have been linked to atherosclerosis and myocardial infarction.[52] As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.[52][53] Myocardial infarction can also occur as a late consequence of Kawasaki disease.[54]

Calcium deposits in the coronary arteries can be detected with CT scans. Calcium seen in coronary arteries can provide predictive information beyond that of classical risk factors.[55] High blood levels of the amino acid homocysteine is associated with premature atherosclerosis;[56] whether elevated homocysteine in the normal range is causal is controversial.[57]

The most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle.[23][58] Plaques can become unstable, rupture, and additionally promote the formation of a blood clot that blocks the artery; this can occur in minutes. Blockage of an artery can lead to tissue death in tissue being supplied by that artery.[59] Atherosclerotic plaques are often present for decades before they result in symptoms.[59]

The gradual buildup of cholesterol and fibrous tissue in plaques in the wall of the coronary arteries or other arteries, typically over decades, is termed atherosclerosis.[60] Atherosclerosis is characterized by progressive inflammation of the walls of the arteries.[59] Inflammatory cells, particularly macrophages, move into affected arterial walls. Over time, they become laden with cholesterol products, particularly LDL, and become foam cells. A cholesterol core forms as foam cells die. In response to growth factors secreted by macrophages, smooth muscle and other cells move into the plaque and act to stabilize it. A stable plaque may have a thick fibrous cap with calcification. If there is ongoing inflammation, the cap may be thin or ulcerate. Exposed to the pressure associated with blood flow, plaques, especially those with a thin lining, may rupture and trigger the formation of a blood clot (thrombus).[59]

Atherosclerotic disease is not the only cause of myocardial infarction, and it may exacerbate or contribute to other causes. A myocardial infarction may result from a heart with a limited blood supply subject to increased oxygen demands, such as in fever, a fast heart rate, hyperthyroidism, too few red blood cells in the bloodstream, or low blood pressure. Damage or failure of procedures such as percutaneous coronary intervention or coronary artery bypass grafts may cause a myocardial infarction. Spasm of coronary arteries, such as Prinzmetal's angina may cause blockage.[24][22]

If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the blocked coronary artery die (infarction), chiefly through necrosis, and do not grow back. A collagen scar forms in their place.[59] When an artery is blocked, cells lack oxygen, needed to produce ATP in mitochondria. ATP is required for the maintenance of electrolyte balance, particularly through the Na/K ATPase. This leads to an ischemic cascade of intracellular changes, necrosis and apoptosis of affected cells.[61]

Cells in the area with the worst blood supply, just below the inner surface of the heart (endocardium), are most susceptible to damage.[62] Ischemia first affects this region, the subendocardial region, and tissue begins to die within 15–30 minutes of loss of blood supply.[63] The dead tissue is surrounded by a zone of potentially reversible ischemia that progresses to become a full-thickness transmural infarct.[61][63] The initial "wave" of infarction can take place over 3–4 hours.[59][61] These changes are seen on gross pathology and cannot be predicted by the presence or absence of Q waves on an ECG.[62] The position, size and extent of an infarct depends on the affected artery, totality of the blockage, duration of the blockage, the presence of collateral blood vessels, oxygen demand, and success of interventional procedures.[24][58]

Tissue death and myocardial scarring alter the normal conduction pathways of the heart, and weaken affected areas. The size and location puts a person at risk of abnormal heart rhythms (arrhythmias) or heart block, aneurysm of the heart ventricles, inflammation of the heart wall following infarction, and rupture of the heart wall that can rupture with catastrophic consequences.[58][64]

An acute myocardial infarction, according to current consensus, is defined by an elevated cardiac biomarker and at least one of the following:[22]

Myocardial infarctions are generally clinically classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG.[22] STEMIs make up about 25 â€“ 40% of myocardial infarctions.[18] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:[22]

There are a number of different biomarkers used to determine the presence of cardiac muscle damage. Troponins, measured through a blood test, are considered to be the best,[18] and are preferred because they have greater sensitivity and specificity for measuring injury to the heart muscle than other tests.[58] A rise in troponin occurs within 2–3 hours of injury to the heart muscle, and peaks within 1–2 days. The gross value of the troponin, as well as a change over time, are useful in measuring and diagnosing or excluding myocardial infarctions, and the diagnostic accuracy of troponin testing is improving over time.[58] One high-sensitivity cardiac troponin is able to rule out a heart attack as long as the ECG is normal.[65]

