Myocardial infarction

From Wikipedia, the free encyclopedia
"Heart attack" redirects here. For other uses, see Heart attack (disambiguation).
Not to be confused with Cardiac arrest.
Myocardial infarction
Classification and external resources

Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA). In the diagram, RCA is the right coronary artery.
ICD-10 I21-I22
ICD-9 410
DiseasesDB 8664
MedlinePlus 000195
eMedicine med/1567 emerg/327 ped/2520
MeSH D009203

Myocardial infarction (from Latin: Infarctus myocardii, MI) or acute myocardial infarction (AMI) is the medical term for an event commonly known as a heart attack. It happens when blood stops flowing properly to part of the heart and the heart muscle is injured due to 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.

A person having an acute MI usually has sudden chest pain that is felt behind the breast bone 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.[1] In many cases, in some estimates as high as 64%, the person does not have chest pain or other symptoms.[2] These are called "silent" myocardial infarctions.

Important risk factors are previous cardiovascular disease, old age, tobacco smoking, high blood levels of certain lipids (low-density lipoprotein cholesterol, triglycerides) and low levels of high density lipoprotein (HDL) cholesterol, diabetes, high blood pressure, lack of physical activity, obesity, chronic kidney disease, excessive alcohol consumption, and the use of cocaine and amphetamines.[3][4] The main way 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. Common blood tests are creatine kinase (CK-MB) and troponin. ECG testing is used to differentiate between two types of myocardial infarctions based on the shape 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.

Immediate treatments for a suspected MI include aspirin, which prevents further blood from clotting, and sometimes nitroglycerin to treat chest pain and oxygen.[5] 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.[6] 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.[7] People who have multiple blockages of their coronary arteries, particularly if they also have diabetes, may also be treated with bypass surgery (CABG).[8][9] 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.[10][11]

Signs and symptoms

Rough diagram of pain zones in myocardial infarction; dark red: most typical area, light red: other possible areas; view of the chest
Back view

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous.[12] 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 epigastrium,[8][13] 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.[14]

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),[15] weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system[16] which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in MIs.[8]

Female, elderly, and diabetic patients report atypical symptoms more frequently than their male and younger counterparts.[17][18] Women also report more numerous symptoms compared with men (2.6 on average vs. 1.8 symptoms in men).[17] 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.[19] Women may also experience back or jaw pain during an episode.[20]

At least one-fourth of all MIs are silent, without chest pain or other symptoms.[2][21] 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%.[2] A silent course is more common in the elderly,[2] in patients with diabetes mellitus[22] and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.[23] In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.[22]

Any group of symptoms compatible with a sudden interruption of the blood flow to the heart are called an acute coronary syndrome.[24]

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.[25]

Causes

Many of these risk factors are modifiable, so many heart attacks can be prevented by maintaining a healthier lifestyle. Physical activity, for example, is associated with a lower risk profile.[26] Nonmodifiable risk factors include age, sex, and family history of an early heart attack, which is thought of as reflecting a genetic predisposition.[citation needed] The effect of education is partially based on its effect on income and marital status.[27]

Lifestyle

Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease.[28] Lack of exercise has been linked to 7-12% of cases.[28][29] Job stress appears to play a minor role, accounting for about 3% of cases.[28] Chronic high stress levels may cause some cases.[30]

Tobacco smoking, including secondhand smoke[31] Short-term exposure to air pollution, including carbon monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone.[32] Lack of physical activity[3] Psychosocial factors including, low socioeconomic status, social isolation, negative emotions and stress increase the risk of and are associated with worse outcomes after MI.Socioeconomic factors such as a shorter education and lowerincome (particularly in women), and unmarried cohabitation are also correlated with a higher risk of MI.[27] Alcohol — prolonged exposure to high quantities of alcohol can increase the risk of heart attack.

Disease

Diabetes mellitus (type 1 or 2),[33] high blood pressure[31] dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoproteinand high triglycerides[31] Obesity[34] (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. There is as of 2013 no evidence of benefit from antibiotics or vaccination, however, calling the association into question.[35][36]

Other

Older age[3] Male sex: at any given age, men are more at risk than women, particularly before menopause,[37] but because in general women live longer than men, ischemic heart disease causes slightly more total deaths in women.[3] 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).[3]

Oral contraceptive pill – women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors, such as smoking.[38]

An increased incidence of a heart attack is associated with time of day especially in the morning hours, more specifically around 9 am.[39][40][41]

