Myocardial infarction(Redirected from Heart attack)
Myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow stops to a part of the heart causing damage to the heart muscle. The most common symptom is chest pain or discomfort which may travel into the shoulder, arm, back, neck, or jaw. Often it is in the center or left side of the chest and lasts for more than a few minutes. The discomfort may occasionally feel like heartburn. Other symptoms may include shortness of breath, nausea, feeling faint, a cold sweat, or feeling tired. About 30% of people have atypical symptoms. Women more often have atypical symptoms than men. Among those over 75 years old, about 5% have had an MI with little or no history of symptoms. An MI may cause heart failure, an irregular heartbeat, cardiogenic shock, or cardiac arrest.
|Synonyms||Acute myocardial infarction (AMI), heart attack|
|Diagram showing the blood supply to the heart by the two major blood vessels, the left and right coronary arteries (labelled LCA and RCA). A myocardial infarction (2) has occurred with blockage of a branch of the left coronary artery (1).|
|Symptoms||Chest pain, shortness of breath, nausea, feeling faint, cold sweat, feeling tired|
|Complications||Heart failure, irregular heartbeat, cardiogenic shock, cardiac arrest|
|Causes||Usually coronary artery disease|
|Risk factors||High blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol|
|Diagnostic method||Electrocardiograms (ECGs), blood tests, coronary angiography|
|Treatment||Percutaneous coronary intervention, thrombolysis|
|Medication||Aspirin, nitroglycerin, heparin|
|Prognosis||STEMI 10% risk of death (developed world)|
|Frequency||15.9 million (2015)|
Most MIs occur due to coronary artery disease. Risk factors include high blood pressure, smoking, diabetes, lack of exercise, obesity, high blood cholesterol, poor diet, and excessive alcohol intake, among others. The mechanism of an MI often involves the complete blockage of a coronary artery caused by a rupture of an atherosclerotic plaque. MIs are less commonly caused by coronary artery spasms, which may be due to cocaine, significant emotional stress, and extreme cold, among others. A number of tests are useful to help with diagnosis, including electrocardiograms (ECGs), blood tests, and coronary angiography. An ECG, which is a recording of the heart's electrical activity, may confirm an ST elevation MI (STEMI) if a change known as ST elevation is present. Commonly used blood tests include troponin and less often creatine kinase MB.
Treatment of an MI is time critical. Aspirin is an appropriate immediate treatment for a suspected MI. Nitroglycerin or opioids may be used to help with chest pain; however, they do not improve overall outcomes. Supplemental oxygen should be used in those with low oxygen levels or shortness of breath. In ST elevation MIs treatments which attempt to restore blood flow to the heart are typically recommended and include percutaneous coronary intervention (PCI), where the arteries are pushed open and may be stented, or thrombolysis, where the blockage is removed using medications. People who have a non-ST elevation myocardial infarction (NSTEMI) are often managed with the blood thinner heparin, with the additional use of PCI in those at high risk. In people with blockages of multiple coronary arteries and diabetes, coronary artery bypass surgery (CABG) may be recommended rather than angioplasty. After an MI, lifestyle modifications, along with long term treatment with aspirin, beta blockers, and statins, are typically recommended.
Worldwide, about 15.9 million myocardial infarctions occurred in 2015. More than 3 million people had an ST elevation MI and more than 4 million had an NSTEMI. STEMIs occur about twice as often in men as women. About one million people have an MI each year in the United States. In the developed world the risk of death in those who have had an STEMI is about 10%. Rates of MI for a given age have decreased globally between 1990 and 2010. In 2011, AMI was one of the top five most expensive conditions during inpatient hospitalizations in the US, with a cost of about $11.5 billion for 612,000 hospital stays.
Myocardial infarction refers to tissue death (infarction) of the heart muscle (myocardium). It is a type of acute coronary syndrome, which describes a sudden or short-term change in symptoms related to blood flow to the heart. Unlike other causes of acute coronary syndromes, such as unstable angina, a myocardial infarction occurs when there is cell death, as measured by a blood test of cardiac enzymes such as troponin or CK-MB. When there is evidence of an MI, it may be classified as an ST elevation myocardial infarction (STEMI) or Non-ST elevation myocardial infarction (NSTEMI) based on the results of an ECG.
