|Classification and external resources|
|eMedicine||med/1567 emerg/327 ped/2520|
Myocardial infarction (MI; Latin: infarctus myocardii) or acute myocardial infarction (AMI), commonly known as a heart attack, occurs when blood stops flowing properly to a part of the heart, and the heart muscle is injured because it is not receiving enough oxygen. Usually, this is because one of the coronary arteries that supplies blood to the heart develops a blockage due to an unstable buildup of white blood cells, cholesterol and fat. The event is called "acute" if it is sudden and serious. Myocardial infarction differs from cardiac arrest, although cardiac arrest can be a consequence of MI.
A person having an acute MI usually has sudden chest pain that is felt behind the sternum and sometimes travels to the left arm or the left side of the neck. Additionally, the person may have shortness of breath, sweating, nausea, vomiting, abnormal heartbeats, and anxiety. Women experience fewer of these symptoms than men, but usually have shortness of breath, weakness, a feeling of indigestion, and fatigue. In many cases, in some estimates as high as 64%, the person does not have chest pain or has vague symptoms. These are called "silent" myocardial infarctions. Important risks are previous cardiovascular disease, old age, tobacco smoking, abnormal blood levels of certain lipids, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, and the use of cocaine and amphetamines. The main ways to determine if a person has had a myocardial infarction are electrocardiograms (ECGs) that trace the electrical signals in the heart and testing the blood for substances associated with damage to the heart muscle. ECG testing is used to differentiate between two types of myocardial infarction based on the appearance of the tracing. An ST section of the tracing higher than the baseline is called an ST elevation MI (STEMI) which usually requires more aggressive treatment. If this is not the case, the diagnosis is confirmed with a blood test (usually troponin). Immediate treatments for a suspected MI often include aspirin, which prevents further blood from clotting; nitroglycerin, sometimes given to treat chest pain; and oxygen. STEMI is treated by restoring circulation to the heart, called reperfusion therapy, and typical methods are angioplasty, where the arteries are pushed open, and thrombolysis, where the blockage is removed using medications. Non-ST elevation myocardial infarction (NSTEMI) may be managed with medication, although angioplasty may be required if the person is considered to be at high risk. People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG). Ischemic heart disease, which includes MI, angina, and heart failure when it happens after MI, was the leading cause of death for both men and women worldwide in 2011.
- Signs and symptoms 1
- Lifestyle 2.1
- Disease 2.2
- Genetic 2.3
- Other 2.4
- Pathological types 3.1
- Classification 4.1
- Electrocardiogram 4.2
- Cardiac biomarkers 4.3
- Imaging 4.4
- Lifestyle 5.1
- Medication 5.2
- STEMI 6.1
- NSTEMI 6.2
- Cardiac rehabilitation 6.3
- Secondary prevention 6.4
- Complications 7.1
- Epidemiology 8
Society and culture 9
- Economics 9.1
- Legal implications 9.2
- Research 10
- References 11
- External links 12
Signs and symptoms
The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute MI and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen, where it may mimic heartburn. Levine's sign, in which patients localize the chest pain by clenching their fists over their sternums, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poor positive predictive value.
Shortness of breath (dyspnea) occurs when the damage to the heart limits the output of the left ventricle, causing left ventricular failure and consequent pulmonary edema. Other symptoms include diaphoresis (an excessive form of sweating), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. 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 MIs.
Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs. 1.8 symptoms in men). The most common symptoms of MI in women include dyspnea, weakness, and fatigue. Fatigue, sleep disturbances, and dyspnea have been reported as frequently occurring symptoms that may manifest as long as one month before the actual clinically manifested ischemic event. In women, chest pain may be less predictive of coronary ischemia than in men. Women may also experience back or jaw pain during an episode.
At least one-fourth of all MIs are silent, without chest pain or other symptoms. These cases can be discovered later on electrocardiograms, using blood enzyme tests or at autopsy without a prior history of related complaints. Estimates of the prevalence of silent MIs vary between 22 and 64%. A silent course is more common in the donor heart is not fully innervated by the nervous system of the recipient. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.
Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.
The differential diagnosis includes other catastrophic causes of chest pain, such as pulmonary embolism, aortic dissection, pericardial effusion causing cardiac tamponade, tension pneumothorax, and esophageal rupture. Other noncatastrophic differentials include gastroesophageal reflux and Tietze's syndrome.
Many of the risk factors for myocardial infarction are modifiable and thus many cases may be preventable.
Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease. Lack of exercise has been linked to 7–12% of cases. Less common causes include stress-related causes such as job stress, which accounts for about 3% of cases, and chronic high stress levels.
Tobacco smoking, including secondhand smoke Short-term exposure to air pollution, including carbon monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone. Lack of physical activity, psychosocial factors including, low socioeconomic status, social isolation and negative emotions increase the risk of and are associated with worse outcomes after MI. Socioeconomic factors such as a shorter education and lower income (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI. Alcohol — prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
Diabetes mellitus (type 1 or 2), high blood pressure, dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
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. As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.
Genome-wide association studies have found 27 genetic variants that are associated with an increased risk of myocardial infarction. Strongest association of MI has been found with the 9p21 genomic locus, which contains genes CDKN2A & 2B, although the single nucleotide polymorphisms that are implicated are within a non-coding region. 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, SMG6, SNF8, LDLR, SLC5A3, MRPS6, KCNE2.
At any given age, men are more at risk than women, particularly before menopause, but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women. Family history of ischaemic heart disease or MI, particularly if one has a first-degree relative (father, brother, mother, sister) who suffered a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women).
An increased incidence of a heart attack is associated with time of day especially in the morning hours, more specifically around 9 am.
Old age increases risk of a heart attack.
Acute myocardial infarction refers to two subtypes of acute coronary syndrome, namely non-ST-elevated and ST-elevated MIs, which are most frequently (but not always) a manifestation of coronary artery disease. The most common triggering event is the disruption of an atherosclerotic plaque in an epicardial coronary artery, which leads to a clotting cascade, sometimes resulting in total occlusion of the artery. Atherosclerosis is the gradual buildup of cholesterol and fibrous tissue in plaques in the wall of arteries (in this case, the coronary arteries), typically over decades. Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis. Plaques can become unstable, rupture, and additionally promote the formation of a blood clot that occludes the artery; this can occur in minutes. When a severe enough plaque rupture occurs in the coronary vasculature, it leads to MI (necrosis of downstream myocardium).