Other tests, such as CK-MB or myoglobin, are discouraged.[66] CK-MB is not as specific as troponins for acute myocardial injury, and may be elevated with past cardiac surgery, inflammation or electrical cardioversion; it rises within 4–8 hours and returns to normal within 2–3 days.[24] Copeptin may be useful to rule out MI rapidly when used along with troponin.[67]

Electrocardiograms (ECGs) are a series of leads placed on a person's chest that measure electrical activity associated with contraction of heart muscle.[68] The taking of an ECG is an important part in the workup of an AMI,[22] and ECGs are often not just taken once, but may be repeated over minutes to hours, or in response to changes in signs or symptoms.[22]

ECG readouts product a waveform with different labelled features.[68] In addition to a rise in biomarkers, a rise in the ST segment, changes in the shape or flipping of T waves, new Q waves, or a new left bundle branch block can be used to diagnose an AMI.[22] In addition, ST elevation can be used to diagnose an ST segment myocardial infarction (STEMI). A rise must be new, in two adjacent adjacent ECG leads, greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15 mV) in females in all leads except for V2 and V3, where it must be greater than 1 mm (0.1 mV).[18][22] ST elevation is associated with infarction, and may be preceded by changes indicating ischemia, such as ST depression or inversion of the T waves.[68] Abnormalities can help localize the location of an infarct, based on the leads that are affected by changes.[15] Early STEMIs may be preceded by peaked T waves.[18] Other ECG abnormalities relating to complications of acute myocardial infarctions may also be evident, such as atrial or ventricular fibrillation.[69]

Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial infarction.[22] Tests such as chest X-rays can be used to explore and exclude alternate causes of a person's symptoms.[22] Tests such as stress echocardiography and myocardial perfusion imaging can confirm a diagnosis when a person's history, physical examination (including cardiac examination) ECG, and cardiac biomarkers suggest the likelihood of a problem.[70]

Echocardiography, an ultrasound scan of the heart, is able to visualize the heart, its size, shape, and any abnormal motion of the heart walls as they beat that may indicate a myocardial infarction. The flow of blood can be imaged, and contrast dyes may be given to improve image.[22] Other scans using radioactive contrast include SPECT CT-scans using thallium, sestamibi (MIBI scans) or tetrofosmin; or a PET scan using Fludeoxyglucose or rubidium-82.[22] These nuclear medicine scans can visualize the perfusion of heart muscle.[22] SPECT may also be used to determine viability of tissue, and whether areas of ischemia are inducible.[22][71]

Medical societies and professional guidelines recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis,[70][72] as such tests are unlikely to change management and result in increased costs.[70] Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging.[70]

Poor movement of the heart due to an MI as seen on ultrasound[73]

Pulmonary edema due to an MI as seen on ultrasound[73]

There are many causes of chest pain, which can originate from the heart, lungs, gastrointestinal tract, aorta, and other muscles, bones and nerves surrounding the chest.[74] In addition to myocardial infarction, other causes include angina, insufficient blood supply (ischemia) to the heart muscles without evidence of cell death, gastroesophageal reflux disease; pulmonary embolism, tumors of the lungs, pneumonia, rib fracture, costochondritis, and other musculoskeletal injuries.[74] Rarer severe differential diagnoses includes aortic dissection, esophageal rupture, tension pneumothorax, and pericardial effusion causing cardiac tamponade.[75] The chest pain in an MI may mimic heartburn.[23] Causes of sudden-onset breathlessness generally involve the lungs or heart â€“ including pulmonary edema, pneumonia, allergic reactions and asthma, and pulmonary embolus, acute respiratory distress syndrome and metabolic acidosis.[74] There are many different causes of fatigue, and myocardial infarction is not a common cause.[76]