Pathophysiology

See also: Acute coronary syndrome
The animation shows how 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.
A myocardial infarction occurs when an atherosclerotic plaque slowly builds up in the inner lining of a coronary artery and then suddenly ruptures, causing catastrophic thrombus formation, totally occluding the artery and preventing blood flow downstream.
Drawing of the heart showing anterior left ventricle wall infarction

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.[42] 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.[43][44] 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.[45] Blood stream column irregularities visible on angiography reflect artery lumen narrowing as a result of decades of advancing atherosclerosis.[46] Plaques can become unstable, rupture, and additionally promote a thrombus (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).[43][44]

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.[47] 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 may or may not 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.[8] Inflammation is known to be an important step in the process ofatherosclerotic plaque formation.[48] 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.[48] Moreover, some drugs for MI might also reduce CRP levels.[48] 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.[49] Whether CRP plays a direct role in atherosclerosis remains uncertain.[48]

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.[50][51][52]

Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with premature atherosclerosis,[53]whether elevated homocysteine in the normal range is causal is contentious.[54]

Pathological types

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.[55] 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.[55] In addition, ST depression is seen on ECG.

Diagnosis

Main article: Myocardial infarction diagnosis

A cardiac troponin rise accompanied by either typical symptoms, pathological Q waves, ST elevation or depression, or coronary intervention is diagnostic of MI.[56]

WHO criteria[57] 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:

  1. Clinical history of ischaemic type chest pain lasting for more than 20 minutes
  2. Changes in serial ECG tracings
  3. Rise and fall of serum cardiac biomarkers

At autopsy, a pathologist can diagnose an MI based onanatomopathological findings.

Classification

Myocardial infarctions are generally classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI).[42] 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.[58] They make up abut 25 to 40 percent of cases.[58]

The phrase "heart attack" is often used none specifically to refer to a myocardial infarction and to sudden cardiac death. A 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.[8]

A 2007 consensus document classifies MI into five main types:[59]

  • 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, anaemia, arrhythmias, hypertension, or hypotension
  • Type 3 – sudden unexpected cardiac death, including cardiac arrest, often with symptoms suggestive of myocardial ischaemia, accompanied by new ST elevation, or new 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 PCI
    • Type 4b – MI associated with stent thrombosis as documented by angiography or at autopsy
  • Type 5 – MI associated with CABG

Electrocardiogram

For a person to quality as having an STEMI, the ECG must show new ST elevation in two or more contiguous leads.[58] 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.[58] A left bundle branch block (LBBB) that is believed to be new used to be considered the same as ST elevation; however, no longer is.[58] In early STEMIs there may just be peaked T wave with ST elevation developing latter.[58]

Cardiac biomarkers

While there are a number of different biomarkers, tropinins, are considered to be the best.[58]

Imaging

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.[60] 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.[60] 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.[61]

Medical societies recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis.[62] Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging.[62] Imaging tests such as stress radionuclide myocardial perfusion imaging or stressechocardiography can confirm a diagnosis when a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem.[62]

Prevention

The risk of a recurrent MI decreases with strict blood pressure management and lifestyle changes, chiefly smoking cessation, regular exercise, a sensible diet for those with heart disease, and limitation of alcohol intake. People are usually started on several long-term medications after an MI, with the aim of preventing further cardiovascular events such MIs, congestive heart failure, or cerebrovascular accident. Unless contraindicated, such medications may include:[63][64]

  • Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent MI. Aspirin is first-line, owing to its low cost and comparable efficacy, with clopidogrel reserved for patients intolerant of aspirin. The combination of clopidogrel and aspirin may further reduce risk of cardiovascular events, but the risk of hemorrhage is increased.[65]
  • Beta blocker therapy such as metoprolol or carvedilol should be started.[66] These have been particularly beneficial in those who are high-risk such as those with left ventricular dysfunction and/or continuing cardiac ischaemia.[67] β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
  • ACE inhibitor therapy should be commenced 24–48 hours after MI in those who are hemodynamically stable, particularly with a history of MI, diabetes mellitus, hypertension, anterior location of infarct (as assessed by ECG), and/or evidence of left ventricular dysfunction. ACE inhibitors reduce mortality, the development of heart failure, and decrease ventricular remodelling.[68]
  • Statin therapy has been shown to reduce mortality and morbidity.[69] The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.[70]
  • The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death after MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above.[71] Spironolactone, another option, is sometimes preferable to eplerenone due to cost.
  • Evidence supports the consumption of polyunsaturated fats instead of saturated fats as a measure of decreasing coronary heart disease.[72] In high-risk people, no clear-cut decrease in potentially fatal arrhythmias occurs due to omega-3 fatty acids.[73] And they may increase risk in some groups.[73]
  • Giving heparin to people with heart conditions like unstable angina and some forms of heart attacks reduces the risk of having another heart attack. However, heparin also increases the chance of minor bleeding.[74]