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 occluded coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in their place. Recent studies indicate that another form of cell death, apoptosis, also plays a role in the process of tissue damage subsequent to MI. As a result, the patient's heart will be permanently damaged. This myocardial scarring also puts the patient at risk for potentially life-threatening arrhythmias, and may result in the formation of a ventricular aneurysm that can rupture with catastrophic consequences.
Injured heart tissue conducts electrical impulses more slowly than normal heart tissue. The difference in conduction velocity between injured and uninjured tissue can trigger re-entry or a feedback loop that is believed to be the cause of many lethal arrhythmias. The most serious of these arrhythmias is ventricular fibrillation (V-Fib/VF), an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (V-tach/VT), which can cause sudden cardiac death. However, VT usually results in rapid heart rates that prevent the heart from pumping blood effectively. Cardiac output and blood pressure may fall to dangerous levels, which can lead to further coronary ischemia and extension of the infarct.
The cardiac defibrillator device was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the patient to depolarize a critical mass of the heart muscle, in effect "rebooting" the heart. This therapy is time-dependent, and the odds of successful defibrillation decline rapidly after the onset of cardiopulmonary arrest.
Myocardial infarction results from atherosclerosis. Inflammation is known to be an important step in the process of atherosclerotic plaque formation. C-reactive protein (CRP) is a sensitive but nonspecific marker for inflammation. Elevated CRP blood levels, especially measured with high-sensitivity assays, can predict the risk of MI, as well as stroke and development of diabetes. Moreover, some drugs for MI might also reduce CRP levels. The use of high-sensitivity CRP assays as a means of screening the general population is advised against, but it may be used optionally at the physician's discretion in patients who already present with other risk factors or known coronary artery disease. Whether CRP plays a direct role in atherosclerosis remains uncertain.
Calcium deposition is another part of atherosclerotic plaque formation. Calcium deposits in the coronary arteries can be detected with CT scans. Several studies have shown that coronary calcium can provide predictive information beyond that of classical risk factors.
Hyperhomocysteinemia (high blood levels of the amino acid homocysteine) in homocysteinuria is associated with premature atherosclerosis; whether elevated homocysteine in the normal range is causal is controversial.
The two main types of acute myocardial infarction, based on pathology, are:
- Transmural AMI is associated with atherosclerosis involving a major coronary artery. It can be subclassified into anterior, posterior, inferior, lateral, or septal. Transmural infarcts extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the area's blood supply. In addition, on ECG, ST elevation and Q waves are seen.
- Subendocardial AMI involves a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles. The subendocardial area is particularly susceptible to ischemia. In addition, ST depression is seen on ECG.
A cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI.
WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with MI if two (probable) or three (definite) of the following criteria are satisfied:
- Clinical history of ischemic type chest pain lasting for more than 20 minutes
- Changes in serial ECG tracings
- Rise and fall of serum cardiac biomarkers
Myocardial infarctions are generally classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). A STEMI is the combination of symptoms related to poor oxygenation of the heart with elevation of the ST segments on the electrocardiogram followed by an increase in proteins in the blood related to heart muscles death. They make up abut 25 to 40 percent of cases.
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, which is the stopping of the heartbeat. 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.
A 2007 consensus document classifies MI into five main types:
- Type 1 – spontaneous MI related to ischemia due to a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection
- Type 2 – MI secondary to ischemia due to either increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension
- Type 3 – sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischemia, accompanied by new ST elevation, or new left bundle branch block (LBBB), or evidence of fresh thrombus in a coronary artery by angiography and/or at autopsy, but death occurring before blood samples could be obtained, or at a time before the appearance of cardiac biomarkers in the blood
Type 4 – associated with coronary angioplasty or stents:
- Type 4a – MI associated with percutaneous coronary intervention (PCI)
- Type 4b – MI associated with stent thrombosis as documented by angiography or at autopsy
- Type 5 – MI associated with CABG
For a person to qualify as having a STEMI, in addition to reported angina, the ECG must show new ST elevation in two or more adjacent ECG leads. This must be greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15mV) in females if in leads V2 and V3 or greater than 1 mm (0.1 mV) if it is in other ECG leads. A left bundle branch block that is believed to be new used to be considered the same as ST elevation; however, this is no longer the case. In early STEMIs there may just be peaked T waves with ST elevation developing later.
While there are a number of different biomarkers, troponins are considered to be the best and reliance on older tests (such as CK-MB) or myoglobin is discouraged. Copeptin may be useful to rule out MI rapidly when used along with troponin.
A chest radiograph and routine blood tests may indicate complications or precipitating causes, and are often performed upon arrival to an emergency department. New regional wall motion abnormalities on an echocardiogram are also suggestive of an MI. Echo may be performed in equivocal cases by the on-call cardiologist. In stable patients whose symptoms have resolved by the time of evaluation, technetium (99mTc) sestamibi (i.e. a "MIBI scan") or thallium-201 chloride can be used in nuclear medicine to visualize areas of reduced blood flow in conjunction with physiological or pharmacological stress. Thallium may also be used to determine viability of tissue, distinguishing whether nonfunctional myocardium is actually dead or merely in a state of hibernation or of being stunned. Medical societies recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging. Imaging tests such as stress radionuclide myocardial perfusion imaging or stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem.
Myocardial infarction and other related cardiovascular diseases can be prevented to a large extent by a number of interventions in terms of lifestyle and medical treatments.
On a population level, public health measures may be used to reduce unhealthy diets (excessive salt, saturated fat and trans fat) including food labelling and marketing requirements as well as requirements for catering and restaurants, and stimulating physical activity. This may be part of regional cardiovascular disease prevention programmes, or through the health impact assessment of regional and local plans and policies.
