Myocardial infarction

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"Heart attack" redirects here. For other uses, see Heart attack (disambiguation).
Not to be confused with cardiac arrest or heart failure.

Myocardial infarction
Other namesAcute myocardial infarction (AMI), heart attack
nitroglycerin, heparin[8][9]
PrognosisSTEMI 10% risk of death (developed world)[8]
Frequency15.9 million (2015)[10]

A myocardial infarction (MI), commonly known as a heart attack, occurs when

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 such pain 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

irregular heartbeat, cardiogenic shock or cardiac arrest.[3][4]

Most MIs occur due to

coronary angiography.[7] An ECG, which is a recording of the heart's electrical activity, may confirm an ST elevation MI (STEMI), if ST elevation is present.[8][15] Commonly used blood tests include troponin and less often creatine kinase MB.[7]

Treatment of an MI is time-critical.

beta blockers and statins, are typically recommended.[8]

Worldwide, about 15.9 million myocardial infarctions occurred in 2015.[10] More than 3 million people had an ST elevation MI, and more than 4 million had an NSTEMI.[18] STEMIs occur about twice as often in men as women.[19] About one million people have an MI each year in the United States.[3] In the developed world, the risk of death in those who have had a STEMI is about 10%.[8] Rates of MI for a given age have decreased globally between 1990 and 2010.[20] In 2011, an MI 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.[21]

Terminology

Main article: Acute coronary syndrome

Myocardial infarction (MI) refers to tissue death (

ECG.[24]

The phrase "heart attack" is often used non-specifically to refer to myocardial infarction. 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 leading to death.[25] 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.[26]

Signs and symptoms

View of the chest with common areas of MI coloured
View of the back with common areas of MI coloured
Areas where pain is experienced in myocardial infarction, showing common (dark red) and less common (light red) areas on the chest (top) and back (bottom).

Chest pain that may or may not radiate to other parts of the body is the most typical and significant symptom of myocardial infarction. It might be accompanied by other symptoms such as sweating.[27]

Pain

positive predictive value.[32]

Typically, chest pain because of ischemia, be it unstable angina or myocardial infarction, lessens with the use of

nitroglycerin, but nitroglycerin may also relieve chest pain arising from non-cardiac causes.[33]

Other

Chest pain may be accompanied by

left ventricle, with breathlessness arising either from low oxygen in the blood, or pulmonary edema.[28][39]

Other less common symptoms include weakness,

sudden death, frequently due to the development of ventricular fibrillation. [41] When the brain was without oxygen for too long due to a myocardial infarction, coma and persistent vegetative state can occur. 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.[24]

Absence

"Silent" myocardial infarctions can happen without any symptoms at all.

diabetes mellitus[16] 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.[42] In heart transplantation, the donor heart is not fully innervated by the nervous system of the recipient.[43]

Risk factors

The most prominent risk factors for myocardial infarction are older age, actively

triglycerides.[46]

Many risk factors for myocardial infarction are potentially modifiable, with the most important being

job stress, which accounts for about 3% of cases,[47] and chronic high stress levels.[49]

Diet

There is varying evidence about the importance of

Trans fats do appear to increase risk.[51] Acute and prolonged intake of high quantities of alcoholic drinks (3–4 or more daily) increases the risk of a heart attack.[54]

Genetics

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.[45]

SLC5A3, MRPS6, KCNE2.[55]

Other

See also: Overwork, Karoshi, and 996 working hour system

The risk of having a myocardial infarction increases with older age, low physical activity, and low socioeconomic status.[45] Heart attacks appear to occur more commonly in the morning hours, especially between 6AM and noon.[56] Evidence suggests that heart attacks are at least three times more likely to occur in the morning than in the late evening.[57] Shift work is also associated with a higher risk of MI.[58] One analysis has found an increase in heart attacks immediately following the start of daylight saving time.[59]

Women who use

non-steroidal anti inflammatory drugs (NSAIDs), even for as short as a week, increases risk.[61]