The phrase "heart attack" is often used non-specifically to refer to a myocardial infarction and to sudden cardiac death. An MI is different from—but can cause—cardiac arrest, where the heart is not contracting at all or so poorly that all vital organs cease to function. 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.
Signs and symptomsEdit
Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and upper abdomen. The pain most suggestive of an acute MI, with the highest likelihood ratio, is pain radiating to the right arm and shoulder. The pain associated with MI is usually diffuse, does not change with position, and lasts for more than 20 minutes. Levine's sign, in which a person localizes the chest pain by clenching one or both fists over their sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed it had a poor positive predictive value.
Chest pain may be accompanied by sweating, nausea or vomiting, and fainting, and these symptoms may also occur without any pain at all. In women, the most common symptoms of myocardial infarction include shortness of breath, weakness, and fatigue. Shortness of breath is a common, and sometimes the only symptoms, that occurs the damage to the heart limits the output of the left ventricle, wither breathlessness arising either from subsequent hypoxemia or pulmonary edema. Other less common symptoms include weakness, light-headedness, palpitations, and abnormalities in heart rate or blood pressure. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system, which occurs in response to pain and the blood flow abnormalities that result from dysfunction of the heart muscle. Loss of consciousness due to inadequate blood flow to the brain and cardiogenic shock, and sudden death, frequently due to the development of ventricular fibrillation, can occur in myocardial infarctions. Atypical symptoms, such as cardiac arrest and palpitations, occur more frequently in women, the elderly, those with diabetes, in people who have just had surgery, and in critically ill patients.
"Silent" myocardial infarctions can happen without any symptoms at all. These cases can be discovered later on electrocardiograms, using blood enzyme tests, or at autopsy after a person has died. Such silent myocardial infarctions represent between 22 and 64% of all infarctions, and are more common in the elderly, in those with diabetes mellitus and after heart transplantation. In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms. In heart transplantation, the donor heart is not fully innervated by the nervous system of the recipient.
The most prominent risk factors for myocardial infarction are older age, actively smoking, high blood pressure, diabetes mellitus, and total cholesterol and high-density lipoprotein levels. Many risk factors of MI are shared with coronary artery disease, the primary cause of myocardial infarction, with other risk factors including male sex, low levels of physical activity, a past family history, obesity, and alcohol use. Risk factors for myocardial disease are often included in risk factor stratification scores, such as the Framingham risk score.
Many risk factors for myocardial infarction are potentially modifiable, with the most important being tobacco smoking (including secondhand smoke). Smoking appears to be the cause of about 36% and obesity the cause of 20% of coronary artery disease. Lack of physical activity 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.
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.
The evidence for saturated fat is unclear. Some state there is evidence of benefit from reducing saturated fat, specifically a benefit from eating polyunsaturated fat instead of saturated fat. While others state there is little evidence that reducing dietary saturated fat or increasing polyunsaturated fat intake affects heart attack risk. Dietary cholesterol does not appear to have a significant effect on blood cholesterol and thus recommendations about its consumption may not be needed. Trans fats do appear to increase risk. Acute and prolonged intake of high quantities of alcoholic drinks (3–4 or more) increase the risk of a heart attack.
Family history of ischemic heart disease or MI, particularly if one has a first-degree relative (father, brother, mother, sister) who had a 'premature' myocardial infarction (defined as occurring at or younger than age 55 years (men) or 65 (women)).
Genome-wide association studies have found 27 genetic variants that are associated with an increased risk of myocardial infarction. The 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, SNF8, LDLR, SLC5A3, MRPS6, KCNE2.
Women who use combined oral contraceptive pills have a modestly increased risk of myocardial infarction, especially in the presence of other risk factors. The use of non-steroidal anti inflammatory drugs (NSAIDs), even for as short as a week, increases risk.
Heart attacks appear to occur more commonly in the morning hours, especially between 6AM and noon. Evidence suggests that heart attacks are at least three times more likely to occur in the morning than in the late evening. Old age increases risk of a heart attack.
Short-term exposure to air pollution such as carbon monoxide, nitrogen dioxide, and sulfur dioxide (but not ozone) have been associated with MI. Other factors that increase the risk of MI and are associated with worse outcomes after an MI include lack of physical activity and psychosocial factors including low socioeconomic status, social isolation, and negative emotions. Shift work is also associated with a higher risk of MI.
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. Myocardial infarction can also occur as a late consequence of Kawasaki disease.