People considered at high risk of cardiovascular disease or with previous cardiovascular problems are advised to keep a diet where less than 30% of the energy intake derives from fat, a diet that contains less than 7% of the energy intake in the form saturated fat, and a diet that contains less than 300 mg/day of cholesterol. Replacing saturated with mono- polyunsaturated fat is also recommended, as the consumption of polyunsaturated fat instead of saturated fat can decrease coronary heart disease. Olive oil, rapeseed oil and related products are to be used instead of saturated fat. Other recommendations include: increased intake of wholegrain starch, reduced sugar intake (particularly of refined sugar), consumption of 5 portions of fruit and vegetables daily, consumption of 2 or more portions of fish per week, and 4–5 portions of unsalted nuts, seeds or legumes per week. Vitamins and mineral supplements are of no proven benefit, and neither are plant stanols or sterols.
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. Keeping a healthy weight, drinking alcohol within the recommended limits, and smoking cessation are measures that may reduce the risk of cardiovascular disease.
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. Nevertheless, many clinical practice guidelines continue to recommend aspirin for primary prevention, and some researchers feel that those with very high cardiovascular risk but low risk of bleeding should continue to receive aspirin.
An MI requires immediate medical attention. Treatment attempts to save as much viable heart muscle as possible and to prevent further complications, hence the phrase "time is [heart] muscle". Aspirin and nitroglycerin may be administered. Nitroglycerin (administered under the tongue or intravenously) may be administered to improve the blood supply to the heart. Morphine may be used if nitroglycerin is not effective. Other analgesics such as nitrous oxide are of unknown benefit.
In the past, high flow oxygen was recommended for everyone with possible myocardial infarction. More recently, routine use was found to lead to increased mortality and infarct size. Therefore, oxygen is currently only used if oxygen levels are found to be low or someone is in respiratory distress.
Thrombolysis involves the administration of medication that activates the enzymes that normally destroy blood clots. The first thrombolysis agent was streptokinase, but most thrombolysis agents used currently are artificial forms of the human enzyme tissue plasminogen activator (tPA): reteplase, alteplase and tenecteplase. They are administered intravenously. Once a STEMI has been diagnosed, and no contraindications are present (such as a high risk of bleeding), thrombolysis can be administered in the pre-hospital or in-hospital setting. There is inconclusive evidence whether pre-hospital thrombolysis reduces death in people with STEMI compared to in-hospital thrombolysis. Pre-hospital thrombolysis reduces time to receipt of thrombolytic treatment, based on studies conducted in higher income countries. 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.
Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a hospital in a timely manner.
If PCI cannot be performed within 90 to 120 minutes then thrombolysis, preferably within 30 minutes of arrival to hospital, is recommended. After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).
In the absence of ST elevation, formal diagnosis of MI is delayed until a blood test for biomarkers (usually troponin) can be performed; this is 3–6 hours after the onset of symptoms. The scenario is referred to as "non-ST elevation acute coronary syndrome" (NSTEACS). In the meantime, the calculated risk of further cardiovascular events (e.g. using the GRACE score) and the presence of other ECG changes and clinical features determines ongoing management.
People with an acute coronary syndrome where no ST elevation is demonstrated (non-ST elevation ACS or NSTEACS) are treated with aspirin. Clopidogrel is added in many cases, particularly if the risk of cardiovascular events is felt to be high and early PCI is being considered. Depending on whether early PCI is planned, an inhibitor of antithrombin (fondaparinux or low molecular weight heparin) may be added. In very high-risk scenarios, inhibitors of the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.
P2Y12 inhibitors such as clopidogrel or ticagrelor do not change the risk of death when given to people with a suspected NSTEMI prior to PCI. They do however increase the risk of bleeding and decrease the risk of further cardiovascular problems. Thus their routine use prior to PCI is of questionable value.
Cardiac rehabilitation benefits many who have experienced myocardial infarction, even if there has been substantial heart damage and resultant left ventricular failure; ideally other medical conditions that could interfere with participation should be managed optimally. It should start soon after discharge from hospital. The programme may include lifestyle advice, exercise, social support, as well as recommendations about driving, flying, sport participation, stress management, and sexual intercourse.
A number of lifestyle recommendations are available to those who have experienced myocardial infarction. This includes the adoption of a Mediterranean-type diet, maintaining alcohol intake within recommended limits, exercising to the point of mild breathlessness for 20–30 minutes every day, stopping smoking, and trying to achieve a healthy weight.
- Aspirin as well as an another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) is continued for up to twelve months, followed by asprin indefinitely. 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. In those who have had a stent more than 12 months of clopidogrel plus aspirin does not affect the risk of death.
- Beta blocker therapy such as metoprolol or carvedilol should be started within 24 hours, provided there is no acute heart failure or heart block. The dose should be increased to the highest tolerated. They should not be used in those who have recently taken cocaine.
- ACE inhibitor therapy should be commenced when stable and continued indefinitely at the highest tolerated dose. Those who cannot tolerate ACE inhibitors may be treated with angiotensin II receptor antagonist.
- Statin therapy has been shown to reduce mortality and morbidity. The protective effects of statins may be due to more than their LDL lowering effects. The general consensus is that statins have the ability to stabilize plaques and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.
- Aldosterone antagonists (spironolactone or eplerenone) may be used if there is evidence of left ventricular dysfunction after an MI, ideally after commencing an ACE inhibitor.
- Previous studies suggesting a benefit from omega-3 fatty acid supplementation has not been confirmed.
The prognosis after MI varies greatly depending on a person's health, the extent of the heart damage, and the treatment given.
In those who have an STEMI in the United States, between 5 to 6 percent die before leaving hospital and 7 to 18 percent die within a year.
Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. One study found 0.4% of patients with a low-risk profile died after 90 days, whereas in high-risk people it was 21.1%.
Some 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. Assessment of left ventricular ejection fraction may increase the predictive power. Prognosis is worse if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs. Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.
Complications may occur immediately following the heart attack (in the acute phase), or may need time to develop (a chronic problem). Acute complications may include heart failure if the damaged heart is no longer able to pump blood adequately around the body; aneurysm or rupture of the myocardium; mitral regurgitation, in particular if the infarction causes dysfunction of the papillary muscle; Dressler's syndrome; and arrhythmias, such as ventricular fibrillation, ventricular tachycardia, atrial fibrillation, and heart block. Longer-term complications include heart failure, atrial fibrillation, and the increased risk of a second MI.
Myocardial infarction is a common presentation of
- Cardiac disorders – Open Directory Project
- American Heart Association's Heart Attack web site — Information and resources for preventing, recognizing and treating heart attack.