Management

Main article: Myocardial infarction management

An MI requires immediate medical attention. Treatment attempts to save as much myocardium as possible and to prevent further complications, hence the phrase "time is muscle".[75] Oxygen, aspirin, and nitroglycerin may be administered. Morphine was classically used if nitroglycerin was not effective; however, it may increase mortality in the setting of NSTEMI.[76] Reviews of high flow oxygen in myocardial infarction found increased mortality and infarct size, calling into question the recommendation about its routine use.[77][78] Other analgesics such as nitrous oxide are of unknown benefit.[7]

STEMI

Immediate

Percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner.[79] If PCI cannot be performed within 90 to 120 minutes then fibrinolysis, preferably within 30 minutes, is recommended.[80][81] If after fibrinolysis, significant cardiogenic shock, continued severe chest pain, or less than a 50% improvement in ST elevation after 90 minutes occurs, then rescue PCI is indicated emergently.[81][82] After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).[83]

Long term

Beta blockers are recommended in those without signs off heart failure or a heart block.[58] If used they should be started in the first 24 hours.[58]

Prognosis

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.[58]

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%.[84]

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.[84][85][86] Assessment of left ventricular ejection fraction may increase the predictive power.[87] Prognosis is worse if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs.[88] Morbidity and mortality from myocardial infarction has improved over the years due to better treatment.[89]

Complications

Main article: Myocardial infarction complications

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.

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;[11] 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.[11] Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year.[90] STEMI's occur about twice as often in men as women.[58]

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.[91] 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.[92] 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.[11]

Society and culture

In the United States, women who have had an MI are often treated less aggressively than men.[58]

Economics

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.[93]

Legal implications

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;[94] however, it may be a work-related injury if it results, for example, from unusual emotional stress or unusual exertion.[95] 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.[96]

Research

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 proceeding.[97]

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.[98]