Endometriosis in women under the age of 40 is an identified risk factor.[62]

Air pollution is also an important modifiable risk. Short-term exposure to air pollution such as carbon monoxide, nitrogen dioxide, and sulfur dioxide (but not ozone) has been associated with MI and other acute cardiovascular events.[63] For sudden cardiac deaths, every increment of 30 units in Pollutant Standards Index correlated with an 8% increased risk of out-of-hospital cardiac arrest on the day of exposure.[64] Extremes of temperature are also associated.[65]

A number of acute and chronic

Chlamydophila pneumoniae, influenza, Helicobacter pylori, and Porphyromonas gingivalis among others have been linked to atherosclerosis and myocardial infarction.[66] As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.[66][67] Myocardial infarction can also occur as a late consequence of Kawasaki disease.[68]

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.[69] High blood levels of the amino acid homocysteine is associated with premature atherosclerosis;[70] whether elevated homocysteine in the normal range is causal is controversial.[71]

In people without evident

coronary spasm or coronary artery dissection.[72]

Mechanism

Atherosclerosis

The animation shows plaque buildup or a coronary artery spasm can lead to a heart attack and how blocked blood flow in a coronary artery can lead to a heart attack.
Further information: Atherosclerosis

The most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle.[41][73] 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.[74] Atherosclerotic plaques are often present for decades before they result in symptoms.[74]

The gradual buildup of

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).[74] The cholesterol crystals have been associated with plaque rupture through mechanical injury and inflammation.[76]

Other causes

Atherosclerotic disease is not the only cause of myocardial infarction, but 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,

Prinzmetal's angina may cause blockage.[24][28]

Tissue death

Cross section showing anterior left ventricle wall infarction

If impaired blood flow to the heart lasts long enough, it triggers a process called the

Na/K ATPase. This leads to an ischemic cascade of intracellular changes, necrosis and apoptosis of affected cells.[77]

Cells in the area with the worst blood supply, just below the inner surface of the heart (endocardium), are most susceptible to damage.[78][79] Ischemia first affects this region, the subendocardial region, and tissue begins to die within 15–30 minutes of loss of blood supply.[80] The dead tissue is surrounded by a zone of potentially reversible ischemia that progresses to become a full-thickness transmural infarct.[77][80] The initial "wave" of infarction can take place over 3–4 hours.[74][77] These changes are seen on gross pathology and cannot be predicted by the presence or absence of Q waves on an ECG.[79] 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.[28][73]

Tissue death and

inflammation of the heart wall following infarction, and rupture of the heart wall that can have catastrophic consequences.[73][81]

Injury to the myocardium also occurs during re-perfusion. This might manifest as ventricular arrhythmia. The re-perfusion injury is a consequence of the calcium and sodium uptake from the cardiac cells and the release of oxygen radicals during reperfusion. No-reflow phenomenon—when blood is still unable to be distributed to the affected myocardium despite clearing the occlusion—also contributes to myocardial injury. Topical endothelial swelling is one of many factors contributing to this phenomenon.[82]

Diagnosis

Main article: Diagnosis of myocardial infarction
right coronary arteries
(labelled LCA and RCA). A myocardial infarction (2) has occurred with blockage of a branch of the left coronary artery (1).

Criteria

A myocardial infarction, according to current consensus, is defined by elevated cardiac

biomarkers with a rising or falling trend and at least one of the following:[83]

Types

See also: Electrocardiography in myocardial infarction
"STEMI" redirects here. For the Christian evangelist organization, see Stephen Tong § Ministry.