A myocardial infarction requires immediate medical attention. Treatment aims to preserve as much heart muscle as possible, and to prevent further complications.[24] Treatment depends on whether the myocardial infarction is a STEMI or NSTEMI.[58] Treatment in general aims to unblock blood vessels, reduce blot clot enlargement, reduce ischemia, and modify risk factors with the aim of preventing future MIs.[24] In addition, the main treatment for myocardial infarctions with ECG evidence of ST elevation (STEMI) include thrombolysis or percutaneous coronary intervention, although PCI is also ideally conducted within 1â€“3 days for NSTEMI.[58] In addition to clinical judgement, risk stratification may be used to guide treatment, sometimes including systems such as the TIMI and GRACE (Global Registry of Acute Coronary Events) scoring systems.[15][58][77]

The pain associated with myocardial infarction may be treated with nitroglycerin or morphine.[24] Nitroglycerin (given under the tongue or intravenously) may improve the blood supply to the heart, and decrease the work the heart must do.[24] It is an important part of therapy for its pain relief, despite there being no benefit to overall mortality.[24][78] Morphine may also be used, and is effective for the pain associated with STEMI.[24] The evidence for benefit from morphine on overall outcomes, however, is poor and there is some evidence of potential harm.[79][80]

Aspirin, an antiplatelet anticoagulant, is given as a loading dose with the goal of reducing the clot size and reduce further clotting in the affected artery.[24][58] It is known to decrease mortality associated with acute myocardial infarction by at least 50%.[58] P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are given concurrently, also as a loading dose, with the dose depending on whether further surgical management or fibrinolysis is planned.[58] Prasugrel and ticagrelor are recommended in European and American guidelines, as they are active more quickly and consistently than clopidogrel.[58] P2Y12 inhibitors are recommended in both NSTEMI and STEMI, including in PCI, with evidence also to suggest improved mortality.[58] Heparins, particularly in the unfractionated form, act at several points in the clotting cascade, help to prevent the enlargement of a clot, and are also given in myocardial infarction, owing to evidence suggesting improved mortality rates.[58] In very high-risk scenarios, inhibitors of the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.[58]

There is varying evidence on the mortality benefits in NSTEMI. A 2014 review of P2Y12 inhibitors such as clopidogrel found they do not change the risk of death when given to people with a suspected NSTEMI prior to PCI,[81] nor do heparins change the risk of death.[82] They do decrease the risk of having a further myocardial infarction.[58][82]

Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner, ideally within 90–120 minutes of contact with a medical provider.[58][83] Some recommend it is also done in NSTEMI within 1–3 days, particularly when considered high-risk.[58] A 2017 review, however, did not find a difference between early versus later PCI in NSTEMI.[84]

PCI involves small probes, inserted through peripheral blood vessels such as the femoral artery or radial artery into the blood vessels of the heart. The probes are then used to identify and clear blockages using small balloons, which are dragged through the blocked segment, dragging away the clot, or the insertion of stents.[24][58] Coronary artery bypass grafting is only considered when the affected area of heart muscle large, and PCI is unsuitable, for example with difficult cardiac anatomy.[85] After PCI, people are generally placed on aspirin indefinitely and on dual antiplatelet therapy (generally aspirin and clopidogrel) for at least a year.[18][58][86]

If PCI cannot be performed within 90 to 120 minutes in STEMI then fibrinolysis, preferably within 30 minutes of arrival to hospital, is recommended.[58][87] If a person has had symptoms for 12 to 24 hours evidence for effectiveness of thrombolysis is less and if they have had symptoms for more than 24 hours it is not recommended.[88] Thrombolysis involves the administration of medication that activates the enzymes that normally dissolve blood clots. These medications include tissue plasminogen activator, reteplase, streptokinase, and tenecteplase.[24] Thrombolysis is not recommended in a number of situations, particularly when associated with a high risk of bleeding or the potential for problematic bleeding, such as active bleeding, past strokes or bleeds into the brain, or severe hypertension. Situations in which thrombolysis may be considered, but with caution, include recent surgery, use of anticoagulants, pregnancy, and proclivity to bleeding.[24] Major risks of thrombolysis are major bleeding and intracranial bleeding.[24] Pre-hospital thrombolysis reduces time to thrombolytic treatment, based on studies conducted in higher income countries, however it is unclear whether this has an impact on mortality rates.[89]

In the past, high flow oxygen was recommended for everyone with a possible myocardial infarction.[66] More recently, no evidence was found for routine use with potential of harm.[90][91][92] Therefore, oxygen is currently only recommended if oxygen levels are found to be low or if someone is in respiratory distress.[24][66]