- Kosuge M, Kimura K, Ishikawa T, Ebina T, Hibi K, Tsukahara K, Kanna M, Iwahashi N, Okuda J, Nozawa N, Ozaki H, Yano H, Nakati T, Kusama I, Umemura S; Kimura; Ishikawa; Ebina; Hibi; Tsukahara; Kanna; Iwahashi; Okuda; Nozawa; Ozaki; Yano; Nakati; Kusama; Umemura (March 2006). "Differences between men and women in terms of clinical features of ST-segment elevation acute myocardial infarction". Circulation Journal 70 (3): 222–6.
- Valensi P, Lorgis L, Cottin Y; Lorgis; Cottin (March 2011). "Prevalence, incidence, predictive factors and prognosis of silent myocardial infarction: a review of the literature". Arch Cardiovasc Dis 104 (3): 178–88.
- Graham I, Atar D, Borch-Johnsen K, Boysen G, Burell G, Cifkova R, Dallongeville J, De Backer G, Ebrahim S, Gjelsvik B, Herrmann-Lingen C, Hoes A, Humphries S, Knapton M, Perk J, Priori SG, Pyorala K, Reiner Z, Ruilope L, Sans-Menendez S, Scholte op Reimer W, Weissberg P, Wood D, Yarnell J, Zamorano JL, Walma E, Fitzgerald T, Cooney MT, Dudina A (October 2007). "European guidelines on cardiovascular disease prevention in clinical practice: executive summary: Fourth Joint Task Force of the European Society of Cardiology and Other Societies on Cardiovascular Disease Prevention in Clinical Practice (Constituted by representatives of nine societies and by invited experts)". Eur. Heart J. 28 (19): 2375–414.
- Devlin RJ, Henry JA (2008). "Clinical review: Major consequences of illicit drug consumption". Crit Care 12 (1): 202.
- Erhardt L, Herlitz J, Bossaert L, Halinen M, Keltai M, Koster R, Marcassa C, Quinn T, van Weert H (2002). "Task force on the management of chest pain" (PDF). Eur. Heart J. 23 (15): 1153–76.
- Roe MT, Messenger JC, Weintraub WS, Cannon CP, Fonarow GC, Dai D, Chen AY, Klein LW, Masoudi FA, McKay C, Hewitt K, Brindis RG, Peterson ED, Rumsfeld JS (July 2010). "Treatments, trends, and outcomes of acute myocardial infarction and percutaneous coronary intervention". J. Am. Coll. Cardiol. 56 (4): 254–63.
- O'Connor RE, Brady W, Brooks SC, Diercks D, Egan J, Ghaemmaghami C, Menon V, O'Neil BJ, Travers AH, Yannopoulos D (November 2010). "Part 10: acute coronary syndromes: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care". Circulation 122 (18 Suppl 3): S787–817.
- Van de Werf F, Bax J, Betriu A, Blomstrom-Lundqvist C, Crea F, Falk V, Filippatos G, Fox K, Huber K, Kastrati A, Rosengren A, Steg PG, Tubaro M, Verheugt F, Weidinger F, Weis M (December 2008). "Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology". Eur. Heart J. 29 (23): 2909–45.
- Hamm CW, Bassand JP, Agewall S, Bax J, Boersma E, Bueno H, Caso P, Dudek D, Gielen S, Huber K, Ohman M, Petrie MC, Sonntag F, Uva MS, Storey RF, Wijns W, Zahger D (December 2011). "ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC)". Eur. Heart J. 32 (23): 2999–3054.
- "The top 10 causes of death".
- World Health Organization (2008). The Global Burden of Disease: 2004 Update. Geneva: World Health Organization.
- National Heart, Lung and Blood Institute. Heart Attack Warning Signs. Retrieved November 22, 2006.
- Berger JP, Buclin T, Haller E, Van Melle G, Yersin B (March 1990). "Right arm involvement and pain extension can help to differentiate coronary diseases from chest pain of other origin: a prospective emergency ward study of 278 consecutive patients admitted for chest pain". J. Intern. Med. 227 (3): 165–72.
- Marcus GM, Cohen J, Varosy PD, Vessey J, Rose E, Massie BM, Chatterjee K, Waters D (2007). "The utility of gestures in patients with chest discomfort".
- Mallinson, T (2010). "Myocardial Infarction". Focus on First Aid (15): 15. Retrieved 2010-06-08.
- Little RA, Frayn KN, Randall PE, Stoner HB, Morton C, Yates DW, Laing GS (1986). "Plasma catecholamines in the acute phase of the response to myocardial infarction". Arch Emerg Med 3 (1): 20–7.
- Canto JG, Goldberg RJ, Hand MM, Bonow RO, Sopko G, Pepine CJ, Long T (December 2007). "Symptom presentation of women with acute coronary syndromes: myth vs reality". Arch. Intern. Med. 167 (22): 2405–13.
- Brown, Anthony (2011). Emergency Medicine Diagnosis and Management 6th Edition.
- McSweeney JC, Cody M, O'Sullivan P, Elberson K, Moser DK, Garvin BJ (2003). "Women's early warning symptoms of acute myocardial infarction". Circulation 108 (21): 2619–23.
- Kannel WB (1986). "Silent myocardial ischemia and infarction: insights from the Framingham Study". Cardiol Clin 4 (4): 583–91.
- Davis TM, Fortun P, Mulder J, Davis WA, Bruce DG (2004). "Silent myocardial infarction and its prognosis in a community-based cohort of Type 2 diabetic patients: the Fremantle Diabetes Study". Diabetologia 47 (3): 395–9.
- Rubin, Emanuel; Gorstein, Fred; Rubin, Raphael; Schwarting, Roland; Strayer, David (2001). Rubin's Pathology — Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins. p. 549.
- Acute Coronary Syndrome. American Heart Association. Retrieved November 25, 2006.
- Boie ET (2005). "Initial evaluation of chest pain".