A myocardial infarction is usually clinically classified as an ST-elevation MI (STEMI) or a non-ST elevation MI (NSTEMI). These are based on

ECG.[24] STEMIs make up about 25–40% of myocardial infarctions.[19] A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:[24]

  1. Spontaneous MI related to plaque erosion and/or rupture fissuring, or dissection
  2. MI related to ischemia, such as from increased oxygen demand or decreased supply, e.g., coronary artery spasm, coronary embolism, anemia, arrhythmias, high blood pressure, or low blood pressure
  3. Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a blood clot is found in a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
  4. Associated with
    coronary angioplasty or stents
  5. Associated with
    CABG
  6. Associated with spontaneous coronary artery dissection in young, fit women

Cardiac biomarkers

There are many different biomarkers used to determine the presence of cardiac muscle damage. Troponins, measured through a blood test, are considered to be the best,[19] and are preferred because they have greater sensitivity and specificity for measuring injury to the heart muscle than other tests.[73] A rise in troponin occurs within 2–3 hours of injury to the heart muscle, and peaks within 1–2 days. The level 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.[73] One high-sensitivity cardiac troponin can rule out a heart attack as long as the ECG is normal.[84][85]

Other tests, such as

CK-MB or myoglobin, are discouraged.[86] 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.[28] Copeptin may be useful to rule out MI rapidly when used along with troponin.[87]

Electrocardiogram

A 12-lead ECG showing an inferior STEMI due to reduced perfusion through the right coronary artery. Elevation of the ST segment can be seen in leads II, III and aVF.

Electrocardiograms (ECGs) are a series of leads placed on a person's chest that measure electrical activity associated with contraction of the heart muscle.[88] The taking of an ECG is an important part of the workup of an AMI,[24] 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.[24]

ECG readouts product a waveform with different labelled features.

adjacent chest or limb leads.[19][24] ST elevation is associated with infarction, and may be preceded by changes indicating ischemia, such as ST depression or inversion of the T waves.[88] Abnormalities can help differentiate the location of an infarct, based on the leads that are affected by changes.[16] Early STEMIs may be preceded by peaked T waves.[19] Other ECG abnormalities relating to complications of acute myocardial infarctions may also be evident, such as atrial or ventricular fibrillation.[89]

ECG : AMI with ST elevation in V2-4

Imaging

Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial infarction.

chest X-rays can be used to explore and exclude alternate causes of a person's symptoms.[24] Echocardiography may assist in modifying clinical suspicion of ongoing myocardial infarction in patients that can't be ruled out or ruled in following initial ECG and Troponin testing.[90] Myocardial perfusion imaging has no role in the acute diagnostic algorithm; however, it can confirm a clinical suspicion of Chronic Coronary Syndrome when the patient's history, physical examination (including cardiac examination) ECG, and cardiac biomarkers suggest coronary artery disease.[91]

Fludeoxyglucose or rubidium-82.[24] These nuclear medicine scans can visualize the perfusion of heart muscle.[24] SPECT may also be used to determine viability of tissue, and whether areas of ischemia are inducible.[24][92]

Medical societies and professional guidelines recommend that the physician confirm a person is at high risk for Chronic Coronary Syndrome before conducting diagnostic non-invasive imaging tests to make a diagnosis,[91][93][90] as such tests are unlikely to change management and result in increased costs.[91] Patients who have a normal ECG and who are able to exercise, for example, most likely do not merit routine imaging.[91]

  • Poor movement of the heart due to an MI as seen on ultrasound[94]
  • Pulmonary edema due to an MI as seen on ultrasound[94]

Differential diagnosis

There are many causes of

acute respiratory distress syndrome and metabolic acidosis.[95] There are many different causes of fatigue, and myocardial infarction is not a common cause.[97]

Prevention

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,[73] because of shared risk factors and an aim to reduce atherosclerosis affecting heart vessels.[28] The influenza vaccine also appear to protect against myocardial infarction with a benefit of 15 to 45%.[98]

Primary prevention

Lifestyle

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.[99] Keeping a healthy weight, drinking alcohol within the recommended limits, and quitting smoking reduce the risk of cardiovascular disease.[99]

Substituting

stanols or sterols.[99]

Public health measures may also act at a population level to reduce the risk of myocardial infarction, for example by reducing 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.[102]

Most guidelines recommend combining different preventive strategies. A 2015 Cochrane Review found some evidence that such an approach might help with 

waist circumference. However, there was insufficient evidence to show an effect on mortality or actual cardio-vascular events.[103]