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 most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle. The gradual buildup of cholesterol and fibrous tissue in plaques in the wall of the coronary arteries or other arteries, typically over decades, is termed atherosclerosis. Plaques can become unstable, rupture, and additionally promote the formation of a blood clot that blocks the artery; this can occur in minutes. Blockage of an artery can lead to tissue death (necrosis) in tissue being supplied by that artery. Atherosclerotic plaques are often present for decades before they result in symptoms.
Atherosclerosis is characterised by progressive inflammation of the walls of the arteries. Inflammatory cells, particularly macrophages, move into affected arterial walls. Over time, they become laden with cholesterol products, particularly LDL, and become foam cells. A cholesterol core forms as foam cells die. In response to growth factors secreted by macrophages, smooth muscle and other cells move into the plqaue and act to stabilise it. A stable plaque may have a thick fibrous cap with calcification. If there is ongoing inflammation, the cap may be thin or ulcerate. Exposed to the pressure associated with blood flow, plaques, especially those with a thin lining, may rupture and trigger the formation of a thrombus.
Atherosclerotic disease is not the only cause of myocardial infarction, and it may exacerbate or contribute to other causes. A heart with a limited blood supply with increased oxygen demands on the heart (such as in fever, tachycardia, hyperthyroidism, anaemia and hypotension). Damage or failure of procedures such as percutaneous coronary intervention or coronary artery bypass grafts may cause a myocardial infarction. Spasm of coronary arteries, such as Prinzmetal's angina may cause blockage.
If impaired blood flow to the heart lasts long enough, it triggers a process called the ischemic cascade; the heart cells in the territory of the blocked coronary artery die (chiefly through necrosis) and do not grow back. A collagen scar forms in their place. When an artery is blocked, cells lack oxygen, needed to produce ATP in mitochondria. ATP is required for the maintenance of electrolyte balance, particularly through the Na/K ATPase. This leads to an ischaemic cascade of intracellular changes, necrosis and apoptosis of affected cells. Cells in the area with the worst blood supply, that just below the inner surface of the heart (endocardium), are most susceptible to damage. Ischaemia first affects this region, the subendocardial region and, if severe enough, progresses to become a full-thickness transmural infarct. The initial "wave" of infarction can take place over 3-4 hours. These changes are seen on gross pathology and cannot be predicted by the presence of absence of Q waves on an ECG. The position, size and extent of an infarct depends on the affected artery, totality of the blockage, duration of the blockage, the presence of collateral vessels, oxygen demand, and success of interventional procedures.
Myocardial scarring also puts the person at risk for potentially life-threatening abnormal heart rhythms (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, an extremely fast and chaotic heart rhythm that is the leading cause of sudden cardiac death. Another life-threatening arrhythmia is ventricular tachycardia (VT), which can cause sudden cardiac death. 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.
- Symptoms relating to ischaemia
- Changes on an electrocardiogram (ECG), such as ST segment changes, new left bundle branch block, or Q waves
- Changes in the motion of the heart wall on imaging
- Demonstration of a thrombus on angiogram or at autopsy.
Myocardial infarctions are generally clinically classified into ST elevation MI (STEMI) and non-ST elevation MI (NSTEMI). These are based on changes to an ECG. STEMIs make up about 25 - 40% of myocardial infarctions. A more explicit classification system, based on international consensus in 2012, also exists. This classifies myocardial infarctions into five types:
- Spontaneous MI related to plaque erosion and/or rupture, fissuring, or dissection
- MI related to ischaemia, such as from increased oxygen demand or decreased supply, e.g. coronary artery spasm, coronary embolism, anemia, arrhythmias, hypertension, or hypotension
- Sudden unexpected cardiac death, including cardiac arrest, where symptoms may suggest MI, an ECG may be taken with suggestive changes, or a thrombus is found a coronary artery by angiography and/or at autopsy, but where blood samples could not be obtained, or at a time before the appearance of cardiac biomarkers in the blood
- Associated with coronary angioplasty or stents
- Associated with percutaneous coronary intervention (PCI)
- Associated with stent thrombosis as documented by angiography or at autopsy
- Associated with CABG
There are a number of different biomarkers used to determine the presence of cardiac muscle damage. Troponins, measured through a blood test, are considered to be the best, and are preferred because they have greater sensitivity and specificity for measuring injury to the heart muscle than other tests. A rise in troponin occurs within 2–3 hours of injury to the heart muscle, and peaks within 1–2 days. The gross value of the troponin, as well as a change over time, are useful in measuring and diagnosing or excluding myocardial infarctions, and the diagnostic accuracy of troponin testing is improving over time. One high-sensitivity cardiac troponin is able to rule out a heart attack as long as the ECG is normal.