References

  1. ↑ Kosuge, M; Kimura K, Ishikawa T et al. (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. doi:10.1253/circj.70.222. PMID 16501283. 
  2. ↑ 2.0 2.1 2.2 2.3 Valensi P, Lorgis L, Cottin Y (March 2011). "Prevalence, incidence, predictive factors and prognosis of silent myocardial infarction: a review of the literature". Arch Cardiovasc Dis 104 (3): 178–88. doi:10.1016/j.acvd.2010.11.013. PMID 21497307. 
  3. ↑ 3.0 3.1 3.2 3.3 3.4 Graham I, Atar D, Borch-Johnsen K, et al. (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. doi:10.1093/eurheartj/ehm316. PMID 17726041. 
  4. ↑ Devlin RJ, Henry JA (2008). "Clinical review: Major consequences of illicit drug consumption". Crit Care 12 (1): 202. doi:10.1186/cc6166. PMC 2374627. PMID 18279535. 
  5. ↑ Erhardt L, Herlitz J, Bossaert L, et al. (2002). "Task force on the management of chest pain" (PDF). Eur. Heart J. 23 (15): 1153–76. doi:10.1053/euhj.2002.3194. PMID 12206127. 
  6. ↑ Roe MT, Messenger JC, Weintraub WS, et al. (July 2010). "Treatments, trends, and outcomes of acute myocardial infarction and percutaneous coronary intervention". J. Am. Coll. Cardiol. 56 (4): 254–63. doi:10.1016/j.jacc.2010.05.008. PMID 20633817. 
  7. ↑ 7.0 7.1 O'Connor RE, Brady W, Brooks SC, et al. (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. doi:10.1161/CIRCULATIONAHA.110.971028. PMID 20956226. 
  8. ↑ 8.0 8.1 8.2 8.3 8.4 Van de Werf F, Bax J, Betriu A, et al. (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. doi:10.1093/eurheartj/ehn416. PMID 19004841. 
  9. ↑ Hamm CW, Bassand JP, Agewall S, et al. (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. doi:10.1093/eurheartj/ehr236. PMID 21873419. 
  10. ↑ "The top 10 causes of death". World Health Organization. Retrieved 13 August 2013. 
  11. ↑ 11.0 11.1 11.2 11.3 World Health Organization (2008). The Global Burden of Disease: 2004 Update. Geneva: World Health Organization. ISBN 92-4-156371-0. 
  12. ↑ National Heart, Lung and Blood Institute. Heart Attack Warning Signs. Retrieved November 22, 2006.
  13. ↑ 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. doi:10.1111/j.1365-2796.1990.tb00138.x. PMID 2313224. 
  14. ↑ Marcus GM, Cohen J, Varosy PD, et al. (2007). "The utility of gestures in patients with chest discomfort". Am. J. Med. 120 (1): 83–9. doi:10.1016/j.amjmed.2006.05.045. PMID 17208083. 
  15. ↑ Mallinson, T (2010). "Myocardial Infarction". Focus on First Aid (15): 15. Retrieved 2010-06-08. 
  16. ↑ Little RA, Frayn KN, Randall PE, et al. (1986). "Plasma catecholamines in the acute phase of the response to myocardial infarction". Arch Emerg Med 3 (1): 20–7. doi:10.1136/emj.3.1.20. PMC 1285314. PMID 3524599. 
  17. ↑ 17.0 17.1 Canto JG, Goldberg RJ, Hand MM, et al. (December 2007). "Symptom presentation of women with acute coronary syndromes: myth vs reality". Arch. Intern. Med. 167 (22): 2405–13. doi:10.1001/archinte.167.22.2405. PMID 18071161. 
  18. ↑ Brown, Anthony (2011). Emergency Medicine Diagnosis and Management 6th Edition. 
  19. ↑ 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. doi:10.1161/01.CIR.0000097116.29625.7C. PMID 14597589. 
  20. ↑ http://feministing.com/2012/02/23/for-women-heart-attacks-look-different-and-so-do-heart-health-outcomes/
  21. ↑ Kannel WB. (1986). "Silent myocardial ischemia and infarction: insights from the Framingham Study". Cardiol Clin 4 (4): 583–91. PMID 3779719. 
  22. ↑ 22.0 22.1 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. doi:10.1007/s00125-004-1344-4. PMID 14963648. 
  23. ↑ Rubin, Emanuel; Gorstein, Fred; Rubin, Raphael; Schwarting, Roland; Strayer, David (2001). Rubin's Pathology — Clinicopathological Foundations of Medicine. Maryland: Lippincott Williams & Wilkins. p. 549. ISBN 0-7817-4733-3. 
  24. ↑ Acute Coronary Syndrome. American Heart Association. Retrieved November 25, 2006.
  25. ↑ Boie ET (2005). "Initial evaluation of chest pain". Emerg. Med. Clin. North Am. 23 (4): 937–57. doi:10.1016/j.emc.2005.07.007. PMID 16199332. 
  26. ↑ Jensen G, Nyboe J, Appleyard M, Schnohr P. (1991). "Risk factors for acute myocardial infarction in Copenhagen, II: Smoking, alcohol intake, physical activity, obesity, oral contraception, diabetes, lipids, and blood pressure". Eur Heart J 12 (3): 298–308. PMID 2040311. 