If despite thrombolysis there is significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation on the ECG recording after 90 minutes, then rescue PCI is indicated emergently.[93][94]

Those who have had cardiac arrest may benefit from targeted temperature management with evaluation for implementation of hypothermia protocols. Furthermore, those with cardiac arrest, and ST elevation at any time, should usually have angiography.[95]

Cardiac rehabilitation benefits many who have experienced myocardial infarction,[58] even if there has been substantial heart damage and resultant left ventricular failure. It should start soon after discharge from the hospital. The program may include lifestyle advice, exercise, social support, as well as recommendations about driving, flying, sport participation, stress management, and sexual intercourse.[96]

There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted as secondary prevention after an initial myocardial infarction,[58] because of shared risk factors and an aim to reduce atherosclerosis affecting heart vessels.[24]

Physical activity can reduce the risk of cardiovascular disease, and people at risk are advised to engage in 150 minutes of moderate or 75 minutes of vigorous intensity aerobic exercise a week.[97] Keeping a healthy weight, drinking alcohol within the recommended limits, and quitting smoking reduce the risk of cardiovascular disease.[97]

Substituting polyunsaturated fats such as olive oil and rapeseed oil instead saturated fats may reduce the risk of myocardial infarction,[39] although there is not universal agreement.[40] Dietary modifications are recommended by some national authorities, with recommendations including increasing the intake of wholegrain starch, reducing sugar intake (particularly of refined sugar), consuming five portions of fruit and vegetables daily, consuming two or more portions of fish per week, and consuming 4â€“5 portions of unsalted nuts, seeds, or legumes per week.[97] The dietary pattern with the greatest support is the Mediterranean diet.[98] Vitamins and mineral supplements are of no proven benefit,[99] and neither are plant stanols or sterols.[97]

Public health measures may also act at a population level to reduce the risk of myocardial infarction, for example by reduce unhealthy diets (excessive salt, saturated fat and trans fat) including food labeling and marketing requirements as well as requirements for catering and restaurants, and stimulating physical activity. This may be part of regional cardiovascular disease prevention programs, or through the health impact assessment of regional and local plans and policies.[100]

Most guidelines recommend combining different preventive strategies. A 2015 Cochrane Review found some evidence that such an approach might help with blood pressure, body mass index and waist circumference. However, there was insufficient evidence to show an effect on mortality or actual cardio-vascular events.[101]

Statins, drugs that act to lower blood cholesterol, decrease the incidence and mortality rates of myocardial infarctions.[102] They are often recommended in those at an elevated risk of cardiovascular diseases.[97]

Aspirin has been studied extensively in people considered at increased risk of myocardial infarction. Based on numerous studies in different groups (e.g. people with or without diabetes), there does not appear to be a benefit strong enough to outweigh the risk of excessive bleeding.[103][104] Nevertheless, many clinical practice guidelines continue to recommend aspirin for primary prevention,[105] and some researchers feel that those with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.[106]

There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted as secondary prevention after an initial myocardial infarct.[58] Recommendations include stopping smoking, a gradual return to exercise, eating a healthy diet, low in saturated fat and low in cholesterol, and drinking alcohol within recommended limits, exercising, and trying to achieve a healthy weight.[58][96] Exercise is both safe and effective even if people have had stents or heart failure,[107] and is recommended to start gradually after 1â€“2 weeks.[58] Counselling should be provided relating to medications used, and for warning signs of depression.[58] Previous studies suggested a benefit from omega-3 fatty acid supplementation but this has not been confirmed.[96]

Following a heart attack, nitrates, when taken for two days, and ACE-inhibitors decrease the risk of death.[108] Other medications include:

Aspirin is continued indefinitely, as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) for up to twelve months.[96] If someone has another medical condition that requires anticoagulation (e.g. with warfarin) this may need to be adjusted based on risk of further cardiac events as well as bleeding risk.[96] In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.[109]

