Myocardial infarction

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Myocardial infarction
Classification and external resources
AMI scheme.png
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[edit]

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 upper abdomen,[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 blood flow to the brain 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[edit]

Many of the risk factors for myocardial infarction are modifiable and thus many cases may be preventable.

Lifestyle[edit]

Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease.[26] Lack of exercise has been linked to 7-12% of cases.[26][27] Job stress appears to play a minor role, accounting for about 3% of cases.[26] Chronic high stress levels may cause some cases.[28]

Tobacco smoking, including secondhand smoke[29] Short-term exposure to air pollution, including carbon monoxide, nitrogen dioxide, and sulfur dioxide, but not ozone.[30] Lack of physical activity,[3] 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.[31] Alcohol — prolonged exposure to high quantities of alcohol can increase the risk of heart attack.

There is little evidence that dietary saturated fat or polyunsaturated fat intake affects risk.[32] Trans fats do appear to increase risk.[32]

Disease[edit]

Diabetes mellitus (type 1 or 2),[33] high blood pressure,[29] dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides[29] 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.[35] As of 2013, there is no evidence of benefit from antibiotics or vaccination, however, calling the association into question.[35][36]

Other[edit]

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]

Old age increases risk of a heart attack.[3]

Pathophysiology[edit]

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 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).[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 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.[8] Inflammation is known to be an important step in the process of atherosclerotic 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 blood levels of the amino acid homocysteine) in homocysteinuria is associated with premature atherosclerosis;[53] whether elevated homocysteine in the normal range is causal is controversial.[54]

Pathological types[edit]

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[edit]

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 on anatomopathological findings.

Classification[edit]

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 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.[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 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 5 – MI associated with CABG

Electrocardiogram[edit]

For a person to qualify as having an STEMI, the ECG must show new ST elevation in two or more adjacent ECG 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 that is believed to be new used to be considered the same as ST elevation; however, this is no longer the case.[58] In early STEMIs there may just be peaked T wave with ST elevation developing later.[58]

Cardiac biomarkers[edit]

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

Imaging[edit]

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 stress echocardiography can confirm a diagnosis when a patient's history, physical exam, ECG, and cardiac biomarkers suggest the likelihood of a problem.[62]

Prevention[edit]

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 strokes. Unless contraindicated, such medications often include the following:[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 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.[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 and may actually 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[edit]

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 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[edit]

Immediate[edit]

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[edit]

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

Prognosis[edit]

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[edit]

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[edit]

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] STEMIs 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[edit]

In the United States, women who have had an MI are often treated with fewer medical interventions than men.[58]

Economics[edit]

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[edit]

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[edit]

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.[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]

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