  27. ↑ 27.0 27.1 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. PMID 2598948. 
  28. ↑ 28.0 28.1 28.2 Kivimäki, Mika; Nyberg, Solja T; Batty, G David et al (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. doi:10.1016/S0140-6736(12)60994-5. PMC 3486012. PMID 22981903. 
  29. ↑ Lee, I-Min; Shiroma, Eric J; Lobelo, Felipe et al (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. doi:10.1016/S0140-6736(12)61031-9. PMC 3645500. PMID 22818936. 
  30. ↑ Steptoe A, Kivimäki M (April 2012). "Stress and cardiovascular disease". Nature Reviews Cardiology 9 (6): 360–70. doi:10.1038/nrcardio.2012.45. PMID 22473079. 
  31. ↑ 31.0 31.1 31.2 Smith, Sidney (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. doi:10.1016/j.jacc.2006.04.026. PMID 16697342. 
  32. ↑ 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. doi:10.1001/jama.2012.126. PMID 22337682. 
  33. ↑ Buse JB, Ginsberg HN, Bakris GL, et al. (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. doi:10.1161/CIRCULATIONAHA.106.179294. PMID 17192512. 
  34. ↑ Yusuf S, Hawken S, Ounpuu S, Bautista L, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Onen CL, Lisheng L, Tanomsup S, Wangai P Jr, Razak F, Sharma AM, Anand SS; INTERHEART Study Investigators. (2005). "Obesity and the risk of myocardial infarction in 27,000 participants from 52 countries: a case-control study". Lancet 366 (9497): 1640–9. doi:10.1016/S0140-6736(05)67663-5. PMID 16271645. 
  35. ↑ Chatzidimitriou, D; Kirmizis, D; Gavriilaki, E; Chatzidimitriou, M; Malisiovas, N (2012 Oct). "Atherosclerosis and infection: is the jury still not in?". Future microbiology 7 (10): 1217–30. PMID 23030426. 
  36. ↑ Charakida, M; Tousoulis, D (2013). "Infections and atheromatous plaque: current therapeutic implications.". Current pharmaceutical design 19 (9): 1638–50. PMID 23016720. 
  37. ↑ 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. doi:10.1161/01.CIR.97.18.1837. PMID 9603539. 
  38. ↑ 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. doi:10.1016/S0010-7824(03)00073-8. PMID 12878281. 
  39. ↑ Muller JE, Stone PH, Turi ZG, et al. (1985). "Circadian variation in the frequency of onset of acute myocardial infarction". N. Engl. J. Med. 313 (21): 1315–22. doi:10.1056/NEJM198511213132103. PMID 2865677. 
  40. ↑ Beamer AD, Lee TH, Cook EF, et al. (1987). "Diagnostic implications for myocardial ischemia of the circadian variation of the onset of chest pain". Am. J. Cardiol. 60 (13): 998–1002. doi:10.1016/0002-9149(87)90340-7. PMID 3673917. 
  41. ↑ Cannon; McCabe, Carolyn H.; Stone, Peter H.; Schactman, Mark; Thompson, Bruce; Theroux, Pierre; Gibson, Robert S.; Feldman, Ted et al. (1997). "Circadian variation in the onset of unstable angina and non-Q-wave acute myocardial infarction (the TIMI III Registry and TIMI IIIB)". Am. J. Cardiol. 79 (3): 253–8. doi:10.1016/S0002-9149(97)00743-1. PMID 9036740. 
  42. ↑ 42.0 42.1 Moe KT, Wong P (March 2010). "Current trends in diagnostic biomarkers of acute coronary syndrome" (PDF). Ann. Acad. Med. Singap. 39 (3): 210–5. PMID 20372757. 
  43. ↑ 43.0 43.1 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. PMID 20387549. 
  44. ↑ 44.0 44.1 Dohi T, Daida H (April 2010). "[Change of concept and pathophysiology in acute coronary syndrome]". Nippon Rinsho (in Japanese) 68 (4): 592–6. PMID 20387546. 
  45. ↑ Woollard KJ, Geissmann F (February 2010). "Monocytes in atherosclerosis: subsets and functions". Nature Reviews Cardiology 7 (2): 77–86. doi:10.1038/nrcardio.2009.228. PMC 2813241. PMID 20065951. 
  46. ↑ Spaan J, Kolyva C, van den Wijngaard J, et al. (September 2008). "Coronary structure and perfusion in health and disease". Philosophical Transactions of the Royal Society A 366 (1878): 3137–53. doi:10.1098/rsta.2008.0075. PMID 18559321. 
  47. ↑ 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. doi:10.1136/jcp.55.11.801. PMC 1769793. PMID 12401816. 
  48. ↑ 48.0 48.1 48.2 48.3 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. doi:10.1016/j.ijcard.2005.01.068. PMID 16337036. 