Other tests, such as CK-MB or myoglobin, are discouraged. CK-MB is not as specific as troponins for acute myocardial injury, and may be elevated with past cardiac surgery, inflammation and electrical cardioversion; it rises within 4–8 hours and returns to normal within 2–3 days. Copeptin may be useful to rule out MI rapidly when used along with troponin.
Electrocardiograms (ECGs) are a series of leads placed on a person's chest that measure electrical activity associated with contraction of heart muscle. The taking of an ECG is an important part in the workup of an AMI, and ECGs are often not just taken once, but may be repeated over minutes to hours, or in response to changes in signs or symptoms.
ECG readouts product a waveform with different labelled features. In addition to a rise in biomarkers, a rise in the ST segment, changes in the shape or flipping of T waves, new Q waves, or a new left bundle branch block can be used to diagnose an AMI. In addition, ST elevation can be used to diagnose an ST segment myocardial infarction (STEMI). A rise must be new, in two adjacent adjacent ECG leads, greater than 2 mm (0.2 mV) for males and greater than 1.5 mm (0.15 mV) in females in all leads except for V2 and V3, where it must be greater than 1 mm (0.1 mV). ST elevation is associated with infarction, and may be preceded by changes indicating ischaemia, such as ST depression or inversion of the T waves. Abnormalities can help localise the location of an infarct, based on the leads that are affected by changes. Early STEMIs may be preceded by peaked T waves. Other ECG abnormalities relating to complications of acute myocardial infarctions may also be evident, such as atrial fibrillation, ventricular fibrillation.
Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial infarction. Tests such as Chest X-rays can be used to explore and exclude alternate causes of a person's symptoms. Tests such as stress echocardiography and myocardial perfusion imaging can confirm a diagnosis when a patient's history, physical examination (including cardiac examination) ECG, and cardiac biomarkers suggest the likelihood of a problem.
Echocardiography, an ultrasound scan of the heart, is able to visualise the heart, its size, shape, and any abnormal motion of the heart walls as they beat that may indicate a myocardial infarction. The flow of blood can be imaged, and contrast dyes may be given to improve image. Other scans using radioactive contrast include SPECT CT-scans using thallium, sestamibi (MIBI scans) or tetrofosmin; or a PET scan using Fludeoxyglucose or rubidium-82. These nuclear medicine scans can visualise the perfusion of heart muscle. SPECT may also be used to determine viability of tissue, and whether areas of ischaemia are inducible.
Medical societies and professional guidelines recommend that the physician confirm a person is at high risk for myocardial infarction before conducting imaging tests to make a diagnosis, as such tests are unlikely to change management and result in increased costs. Patients who have a normal ECG and who are able to exercise, for example, do not merit routine imaging.
In addition to myocardial, the differential diagnosis for chest pain includes angina, insufficient blood supply (ischemia) to the heart muscles without evidence of cell death, gastroesophageal reflux, and other causes such as pulmonary embolism. Rarer severe differential diagnosis includes aortic dissection, esophageal rupture, tension pneumothorax, pericardial effusion causing cardiac tamponade, and Tietze's syndrome. The chest pain in an MI may mimic heartburn.
A myocardial infarction requires immediate medical attention. Treatment aims to preserve as much heart muscle as possible, and to prevent further complications. Treatment depends on whether the myocardial infarction is a STEMI or NSTEMI, and begins with risk factor stratification using a scoring system such as the thrombosis in myocardial ischaemia (TIMI) or GRACE scores. Aspirin, an anti-platelet anticoagulant, is given with the goal of reducing the clot size and reduce further clotting in the affected artery.
The pain associated with myocardial infarction is treated with nitroglycerin and morphine. Nitroglycerin (administered under the tongue or intravenously) may be administered to improve the blood supply to the heart, and decreasing the work the heart must do by decreasing the amount of blood per heartbeat. It is an important part of therapy for its pain relief, despite there being no benefit to overall mortality. Morphine may also be used, and is particularly effective for the pain associated with STEMI. Pain that responds to nitroglycerin does not indicate the presence or absence of a myocardial infarction.