- Kivimäki M, Nyberg ST, Batty GD, Fransson EI, Heikkilä K, Alfredsson L, Bjorner JB, Borritz M, Burr H, Casini A, Clays E, De Bacquer D, Dragano N, Ferrie JE, Geuskens GA, Goldberg M, Hamer M, Hooftman WE, Houtman IL, Joensuu M, Jokela M, Kittel F, Knutsson A, Koskenvuo M, Koskinen A, Kouvonen A, Kumari M, Madsen IE, Marmot MG, Nielsen ML, Nordin M, Oksanen T, Pentti J, Rugulies R, Salo P, Siegrist J, Singh-Manoux A, Suominen SB, Väänänen A, Vahtera J, Virtanen M, Westerholm PJ, Westerlund H, Zins M, Steptoe A, Theorell T (31 August 2012). "Job strain as a risk factor for coronary heart disease: a collaborative meta-analysis of individual participant data". The Lancet 380 (9852): 1491–7.
- Lee IM, Shiroma EJ, Lobelo F, Puska P, Blair SN, Katzmarzyk PT (1 July 2012). "Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy". The Lancet 380 (9838): 219–29.
- Steptoe A, Kivimäki M (April 2012). "Stress and cardiovascular disease". Nature Reviews Cardiology 9 (6): 360–70.
- Smith SC, Allen J, Blair SN, Bonow RO, Brass LM, Fonarow GC, Grundy SM, Hiratzka L, Jones D, Krumholz HM, Mosca L, Pearson T, Pfeffer MA, Taubert KA (May 2006). "AHA/ACC guidelines for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update endorsed by the National Heart, Lung, and Blood Institute". J. Am. Coll. Cardiol. 47 (10): 2130–9.
- Mustafic H, Jabre P, Caussin C, Murad MH, Escolano S, Tafflet M, Périer MC, Marijon E, Vernerey D, Empana JP, Jouven X (Feb 15, 2012). "Main air pollutants and myocardial infarction: a systematic review and meta-analysis". JAMA: the Journal of the American Medical Association 307 (7): 713–21.
- Nyboe J, Jensen G, Appleyard M, Schnohr P (1989). "Risk factors for acute myocardial infarction in Copenhagen. I: Hereditary, educational and socioeconomic factors. Copenhagen City Heart Study". Eur Heart J 10 (10): 910–6.
- Chowdhury R, Warnakula S, Kunutsor S, Crowe F, Ward HA, Johnson L, Franco OH, Butterworth AS, Forouhi NG, Thompson SG, Khaw KT, Mozaffarian D, Danesh J, Di Angelantonio E (2014). "Association of dietary, circulating, and supplement fatty acids with coronary risk: a systematic review and meta-analysis". Ann. Intern. Med. 160 (6): 398–406.
- Buse JB, Ginsberg HN, Bakris GL, Clark NG, Costa F, Eckel R, Fonseca V, Gerstein HC, Grundy S, Nesto RW, Pignone MP, Plutzky J, Porte D, Redberg R, Stitzel KF, Stone NJ (January 2007). "Primary prevention of cardiovascular diseases in people with diabetes mellitus: a scientific statement from the American Heart Association and the American Diabetes Association". Circulation 115 (1): 114–26.
- Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Onen CL, Lisheng L, Tanomsup S, Wangai P, Razak F, Sharma AM, Anand SS (2005). "Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study". Lancet 366 (9497): 1640–9.
- Chatzidimitriou D, Kirmizis D, Gavriilaki E, Chatzidimitriou M, Malisiovas N (Oct 2012). "Atherosclerosis and infection: is the jury still not in?". Future microbiology 7 (10): 1217–30.
- Charakida M, Tousoulis D (2013). "Infections and atheromatous plaque: current therapeutic implications.". Current pharmaceutical design 19 (9): 1638–50.
- Feero, W. Gregory; Guttmacher, Alan E.; O'Donnell, Christopher J.; Nabel, Elizabeth G. (Dec 2011). "Genomics of Cardiovascular Disease". New England Journal of Medicine 365 (22): 2098–2109.
- Wilson PW, D'Agostino RB, Levy D, Belanger AM, Silbershatz H, Kannel WB (1998). "Prediction of coronary heart disease using risk factor categories" (PDF). Circulation 97 (18): 1843–44.
- Khader YS, Rice J, John L, Abueita O (2003). "Oral contraceptives use and the risk of myocardial infarction: a meta-analysis". Contraception 68 (1): 11–7.
- Muller JE, Stone PH, Turi ZG, Rutherford JD, Czeisler CA, Parker C, Poole WK, Passamani E, Roberts R, Robertson T (1985). "Circadian variation in the frequency of onset of acute myocardial infarction".
- Beamer AD, Lee TH, Cook EF, Brand DA, Rouan GW, Weisberg MC, Goldman L (1987). "Diagnostic implications for myocardial ischemia of the circadian variation of the onset of chest pain".
- Cannon CP, McCabe CH, Stone PH, Schactman M, Thompson B, Theroux P, Gibson RS, Feldman T, Kleiman NS, Tofler GH, Muller JE, Chaitman BR, Braunwald E (1997). "Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB)".
- Moe KT, Wong P (March 2010). "Current trends in diagnostic biomarkers of acute coronary syndrome" (PDF). Ann. Acad. Med. Singap. 39 (3): 210–5.
- Tsujita K, Kaikita K, Soejima H, Sugiyama S, Ogawa H (April 2010). "[Acute coronary syndrome-initiating factors]". Nippon Rinsho (in Japanese) 68 (4): 607–14.
- Dohi T, Daida H (April 2010). "[Change of concept and pathophysiology in acute coronary syndrome]". Nippon Rinsho (in Japanese) 68 (4): 592–6.
- Woollard KJ, Geissmann F (February 2010). "Monocytes in atherosclerosis: subsets and functions". Nature Reviews Cardiology 7 (2): 77–86.
- Spaan J, Kolyva C, van den Wijngaard J, ter Wee R, van Horssen P, Piek J, Siebes M (September 2008). "Coronary structure and perfusion in health and disease".
- Krijnen PA, Nijmeijer R, Meijer CJ, Visser CA, Hack CE, Niessen HW (2002). "Apoptosis in myocardial ischaemia and infarction". J Clin Pathol 55 (11): 801–11.
- Wilson AM, Ryan MC, Boyle AJ (2006). "The novel role of C-reactive protein in cardiovascular disease: risk marker or pathogen". Int J Cardiol 106 (3): 291–7.
- Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO, Criqui M, Fadl YY, Fortmann SP, Hong Y, Myers GL, Rifai N, Smith SC, Taubert K, Tracy RP, Vinicor F (2003). "Markers of inflammation and cardiovascular disease: application to clinical and public health practice: A statement for healthcare professionals from the Centers for Disease Control and Prevention and the American Heart Association" (PDF). Circulation 107 (3): 499–511.
- Greenland P, LaBree L, Azen SP, Doherty TM, Detrano RC (2004). "Coronary artery calcium score combined with Framingham score for risk prediction in asymptomatic individuals". JAMA 291 (2): 210–5.
- Detrano R, Guerci AD, Carr JJ, Bild DE, Burke G, Folsom AR, Liu K, Shea S, Szklo M, Bluemke DA, O'Leary DH, Tracy R, Watson K, Wong ND, Kronmal RA (2008). "Coronary calcium as a predictor of coronary events in four racial or ethnic groups". N. Engl. J. Med. 358 (13): 1336–45.
- Arad Y, Goodman KJ, Roth M, Newstein D, Guerci AD (2005). "Coronary calcification, coronary disease risk factors, C-reactive protein, and atherosclerotic cardiovascular disease events: the St. Francis Heart Study". J. Am. Coll. Cardiol. 46 (1): 158–65.
- Clarke R, Halsey J, Bennett D, Lewington S (February 2011). "Homocysteine and vascular disease: review of published results of the homocysteine-lowering trials". J. Inherit. Metab. Dis. 34 (1): 83–91.
- Lonn E (September 2007). "Homocysteine in the prevention of ischemic heart disease, stroke and venous thromboembolism: therapeutic target or just another distraction?". Current Opinion in Hematology 14 (5): 481–7.
- Reznik AG (2010). "[Morphology of acute myocardial infarction at prenecrotic stage]". Kardiologiia (in Russian) 50 (1): 4–8.
- Alpert JS, Thygesen K, Antman E, Bassand JP (2000). "Myocardial infarction redefined—a consensus document of The Joint European Society of Cardiology/American College of Cardiology Committee for the redefinition of myocardial infarction". J Am Coll Cardiol 36 (3): 959–69.
- Anonymous (March 1979). "Nomenclature and criteria for diagnosis of ischemic heart disease. Report of the Joint International Society and Federation of Cardiology/World Health Organization task force on standardization of clinical nomenclature". Circulation 59 (3): 607–9.
- O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA, Ettinger SM, Fang JC, Fesmire FM, Franklin BA, Granger CB, Krumholz HM, Linderbaum JA, Morrow DA, Newby LK, Ornato JP, Ou N, Radford MJ, Tamis-Holland JE, Tommaso CL, Tracy CM, Woo YJ, Zhao DX, Anderson JL, Jacobs AK, Halperin JL, Albert NM, Brindis RG, Creager MA, DeMets D, Guyton RA, Hochman JS, Kovacs RJ, Kushner FG, Ohman EM, Stevenson WG, Yancy CW (Jan 29, 2013). "2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.". Circulation 127 (4): e362–425.
- Thygesen K, Alpert JS, White HD (October 2007). "Universal definition of myocardial infarction". Eur. Heart J. 28 (20): 2525–38.
- Amsterdam, E. A.; Wenger, N. K.; Brindis, R. G.; Casey, D. E.; Ganiats, T. G.; Holmes, D. R.; Jaffe, A. S.; Jneid, H.; Kelly, R. F.; Kontos, M. C.; Levine, G. N.; Liebson, P. R.; Mukherjee, D.; Peterson, E. D.; Sabatine, M. S.; Smalling, R. W.; Zieman, S. J. (23 September 2014). "2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines". Circulation (Online first).
- Lipinski, MJ; Escárcega, RO; D'Ascenzo, F; Magalhães, MA; Baker, NC; Torguson, R; Chen, F; Epstein, SE; Miró, O; Llorens, P; Giannitsis, E; Lotze, U; Lefebvre, S; Sebbane, M; Cristol, JP; Chenevier-Gobeaux, C; Meune, C; Eggers, KM; Charpentier, S; Twerenbold, R; Mueller, C; Biondi-Zoccai, G; Waksman, R (May 1, 2014). "A systematic review and collaborative meta-analysis to determine the incremental value of copeptin for rapid rule-out of acute myocardial infarction.". The American journal of cardiology 113 (9): 1581–91.
- Myocardial infarction~workup at eMedicine
- Skoufis E, McGhie AI (1998). "Radionuclide techniques for the assessment of myocardial viability".
, which cites
- Hendel RC, Berman DS, Di Carli MF, Heidenreich PA, Henkin RE, Pellikka PA, Pohost GM, Williams KA (2009). "ACCF/ASNC/ACR/AHA/ASE/SCCT/SCMR/SNM 2009 Appropriate Use Criteria for Cardiac Radionuclide Imaging". Journal of the American College of Cardiology 53 (23): 2201–2229.
- Taylor AJ, Cerqueira M, Hodgson JM, Mark D, Min J, O'Gara P, Rubin GD, Kramer CM, Berman D, Brown A, Chaudhry FA, Cury RC, Desai MY, Einstein AJ, Gomes AS, Harrington R, Hoffmann U, Khare R, Lesser J, McGann C, Rosenberg A, Schwartz R, Shelton M, Smetana GW, Smith SC (2010). "ACCF/SCCT/ACR/AHA/ASE/ASNC/NASCI/SCAI/SCMR 2010 Appropriate Use Criteria for Cardiac Computed Tomography". Journal of the American College of Cardiology 56 (22): 1864–1894.
- Anderson, J. L.; Adams, C. D.; Antman, E. M.; Bridges, C. R.; Califf, R. M.; Casey, D. E.; Chavey, W. E.; Fesmire, F. M.; Hochman, J. S.; Levin, T. N.; Lincoff, A. M.; Peterson, E. D.; Theroux, P.; Wenger, N. K.; Wright, R. S. (2007). "ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction): Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons: Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". Circulation 116 (7): 803.
- McPherson K et al (June 2010). "Prevention of cardiovascular disease – NICE public health guidance 25". London:
- National Institute for Health and Clinical Excellence. Clinical guideline 181: Lipid modification: cardiovascular risk assessment and the modification of blood lipids for the primary and secondary prevention of cardiovascular disease. London, 2014.