  49. ↑ Pearson TA, Mensah GA, Alexander RW, Anderson JL, Cannon RO 3rd, Criqui M, Fadl YY, Fortmann SP, Hong Y, Myers GL, Rifai N, Smith SC Jr, Taubert K, Tracy RP, Vinicor F; Centers for Disease Control and Prevention; American Heart Association. (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. doi:10.1161/01.CIR.0000052939.59093.45. PMID 12551878. 
  50. ↑ 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. doi:10.1001/jama.291.2.210. PMID 14722147. 
  51. ↑ Detrano R, Guerci AD, Carr JJ, et al. (2008). "Coronary calcium as a predictor of coronary events in four racial or ethnic groups". N. Engl. J. Med. 358 (13): 1336–45. doi:10.1056/NEJMoa072100. PMID 18367736. 
  52. ↑ 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. doi:10.1016/j.jacc.2005.02.088. PMID 15992651. 
  53. ↑ 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. doi:10.1007/s10545-010-9235-y. PMID 21069462. 
  54. ↑ 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. doi:10.1097/MOH.0b013e3282c48bd8. PMID 17934354. 
  55. ↑ 55.0 55.1 Reznik, AG (2010). "[Morphology of acute myocardial infarction at prenecrotic stage]". Kardiologiia (in Russian) 50 (1): 4–8. PMID 20144151. 
  56. ↑ 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. doi:10.1016/S0735-1097(00)00804-4. PMID 10987628. 
  57. ↑ 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. doi:10.1161/01.CIR.59.3.607. PMID 761341. 
  58. ↑ 58.0 58.1 58.2 58.3 58.4 58.5 58.6 58.7 58.8 58.9 58.10 58.11 O'Gara, PT; Kushner, FG; Ascheim, DD; Casey DE, Jr; 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; American College of Cardiology Foundation/American Heart Association Task Force on Practice, Guidelines (2013 Jan 29). "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. PMID 23247304. 
  59. ↑ Thygesen K, Alpert JS, White HD (October 2007). "Universal definition of myocardial infarction". Eur. Heart J. 28 (20): 2525–38. doi:10.1093/eurheartj/ehm355. PMID 17951287. 
  60. ↑ 60.0 60.1 Myocardial infarction~workup at eMedicine
  61. ↑ Skoufis E, McGhie AI (1998). "Radionuclide techniques for the assessment of myocardial viability". Tex Heart Inst J 25 (4): 272–9. PMC 325572. PMID 9885104. 
  62. ↑ 62.0 62.1 62.2 American Society of Nuclear Cardiology. "Five Things Physicians and Patients Should Question". Choosing Wisely: an initiative of the ABIM Foundation (American Society of Nuclear Cardiology). Retrieved August 17, 2012 , which cites
    • Hendel, R. C.; Berman, D. S.; Di Carli, M. F.; Heidenreich, P. A.; Henkin, R. E.; Pellikka, P. A.; Pohost, G. M.; Williams, K. A.; American College of Cardiology Foundation Appropriate Use Criteria Task Force; American Society of Nuclear Cardiology; American College Of, R.; American Heart, A.; American Society of Echocardiology; Society of Cardiovascular Computed Tomography; Society for Cardiovascular Magnetic Resonance; Society Of Nuclear, M. (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. doi:10.1016/j.jacc.2009.02.013. PMID 19497454. 
    • Taylor, A. J.; Cerqueira, M.; Hodgson, J. M. .; Mark, D.; Min, J.; O'Gara, P.; Rubin, G. D.; American College of Cardiology Foundation Appropriate Use Criteria Task Force; Society of Cardiovascular Computed Tomography; American College Of, R.; American Heart, A.; American Society of Echocardiography; American Society of Nuclear Cardiology; North American Society for Cardiovascular Imaging; Society for Cardiovascular Angiography Interventions; Society for Cardiovascular Magnetic Resonance; Kramer, C. M.; Berman; Brown; Chaudhry, F. A.; Cury, R. C.; Desai, M. Y.; Einstein, A. J.; Gomes, A. S.; Harrington, R.; Hoffmann, U.; Khare, R.; Lesser; McGann; Rosenberg, A. (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. doi:10.1016/j.jacc.2010.07.005. PMID 21087721. 