In the past, high flow oxygen was recommended for everyone with a possible myocardial infarction. More recently, no evidence was found for routine use with potential of harm. Therefore, oxygen is currently only recommended if oxygen levels are found to be low or if someone is in respiratory distress.
Treatment of a NSTEMI involves medications to dissolve blood clots and reduce enlargement, medications to reduce ischaemia, surgical intervention in high-risk patients, and risk factor modification with the aim of preventing future events. In addition to nitroglycerin, aspirin is a mainstay of treatment. P2Y12 inhibitors such as clopidogrel, prasugrel and ticagrelor are given concurrently in those without a high risk of bleeding, and are recommended for 12 months following NSTEMI in Europe.
Depending on whether early PCI is planned, a factor Xa inhibitor or a potentiator of antithrombin (fondaparinux or low molecular weight heparin respectively) may be added. In very high-risk scenarios, inhibitors of the platelet glycoprotein αIIbβ3a receptor such as eptifibatide or tirofiban may be used.
A 2014 review of P2Y12 inhibitors such as clopidogrel found they do not change the risk of death when given to people with a suspected NSTEMI prior to PCI. They do however increase the risk of bleeding and decrease the risk of further cardiovascular problems. The authors thus concluded that their routine use prior to PCI is of questionable value.
The main treatment for myocardial infarctions with ECG evidence of ST elevation (STEMI) include thrombolysis and percutaneous coronary intervention. Primary percutaneous coronary intervention (PCI) is the treatment of choice for STEMI if it can be performed in a timely manner, ideally within 90–120 minutes of contact with a medical provider. PCI involves small probes, inserted through peripheral blood vessels such as the femoral artery into the blood vessels of the heart. The probes are then used to identify and clear blockages using small balloons, which are dragged through the blocked segment, dragging away the clot, or the insertion of stents. Coronary artery bypass grafting is only considered when the affected area of heart muscle large, and PCI is unsuitable, for example with difficult cardiac anatomy.
If PCI cannot be performed within 90 to 120 minutes then thrombolysis, preferably within 30 minutes of arrival to hospital, is recommended. If a person has had symptoms for 12 to 24 hours evidence for effectiveness of thrombolysis is less and if they have had symptoms for more than 24 hours it is not recommended. Thrombolysis involves the administration of medication that activates the enzymes that normally dissolve blood clots. These medications include tissue plasminogen activator, reteplase, streptokinase, and tenecteplase. Thrombolysis is not recommended in a number of situations, particularly when associated with a high risk of bleeding, past strokes or bleeds into the brain, severe hypertension, and active bleeding. Situations in which thrombolysis may be considered, but with caution, include recent surgery, use of anticoagulants, pregnancy, and proclivity to bleeding. Major risks of thrombolysis are major bleeding and intracranial bleeding. Pre-hospital thrombolysis reduces time to thrombolytic treatment, based on studies conducted in higher income countries, however it is unclear whether this has an impact on mortality rates.
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 the hospital. The program may include lifestyle advice, exercise, social support, as well as recommendations about driving, flying, sport participation, stress management, and sexual intercourse.
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. After PCI, people are generally placed on dual antiplatelet therapy for at least a year (which is generally aspirin and clopidogrel).
Those who have had cardiac arrest may benefit from targeted temperature management with evaluation for implementation of hypothermia protocols. Furthermore, those with cardiac arrest, and ST elevation at any time, should usually have angiography.
Myocardial infarction and other related cardiovascular diseases can be prevented to a large extent by a number of lifestyle changes and medical treatments.
Recommendations include increasing the intake of wholegrain starch, reducing sugar intake (particularly of refined sugar), consuming five portions of fruit and vegetables daily, consuming two or more portions of fish per week, and consuming 4–5 portions of unsalted nuts, seeds, or legumes per week. The dietary pattern with the greatest support is the Mediterranean diet. Vitamins and mineral supplements are of no proven benefit, and neither are plant stanols or sterols.
There is some controversy surrounding the effect of dietary fat on the development of cardiovascular disease. People are often 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 of 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 may decrease coronary heart disease. Olive oil, rapeseed oil and related products are to be used instead of saturated fat.