- Mozaffarian D, Micha R, Wallace S (2010). Katan, Martijn B, ed. "Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials". PLoS Med. 7 (3): e1000252.
- Fortmann, SP; Burda, BU; Senger, CA; Lin, JS; Whitlock, EP (17 December 2013). "Vitamin and mineral supplements in the primary prevention of cardiovascular disease and cancer: An updated systematic evidence review for the U.S. Preventive Services Task Force.". Annals of internal medicine 159 (12): 824–34.
- Antithrombotic Trialists' (ATT), Collaboration; Baigent, C; Blackwell, L; Collins, R; Emberson, J; Godwin, J; Peto, R; Buring, J; Hennekens, C; Kearney, P; Meade, T; Patrono, C; Roncaglioni, MC; Zanchetti, A (30 May 2009). "Aspirin in the primary and secondary prevention of vascular disease: collaborative meta-analysis of individual participant data from randomised trials.". Lancet 373 (9678): 1849–60.
- Sutcliffe, P; Connock, M; Gurung, T; Freeman, K; Johnson, S; Kandala, NB; Grove, A; Gurung, B; Morrow, S; Clarke, A (September 2013). "Aspirin for prophylactic use in the primary prevention of cardiovascular disease and cancer: a systematic review and overview of reviews.". Health technology assessment (Winchester, England) 17 (43): 1–253.
- Matthys, F; De Backer, T; De Backer, G; Stichele, RV (March 2014). "Review of guidelines on primary prevention of cardiovascular disease with aspirin: how much evidence is needed to turn a tanker?". European journal of preventive cardiology 21 (3): 354–65.
- Halvorsen, S; Andreotti, F; ten Berg, JM; Cattaneo, M; Coccheri, S; Marchioli, R; Morais, J; Verheugt, FW; De Caterina, R (22 July 2014). "Aspirin therapy in primary cardiovascular disease prevention: a position paper of the European Society of Cardiology working group on thrombosis.". Journal of the American College of Cardiology 64 (3): 319–27.
- Gulli, American Academy of Orthopaedic Surgeons ; editors, Leaugeay Barnes, Joseph A. Ciotola, Benjamin (2010-03-23). Emergency care and transportation of the sick and injured. (10th ed.). Sudbury, Mass.: Jones and Bartlett. p. 575.
- Wijesinghe M, Perrin K, Ranchord A, Simmonds M, Weatherall M, Beasley R (March 2009). "Routine use of oxygen in the treatment of myocardial infarction: systematic review". Heart 95 (3): 198–202.
- Cabello JB, Burls A, Emparanza JI, Bayliss S, Quinn T (2013). Cabello, Juan B, ed. "Oxygen therapy for acute myocardial infarction". Cochrane Database Syst Rev 8: CD007160.
- Bates ER, Menees DS (Oct 2012). "Acute ST-elevation myocardial infarction". Current Opinion in Critical Care. 5 18 (5): 417–23.
- McCaul, M; Lourens, A; Kredo, T (Sep 10, 2014). "Pre-hospital versus in-hospital thrombolysis for ST-elevation myocardial infarction.". The Cochrane database of systematic reviews 9: CD010191.
- Wang, edited by Reza Ardehali, Marco Perez, Paul (2011). A practical approach to cardiovascular medicine. Chichester, West Sussex, UK: Wiley-Blackwell. p. 57.
- Jindal, editor-in-chief SK (2011). Textbook of pulmonary and critical care medicine. New Delhi: Jaypee Brothers Medical Publishers. p. 1758.
- Bagai, A; Dangas, GD; Stone, GW; Granger, CB (6 June 2014). "Reperfusion strategies in acute coronary syndromes.". Circulation research 114 (12): 1918–28.
- Lassen JF, Bøtker HE, Terkelsen CJ (Jan 2013). "Timely and optimal treatment of patients with STEMI". Nature Reviews Cardiology. 1 10 (1): 41–8.
- Brilakis ES, Patel VG, Banerjee S (Jul 10, 2013). "Medical management after coronary stent implantation: a review". JAMA: the Journal of the American Medical Association 310 (2): 189–98.
- National Institute for Health and Clinical Excellence. Clinical guideline cg94: Unstable angina and NSTEMI. London, 2010.
- Andrade-Castellanos, CA; Colunga-Lozano, LE; Delgado-Figueroa, N; Magee, K (Jun 27, 2014). "Heparin versus placebo for non-ST elevation acute coronary syndromes.". The Cochrane database of systematic reviews 6: CD003462.
- Bellemain-Appaix, A.; Kerneis, M.; O'Connor, S. A.; Silvain, J.; Cucherat, M.; Beygui, F.; Barthelemy, O.; Collet, J.-P.; Jacq, L.; Bernasconi, F.; Montalescot, G. (24 October 2014). "Reappraisal of thienopyridine pretreatment in patients with non-ST elevation acute coronary syndrome: a systematic review and meta-analysis". BMJ 347 (aug06 2): g6269–g6269.
- National Institute for Health and Clinical Excellence. Clinical guideline 172: Secondary prevention in primary and secondary care for patients following a myocardial infarction. London, 2013.
- Elmariah, Sammy; Mauri, Laura; Doros, Gheorghe; Galper, Benjamin Z; O'Neill, Kelly E; Steg, Philippe Gabriel; Kereiakes, Dean J; Yeh, Robert W (November 2014). "Extended duration dual antiplatelet therapy and mortality: a systematic review and meta-analysis". The Lancet.
- McCord, J; Jneid, H; Hollander, JE; de Lemos, JA; Cercek, B; Hsue, P; Gibler, WB; Ohman, EM; Drew, B; Philippides, G; Newby, LK; American Heart Association Acute Cardiac Care Committee of the Council on Clinical, Cardiology (8 April 2008). "Management of cocaine-associated chest pain and myocardial infarction: a scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology.". Circulation 117 (14): 1897–907.
- Taylor F, Huffman MD, Macedo AF, Moore TH, Burke M, Davey Smith G, Ward K, Ebrahim S; Huffman; MacEdo; Moore; Burke; Davey Smith; Ward; Ebrahim (Jan 31, 2013). "Statins for the primary prevention of cardiovascular disease". The Cochrane database of systematic reviews 1: CD004816.