Beta blocker therapy such as metoprolol or carvedilol is recommended to be started within 24 hours, provided there is no acute heart failure or heart block.[18][66] The dose should be increased to the highest tolerated.[96] Contrary to what was long believed, the use of beta blockers does not appear to affect the risk of death, possibly because other treatments for MI have improved.[110] When beta blocker medication is given within the first 24â€“72 hours of a STEMI no lives are saved. However, 1 in 200 people were prevented from a repeat heart attack, and another 1 in 200 from having an abnormal heart rhythm. Additionally, for 1 in 91 the medication causes a temporary decrease in the heart's ability to pump blood.[111]

ACE inhibitor therapy should be started within 24 hours, and continued indefinitely at the highest tolerated dose. This is provided there is no evidence of worsening kidney failure, high potassium, low blood pressure, or known narrowing of the renal arteries.[58] Those who cannot tolerate ACE inhibitors may be treated with an angiotensin II receptor antagonist.[96]

Statin therapy has been shown to reduce mortality and subsequent cardiac events, and should be commenced with the aim of lowering LDL cholesterol. Other medications, such as ezetimibe, may also be added with this goal in mind.[58]

Aldosterone antagonists (spironolactone or eplerenone) may be used if there is evidence of left ventricular dysfunction after an MI, ideally after beginning treatment with an ACE inhibitor.[96]

A defibrillator, an electric device connected to the heart and surgically inserted under the skin, may be recommended. This is particularly if there are any ongoing signs of heart failure, with a low left ventricular ejection fraction and a New York Heart Association grade II or III after 40 days of the infarction.[58] Defibrillators detect potentially fatal arrhythmia and deliver an electrical shock to the person to depolarize a critical mass of the heart muscle.[112]

The prognosis after myocardial infarction varies greatly depending on the extent and location of the affected heart muscle, and the development and management of complications.[15] Prognosis is worse with older age, and social isolation.[15] Anterior infarcts, persistent ventricular tachycardia or fibrillation, development of heart blocks, and left ventricular impairment are all associated with poorer prognosis.[15] Without treatment, about a quarter of those affected by MI die within minutes, and about forty percent within the first month.[15] Morbidity and mortality from myocardial infarction has however improved over the years due to earlier and better treatment:[25] in those who have an STEMI in the United States, between 5 and 6 percent die before leaving the hospital and 7 to 18 percent die within a year.[18]

Heart failure may develop as a long-term consequence, with an impaired ability of heard muscle to pump, scarring, and increase in size of the existing muscle. Aneurysm of the left ventricle myocardium develops in about 10% of MI and is itself a risk factor for heart failure, ventricular arrhythmia and the development of clots.[15]

Risk factors for complications and death risk factors for death include age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease, and elevation of cardiac markers.[113][114][115]

Myocardial infarction is a common presentation of coronary artery disease. The World Health Organization estimated in 2004, that 12.2% of worldwide deaths were from ischemic heart disease;[116] with it being the leading cause of death in high- or middle-income countries and second only to lower respiratory infections in lower-income countries.[116] Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[17] STEMIs occur about twice as often in men as women.[18]

Rates of death from ischemic heart disease (IHD) have slowed or declined in most high-income countries, although cardiovascular disease still accounted for one in three of all deaths in the USA in 2008.[117] For example, rates of death from cardiovascular disease have decreased almost a third between 2001 and 2011 in the United States.[118]

In contrast, IHD is becoming a more common cause of death in the developing world. For example, in India, IHD had become the leading cause of death by 2004, accounting for 1.46 million deaths (14% of total deaths) and deaths due to IHD were expected to double during 1985â€“2015.[119] Globally, disability adjusted life years (DALYs) lost to ischemic heart disease are predicted to account for 5.5% of total DALYs in 2030, making it the second-most-important cause of disability (after unipolar depressive disorder), as well as the leading cause of death by this date.[116]

Depictions of heart attacks in popular media often include collapsing or loss of consciousness which are not common symptoms; these depictions contribute to widespread misunderstanding about the symptoms of myocardial infarctions, which in turn contributes to people not getting care when they should.[120]

At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in the administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered;[121] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion.[122] In addition, in some jurisdictions, heart attacks suffered by persons in particular occupations such as police officers may be classified as line-of-duty injuries by statute or policy. In some countries or states, a person having suffered from an MI may be prevented from participating in activity that puts other people's lives at risk, for example driving a car or flying an airplane.[123]