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, non drinking or drinking alcohol within the recommended limits, and quitting smoking are measures that also appear to reduce the risk of cardiovascular disease.
On a population level, public health measures may be used to reduce unhealthy diets (excessive salt, saturated fat and trans fat) including food labeling and marketing requirements as well as requirements for catering and restaurants, and stimulating physical activity. This may be part of regional cardiovascular disease prevention programs, or through the health impact assessment of regional and local plans and policies.
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.
A number of lifestyle recommendations are advised 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. Exercise is both safe and effective even if people have had stents or heart failure.
- Aspirin as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT), is continued for up to twelve months, followed by aspirin 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 is recommended to be started within 24 hours, provided there is no acute heart failure or heart block. The dose should be increased to the highest tolerated. Contrary to what was long believed, the use of beta blockers does not appear to affect the risk of death, possibly because other treatments for MI have improved. They should not be used in those who have recently taken cocaine. When beta blocker medication is given within the first 24–72 hours of a STEMI no lives are saved. However, 1 in 200 people were prevented from a repeat heart attack, and another 1 in 200 from having an abnormal heart rhythm. Additionally, for 1 in 91 the drug causes a temporary poor ability of the heart to pump blood.
- ACE inhibitor therapy should be started when stable and continued indefinitely at the highest tolerated dose. Those who cannot tolerate ACE inhibitors may be treated with an 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 beginning treatment with an ACE inhibitor.
- Previous studies suggested a benefit from omega-3 fatty acid supplementation but this has not been confirmed.
- The cardiac defibrillator device was specifically designed to terminate these potentially fatal arrhythmias. The device works by delivering an electrical shock to the person 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.
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 and 6 percent die before leaving the hospital and 7 to 18 percent die within a year. Morbidity and mortality from myocardial infarction has improved over the years due to earlier and better treatment.
Using variables available in the emergency room, people with a higher risk of adverse outcome can be identified. Throughout hospital departments, practitioners use TIMI scores to assess mortality risk. There are TIMI (Thrombolysis in Myocardial Infarction) scores for unstable angina or NSTEMI and STEMI, both using routine patient data from history taking, medication use and lab results. Both scores have been found effective and reliable in multiple settings, including the emergency room.
Complications may occur immediately following the myocardial infarction or may need time to develop. Disturbances of heart rhythms, including ventricular tachycardia and fibrillation and heart block can arise as a result of ischaemia, cardiac scarring, and infarct location. Stroke is also a risk, either as a result of clots transmitted from the heart during PCI, as a result of bleeding following anticoagulation, or as a result of disturbances in the heart's ability to pump effectively as a result of the infarction, including aneurysm of the left ventricle myocardium; ventricular septal rupture or free wall rupture. Regurgitation of blood through the mitral valve is possible, particularly if the infarction causes dysfunction of the papillary muscle. Cardiogenic shock as a result of the heart being unable to pump blood adequately may develop, dependent on cardiac size, is most likely to occur within the days following an acute myocardial infarction, and the largest cause of in-hospital mortality. Rupture of the ventricular dividing wall or left ventricular wall may occur within the initial weeks. Dressler's syndrome, a reaction following larger infarcts and a cause of pericarditis is also possible.
Longer-term complications include heart failure, atrial fibrillation, and an increased risk of a second MI. Prognosis is worse if a mechanical complication such as papillary muscle or myocardial free wall rupture occurs.
Risk factors for complications and death risk factors for death include age, hemodynamic parameters (such as heart failure, cardiac arrest on admission, systolic blood pressure, or Killip class of two or greater), ST-segment deviation, diabetes, serum creatinine, peripheral vascular disease, and elevation of cardiac markers.
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; 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. Worldwide, more than 3 million people have STEMIs and 4 million have NSTEMIs a year. STEMIs occur about twice as often in men as women.
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. For example, rates of death from cardiovascular disease have decreased almost a third between 2001 and 2011 in the United States.
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.
Society and cultureEdit
Depictions of heart attacks in popular media often include collapsing or loss of consciousness which are not common symptoms; these depictions contribute to widespread misunderstanding about the symptoms of myocardial infarctions, which in turn contributes to people not getting care when they should.
At common law, in general, a myocardial infarction is a disease, but may sometimes be an injury. This can create coverage issues in the administration of no-fault insurance schemes such as workers' compensation. In general, a heart attack is not covered; 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.
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