Medication

Statins, drugs that act to lower blood cholesterol, decrease the incidence and mortality rates of myocardial infarctions.[104] They are often recommended in those at an elevated risk of cardiovascular diseases.[99]

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.

clinical practice guidelines continue to recommend aspirin for primary prevention,[107] and some researchers feel that those with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.[108]

Secondary prevention

There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted as

drinking alcohol within recommended limits, exercising, and trying to achieve a healthy weight.[73][109] Exercise is both safe and effective even if people have had stents or heart failure,[110] and is recommended to start gradually after 1–2 weeks.[73] Counselling should be provided relating to medications used, and for warning signs of depression.[73] Previous studies suggested a benefit from omega-3 fatty acid supplementation but this has not been confirmed.[109]

Medications

Following a heart attack, nitrates, when taken for two days, and ACE-inhibitors decrease the risk of death.[111] 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.[109] 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.[109] In those who have had a stent, more than 12 months of clopidogrel plus aspirin does not affect the risk of death.[112]

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.[19][86] The dose should be increased to the highest tolerated.[109] Contrary to most guidelines, the use of beta blockers does not appear to affect the risk of death,[113][114] possibly because other treatments for MI have improved. When beta blocker medication is given within the first 24–72 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.[115]

angiotensin II receptor antagonist.[109]

Statin therapy has been shown to reduce mortality and subsequent cardiac events and should be commenced to lower LDL cholesterol. Other medications, such as ezetimibe, may also be added with this goal in mind.[73]

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.[109][116]

Other

A

left ventricular ejection fraction and a New York Heart Association grade II or III after 40 days of the infarction.[73] Defibrillators detect potentially fatal arrhythmia and deliver an electrical shock to the person to depolarize a critical mass of the heart muscle.[117]

First aid

Further information: Management_of_acute_coronary_syndrome § Patient-dependent_initial_measures

Taking aspirin helps to reduce the risk of mortality in people with myocardial infarction.[118]

Management

Main article: Management of acute coronary syndrome

A myocardial infarction requires immediate medical attention. Treatment aims to preserve as much heart muscle as possible, and to prevent further complications.

TIMI and GRACE scoring systems.[16][73][119]

Pain

The pain associated with myocardial infarction is often treated with

vasodilator, or opioid medications such as morphine.[28] Nitroglycerin (given under the tongue or injected into a vein) may improve blood supply to the heart.[28] It is an important part of therapy for its pain relief effects, though there is no proven benefit to mortality.[28][120] Morphine or other opioid medications may also be used, and are effective for the pain associated with STEMI.[28] There is poor evidence that morphine shows any benefit to overall outcomes, and there is some evidence of potential harm.[121][122]

Antithrombotics

clotting cascade, help to prevent the enlargement of a clot, and are also given in myocardial infarction, owing to evidence suggesting improved mortality rates.[73] In very high-risk scenarios, inhibitors of the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.[73]

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,[123] nor do heparins change the risk of death.[124] They do decrease the risk of having a further myocardial infarction.[73][124]

Inserting a stent to widen the artery.

Angiogram

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.[73][125] Some recommend it is also done in NSTEMI within 1–3 days, particularly when considered high-risk.[73] A 2017 review, however, did not find a difference between early versus later PCI in NSTEMI.[126]

PCI involves small probes, inserted through peripheral blood vessels such as the

Coronary artery bypass grafting is only considered when the affected area of heart muscle is large, and PCI is unsuitable, for example with difficult cardiac anatomy.[127] After PCI, people are generally placed on aspirin indefinitely and on dual antiplatelet therapy (generally aspirin and clopidogrel) for at least a year.[19][73][128]

Fibrinolysis

Main article: Thrombolysis

If PCI cannot be performed within 90 to 120 minutes in STEMI then fibrinolysis, preferably within 30 minutes of arrival to hospital, is recommended.

intracranial bleeding.[28] 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.[131]