- Ray KK, Cannon CP; Cannon (2005). "The potential relevance of the multiple lipid-independent (pleiotropic) effects of statins in the management of acute coronary syndromes". J. Am. Coll. Cardiol. 46 (8): 1425–33.
- López de Sá E, López-Sendón J, Anguera I, Bethencourt A, Bosch X; López-Sendón; Anguera; Bethencourt; Bosch; Proyecto de Estudio del Pronostico de la Angina (PEPA) Investigators (November 2002). "Prognostic value of clinical variables at presentation in patients with non-ST-segment elevation acute coronary syndromes: results of the Proyecto de Estudio del Pronóstico de la Angina (PEPA)". Medicine (Baltimore) 81 (6): 434–42.
- Fox KA, Dabbous OH, Goldberg RJ, Pieper KS, Eagle KA, Van de Werf F, Avezum A, Goodman SG, Flather MD, Anderson FA, Granger CB; Dabbous; Goldberg; Pieper; Eagle; Van De Werf; Avezum; Goodman; Flather; Anderson Jr; Granger (November 2006). "Prediction of risk of death and myocardial infarction in the six months after presentation with acute coronary syndrome: prospective multinational observational study (GRACE)". BMJ 333 (7578): 1091.
- Weir RA, McMurray JJ, Velazquez EJ; McMurray; Velazquez (2006). "Epidemiology of heart failure and left ventricular systolic dysfunction after acute myocardial infarction: prevalence, clinical characteristics, and prognostic importance". Am J Cardiol 97 (10A): 13F–25F.
- Bosch X, Théroux P; Théroux (2005). "Left ventricular ejection fraction to predict early mortality in patients with non-ST-segment elevation acute coronary syndromes". Am Heart J 150 (2): 215–20.
- Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ; Gore; Lambrew; Weaver; Rubison; French; Tiefenbrunn; Bowlby; Rogers (1996). "A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction". J Am Coll Cardiol 27 (6): 1321–6.
- Liew R, Sulfi S, Ranjadayalan K, Cooper J, Timmis AD; Sulfi; Ranjadayalan; Cooper; Timmis (2006). "Declining case fatality rates for acute myocardial infarction in South Asian and white patients in the past 15 years". Heart 92 (8): 1030–4.
- White HD, Chew DP; Chew (August 2008). "Acute myocardial infarction". Lancet 372 (9638): 570–84.
- Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, Bravata DM, Dai S, Ford ES, Fox CS, Fullerton HJ, Gillespie C, Hailpern SM, Heit JA, Howard VJ, Kissela BM, Kittner SJ, Lackland DT, Lichtman JH, Lisabeth LD, Makuc DM, Marcus GM, Marelli A, Matchar DB, Moy CS, Mozaffarian D, Mussolino ME, Nichol G, Paynter NP, Soliman EZ, Sorlie PD, Sotoodehnia N, Turan TN, Virani SS, Wong ND, Woo D, Turner MB; Go; Lloyd-Jones; Benjamin; Berry; Borden; Bravata; Dai; Ford; Fox; Fullerton; Gillespie; Hailpern; Heit; Howard; Kissela; Kittner; Lackland; Lichtman; Lisabeth; Makuc; Marcus; Marelli; Matchar; Moy; Mozaffarian; Mussolino; Nichol; Paynter; Soliman (January 2012). "Executive summary: heart disease and stroke statistics—2012 update: a report from the American Heart Association". Circulation 125 (1): 188–97.
- Gupta R, Joshi P, Mohan V, Reddy KS, Yusuf S; Joshi; Mohan; Reddy; Yusuf (January 2008). "Epidemiology and causation of coronary heart disease and stroke in India". Heart 94 (1): 16–26.
- Torio CM, Andrews RM. National Inpatient Hospital Costs: The Most Expensive Conditions by Payer, 2011. HCUP Statistical Brief #160. Agency for Healthcare Research and Quality, Rockville, MD. August 2013. 
- Workers' Compensation FAQ. Prairie View A&M University. Retrieved November 22, 2006.
- SIGNIFICANT DECISIONS Subject Index. Board of Industrial Insurance Appeals. Retrieved November 22, 2006.
- "Classification of Drivers' Licenses Regulations". Nova Scotia Registry of Regulations. May 24, 2000. Retrieved April 22, 2007.
- Schächinger V, Erbs S, Elsässer A, Haberbosch W, Hambrecht R, Hölschermann H, Yu J, Corti R, Mathey DG, Hamm CW, Süselbeck T, Assmus B, Tonn T, Dimmeler S, Zeiher AM; Erbs; Elsässer; Haberbosch; Hambrecht; Hölschermann; Yu; Corti; Mathey; Hamm; Süselbeck; Assmus; Tonn; Dimmeler; Zeiher; Repair-Ami (2006). "Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction". N Engl J Med 2006 355 (12): 1210–21.
- Christman KL, Lee RJ; Lee (September 2006). "Biomaterials for the treatment of myocardial infarction". J. Am. Coll. Cardiol. 48 (5): 907–13.
Currently, three biomaterial and tissue engineering approaches are used for the treatment of post-MI conditions, but these are in an even earlier stage of medical research. Many questions and issues must be addressed before they can be applied to patients. The first involves polymeric left ventricular restraints in the prevention of heart failure. The second uses in vitro-engineered cardiac tissue, which is subsequently implanted in vivo. The final approach entails injecting cells and/or a scaffold into the myocardium to create in situ-engineered cardiac tissue.
Patients who receive stem cell treatment by coronary artery injections of stem cells derived from their own bone marrow after an MI show improvements in left ventricular ejection fraction and end-diastolic volume not seen with placebo. The larger the initial infarct size, the greater the effect of the infusion. Clinical trials of progenitor cell infusion as a treatment approach to STEMI are underway.
At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered; however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion. 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.
In 2011, AMI was one of the top five most expensive conditions seen during inpatient hospitalizations in the U.S., with an aggregate cost of about $11.5 billion for 612,000 hospital stays.
In the United States, women who have had an MI are often treated with fewer medical interventions than men.
Society and culture
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. 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 1985–2015. 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.
 STEMIs occur about twice as often in men as women. Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year..lower-income countries in lower respiratory infections with it being the leading cause of death in high- or middle-income countries and second only to