    • Anderson, J. L.; Adams, C. D.; Antman, E. M.; Bridges, C. R.; Califf, R. M.; Casey, D. E.; Chavey, W. E.; Fesmire, F. M.; Hochman, J. S.; Levin, T. N.; Lincoff, A. M.; Peterson, E. D.; Theroux, P.; Wenger, N. K.; Wright, R. S. (2007). "ACC/AHA 2007 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines for the Management of Patients with Unstable Angina/Non-ST-Elevation Myocardial Infarction): Developed in Collaboration with the American College of Emergency Physicians, the Society for Cardiovascular Angiography and Interventions, and the Society of Thoracic Surgeons: Endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation and the Society for Academic Emergency Medicine". Circulation 116 (7): 803. doi:10.1161/CIRCULATIONAHA.107.185752. 
  63. ↑ Rossi, S., ed. (2006). Australian Medicines Handbook 2006. Adelaide: Australian Medicines Handbook. ISBN 0-9757919-2-3. 
  64. ↑ Smith A, Aylward P, Campbell T, et al. (2003). Therapeutic Guidelines: Cardiovascular (4th ed.). North Melbourne: Therapeutic Guidelines. ISSN 1327-9513. 
  65. ↑ Peters RJ, Mehta SR, Fox KA, Zhao F, Lewis BS, Kopecky SL, Diaz R, Commerford PJ, Valentin V, Yusuf S; Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) Trial Investigators. (2003). "Effects of aspirin dose when used alone or in combination with clopidogrel in patients with acute coronary syndromes: observations from the Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) study". Circulation 108 (14): 1682–7. doi:10.1161/01.CIR.0000091201.39590.CB. PMID 14504182. 
  66. ↑ Fonarow, GC (2006 Winter). "Beta-blockers for the post-myocardial infarction patient: current clinical evidence and practical considerations.". Reviews in cardiovascular medicine 7 (1): 1–9. PMID 16534490. 
  67. ↑ Dargie HJ. (2001). "Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomised trial". Lancet 357 (9266): 1385–90. doi:10.1016/S0140-6736(00)04560-8. PMID 11356434. 
  68. ↑ Pfeffer MA, Braunwald E, Moye LA, Basta L, Brown EJ Jr, Cuddy TE, Davis BR, Geltman EM, Goldman S, Flaker GC, et al. (1992). "Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. Results of the survival and ventricular enlargement trial. The SAVE Investigators". N Engl J Med. 327 (10): 669–77. doi:10.1056/NEJM199209033271001. PMID 1386652. 
  69. ↑ Taylor, F; Huffman, MD; Macedo, AF; Moore, TH; Burke, M; Davey Smith, G; Ward, K; Ebrahim, S (2013 Jan 31). "Statins for the primary prevention of cardiovascular disease.". The Cochrane database of systematic reviews 1: CD004816. PMID 23440795. 
  70. ↑ Ray KK, Cannon CP (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. doi:10.1016/j.jacc.2005.05.086. PMID 16226165. 
  71. ↑ Keating G, Plosker G (2004). "Eplerenone: a review of its use in left ventricular systolic dysfunction and heart failure after acute myocardial infarction". Drugs 64 (23): 2689–707. doi:10.1157/13089615. PMID 15537370. 
  72. ↑ Mozaffarian D, Micha R, Wallace S (2010). "Effects on Coronary Heart Disease of Increasing Polyunsaturated Fat in Place of Saturated Fat: A Systematic Review and Meta-Analysis of Randomized Controlled Trials". In Katan, Martijn B. PLoS Med. 7 (3): e1000252. doi:10.1371/journal.pmed.1000252. PMC 2843598. PMID 20351774. 
  73. ↑ 73.0 73.1 Jenkins, DJ; Josse, AR; Dorian, P; Burr, ML; LaBelle Trangmar, R; Kendall, CW; Cunnane, SC (June 2008). "Heterogeneity in randomized controlled trials of long chain (fish) omega-3 fatty acids in restenosis, secondary prevention and ventricular arrhythmias". Journal of the American College of Nutrition 27 (3): 367–78. doi:10.1080/07315724.2008.10719713. PMID 18838524. 
  74. ↑ Magee KD, Campbell SG, Moher D, Rowe BH (2008). "Heparin versus placebo for acute coronary syndromes". In Magee, Kirk. Cochrane Database Syst Rev (2): CD003462. doi:10.1002/14651858.CD003462.pub2. PMID 18425889. 
  75. ↑ 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. ISBN 978-0-7637-7828-6. 
  76. ↑ Meine TJ, Roe MT, Chen AY, et al. (2005). "Association of intravenous morphine use and outcomes in acute coronary syndromes: results from the CRUSADE Quality Improvement Initiative". Am Heart J 149 (6): 1043–9. doi:10.1016/j.ahj.2005.02.010. PMID 15976786. 
  77. ↑ 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. doi:10.1136/hrt.2008.148742. PMID 18708420. 
  78. ↑ Cabello, JB.; Burls, A.; Emparanza, JI.; Bayliss, S.; Quinn, T. (2013). "Oxygen therapy for acute myocardial infarction". In Cabello, Juan B. Cochrane Database Syst Rev 8: CD007160. doi:10.1002/14651858.CD007160.pub3. PMID 23963794. 