Other

In the past, high flow oxygen was recommended for everyone with a possible myocardial infarction.[86] More recently, no evidence was found for routine use in those with normal oxygen levels and there is potential harm from the intervention.[132][133][134][135][136] Therefore, oxygen is currently only recommended if oxygen levels are found to be low or if someone is in respiratory distress.[28][86]

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.[137][138]

Those who have had

Aldosterone antagonists appear to be useful in people who have had an STEMI and do not have heart failure.[139]

Rehabilitation and exercise

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, sports participation, stress management, and sexual intercourse.[109] Returning to sexual activity after myocardial infarction is a major concern for most patients, and is an important area to be discussed in the provision of holistic care.[140][141]

In the short-term, exercise-based cardiovascular rehabilitation programs may reduce the risk of a myocardial infarction, reduces a large number of hospitalizations from all causes, reduces hospital costs, improves

all-cause mortality.[142]
Longer-term studies indicate that exercise-based cardiovascular rehabilitation programs may reduce cardiovascular mortality and myocardial infarction.

Prognosis

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.[16] Prognosis is worse with older age and social isolation.[16] Anterior infarcts, persistent ventricular tachycardia or fibrillation, development of heart blocks, and left ventricular impairment are all associated with poorer prognosis.[16] Without treatment, about a quarter of those affected by MI die within minutes and about forty percent within the first month.[16] Morbidity and mortality from myocardial infarction has, however, improved over the years due to earlier and better treatment:[30] in those who have a STEMI in the United States, between 5 and 6 percent die before leaving the hospital and 7 to 18 percent die within a year.[19]

It is unusual for babies to experience a myocardial infarction, but when they do, about half die.[143] In the short-term, neonatal survivors seem to have a normal quality of life.[143]

Complications

Main article: Myocardial infarction complications

Complications may occur immediately following the myocardial infarction or may take time to develop.

Dressler's syndrome, a reaction following larger infarcts and a cause of pericarditis is also possible.[73]

Heart failure may develop as a long-term consequence, with an impaired ability of heart muscle to pump, scarring, and an increase in the 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.[16]

Risk factors for complications and death include age,

peripheral vascular disease, and elevation of cardiac markers.[144][145][146]

Epidemiology

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;[147] 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.[147] Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[18] STEMIs occur about twice as often in men as women.[19]

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 US in 2008.[148] For example, rates of death from cardiovascular disease have decreased almost a third between 2001 and 2011 in the United States.[149]

In contrast, IHD is becoming a more common cause of death in the developing world. For example, in

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.[147]

Social determinants of health

Social determinants such as neighborhood disadvantage, immigration status, lack of social support, social isolation, and access to health services play an important role in myocardial infarction risk and survival.[151][152][153][154] Studies have shown that low socioeconomic status is associated with an increased risk of poorer survival. There are well-documented disparities in myocardial infarction survival by socioeconomic status, race, education, and census-tract-level poverty.[155]

Race: In the U.S.

morbidity and mortality.[156] Similarly, South Asians (including South Asians that have migrated to other countries around the world) experience higher rates of acute myocardial infarctions at younger ages, which can be largely explained by a higher prevalence of risk factors at younger ages.[157]

Socioeconomic status: Among individuals who live in the low-socioeconomic (SES) areas, which is close to 25% of the US population, myocardial infarctions (MIs) occurred twice as often compared with people who lived in higher SES areas.[158]

Immigration status: In 2018 many lawfully present

undocumented immigrants are ineligible for coverage options due to their immigration status.[159]

Health care access: Lack of health insurance and financial concerns about accessing care were associated with delays in seeking emergency care for acute myocardial infarction which can have significant, adverse consequences on patient outcomes.[160]

Education: Researchers found that compared to people with

cardiovascular event, and overall death.[161]

Society and culture

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.[162]

Legal implications

At

work-related injury if it results, for example, from unusual emotional stress or unusual exertion.[164] In addition, in some jurisdictions, heart attacks had 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 had 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.[165]

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Sources

Further reading

External links
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