  79. ↑ Bates, ER; Menees, DS (Oct 2012). "Acute ST-elevation myocardial infarction". Current Opinion in Critical Care. 5 18 (5): 417–23. doi:10.1097/MCC.0b013e328357f07b. PMID 22889871. 
  80. ↑ Lassen, JF; Bøtker, HE; Terkelsen, CJ (Jan 2013). "Timely and optimal treatment of patients with STEMI". Nature Reviews Cardiology. 1 10 (1): 41–8. doi:10.1038/nrcardio.2012.156. PMID 23165072. 
  81. ↑ 81.0 81.1 Wang, edited by Reza Ardehali, Marco Perez, Paul (2011). A practical approach to cardiovascular medicine. Chichester, West Sussex, UK: Wiley-Blackwell. p. 57. ISBN 9781444393873. 
  82. ↑ Jindal, editor-in-chief SK (2011). Textbook of pulmonary and critical care medicine. New Delhi: Jaypee Brothers Medical Publishers. p. 1758. ISBN 9789350250730. 
  83. ↑ 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. doi:10.1001/jama.2013.7086. PMID 23839753. 
  84. ↑ 84.0 84.1 López de Sá E, López-Sendón J, Anguera I, Bethencourt A, Bosch X (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. doi:10.1097/00005792-200211000-00004. PMID 12441900. 
  85. ↑ Fox KA, Dabbous OH, Goldberg RJ, et al. (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. doi:10.1136/bmj.38985.646481.55. PMC 1661748. PMID 17032691. 
  86. ↑ Weir RA, McMurray JJ, Velazquez EJ. (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. doi:10.1016/j.amjcard.2006.03.005. PMID 16698331. 
  87. ↑ Bosch X, Theroux P. (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. doi:10.1016/j.ahj.2004.09.027. PMID 16086920. 
  88. ↑ Becker RC, Gore JM, Lambrew C, Weaver WD, Rubison RM, French WJ, Tiefenbrunn AJ, Bowlby LJ, Rogers WJ. (1996). "A composite view of cardiac rupture in the United States National Registry of Myocardial Infarction". J Am Coll Cardiol 27 (6): 1321–6. doi:10.1016/0735-1097(96)00008-3. PMID 8626938. 
  89. ↑ Liew R, Sulfi S, Ranjadayalan K, Cooper J, Timmis AD. (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. doi:10.1136/hrt.2005.078634. PMC 1861115. PMID 16387823. 
  90. ↑ White HD, Chew DP (August 2008). "Acute myocardial infarction". Lancet 372 (9638): 570–84. doi:10.1016/S0140-6736(08)61237-4. PMID 18707987. 
  91. ↑ Roger VL, Go AS, Lloyd-Jones DM, et al. (January 2012). "Executive summary: heart disease and stroke statistics--2012 update: a report from the American Heart Association". Circulation 125 (1): 188–97. doi:10.1161/CIR.0b013e3182456d46. PMID 22215894. 
  92. ↑ Gupta R, Joshi P, Mohan V, Reddy KS, Yusuf S (January 2008). "Epidemiology and causation of coronary heart disease and stroke in India". Heart 94 (1): 16–26. doi:10.1136/hrt.2007.132951. PMID 18083949. 
  93. ↑ 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.
  94. ↑ Workers' Compensation FAQ. Prairie View A&M University. Retrieved November 22, 2006.
  95. ↑ SIGNIFICANT DECISIONS Subject Index. Board of Industrial Insurance Appeals. Retrieved November 22, 2006.
  96. ↑ "Classification of Drivers' Licenses Regulations". Nova Scotia Registry of Regulations. May 24, 2000. Retrieved April 22, 2007. 
  97. ↑ Schachinger V, Erbs S, Elsasser A, Haberbosch W, Hambrecht R, Holschermann H, Yu J, Corti R, Mathey DG, Hamm CW, Suselbeck T, Assmus B, Tonn T, Dimmeler S, Zeiher AM; REPAIR-AMI Investigators (2006). "Intracoronary bone marrow-derived progenitor cells in acute myocardial infarction". N Engl J Med 2006 355 (12): 1210–21. doi:10.1056/NEJMoa060186. PMID 16990384. 
  98. ↑ Christman KL, Lee RJ (September 2006). "Biomaterials for the treatment of myocardial infarction". J. Am. Coll. Cardiol. 48 (5): 907–13. doi:10.1016/j.jacc.2006.06.005. PMID 16949479. 

External links

Find more about Myocardial infarction at Wikipedia's sister projects
Definitions and translations from Wiktionary
Media from Commons
Quotations from Wikiquote
Source texts from Wikisource
Textbooks from Wikibooks
Learning resources from Wikiversity
Decreases
general:
regional:
Increases
general
regional
general
regional
Other

This article is issued from Wikipedia. The text is available under the Creative Commons Attribution/Share Alike; additional terms may apply for the media files.