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Myocardial infarction

A myocardial infarction (MI), commonly known as a heart attack, occurs when blood flow decreases or stops in one of the arteries of the heart, causing infarction to the heart muscle. The most common symptom is retrosternal chest pain or discomfort that classically radiates to the left shoulder, arm, or jaw. The pain may occasionally feel like heartburn. This is the dangerous type of acute coronary syndrome.

Terminology
Myocardial infarction (MI) refers to tissue death (infarction) of a part of the heart muscle (myocardium), caused by ischemia, the lack of oxygen delivery to myocardial tissue. 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 the other type of acute coronary syndrome, unstable angina, a myocardial infarction occurs when there is cell death, which can be estimated by a blood test that measures biomarkers (the cardiac protein troponin). 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 myocardial infarction. An MI is different from — but can cause — cardiac arrest, where the heart is not contracting at all or so poorly that all vital organs cease to function, thus leading to death. 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 symptoms ==
Signs and symptoms
Chest pain that may or may not radiate to other parts of the body is the most typical and significant symptom of myocardial infarction. It might be accompanied by other symptoms such as sweating. Pain Chest pain is one of the most common symptoms 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. Similarly, chest pain similar to a previous heart attack is also suggestive. The pain associated with MI is usually diffuse, does not change with position, and lasts for more than 20 minutes. It might be described as pressure, tightness, knifelike, tearing, burning sensation (all these are also manifested during other diseases). It could be felt as an unexplained anxiety, and pain might be absent altogether. 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. Typically, chest pain because of ischemia, be it unstable angina or myocardial infarction, lessens with the use of nitroglycerin, but nitroglycerin may also relieve chest pain arising from non-cardiac causes. Other Chest pain may be accompanied by sweating, nausea or vomiting, and fainting, Females are more likely to have unusual or unexplained tiredness and nausea or vomiting as symptoms. Females having heart attacks are more likely to have palpitations, back pain, labored breath, vomiting, and left arm pain than males, although the studies showing these differences had high variability. Females are less likely to report chest pain during a heart attack and more likely to report nausea, jaw pain, neck pain, cough, and fatigue, although these findings are inconsistent across studies. Females with heart attacks also had more indigestion, dizziness, loss of appetite, and loss of consciousness. Shortness of breath is a common, and sometimes the only symptom, occurring when damage to the heart limits the output of the left ventricle, with breathlessness arising either from low oxygen in the blood or pulmonary edema. Other less common symptoms include weakness, light-headedness, palpitations, and abnormalities in heart rate or blood pressure. Loss of consciousness can occur in myocardial infarctions due to inadequate blood flow to the brain and cardiogenic shock, and sudden death, frequently due to the development of ventricular fibrillation. When the brain was without oxygen for too long due to a myocardial infarction, coma and persistent vegetative state can occur. Cardiac arrest, and atypical symptoms such as palpitations, occur more frequently in females, the elderly, those with diabetes, in people who have just had surgery, and in critically ill patients. In heart transplantation, the donor heart is not fully innervated by the nervous system of the recipient. == Risk factors ==
Risk factors
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 myocardial infarction are shared with coronary artery disease, the primary cause of myocardial infarction, High levels of blood cholesterol is a known risk factor, particularly high low-density lipoprotein, low high-density lipoprotein, and high triglycerides. Many risk factors for myocardial infarction are potentially modifiable, with the most important being tobacco smoking (including secondhand smoke). Less common causes include stress-related causes such as job stress, which accounts for about 3% of cases, and chronic high stress levels. Diet There is varying evidence about the importance of saturated fat in the development of myocardial infarctions. Eating polyunsaturated fat instead of saturated fats has been shown in studies to be associated with a decreased risk of myocardial infarction, while other studies find 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. Genetics Family history of ischemic heart disease or MI, particularly if one has a male first-degree relative (father, brother) who had a myocardial infarction before age 55 years, or a female first-degree relative (mother, sister) less than age 65 increases a person's risk of MI. Other The risk of having a myocardial infarction increases with older age, low physical activity, and low socioeconomic status. Evidence suggests that heart attacks are at least three times more likely to occur in the morning than in the late evening. Shift work is also associated with a higher risk of MI. One analysis has found an increase in heart attacks immediately following the start of daylight saving time. 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. Endometriosis in women under the age of 40 is an identified risk factor. Air pollution is also an important modifiable risk. Short-term exposure to air pollution such as carbon monoxide, nitrogen dioxide, and sulfur dioxide (but not ozone) has been associated with MI and other acute cardiovascular events. For sudden cardiac deaths, every increment of 30 units in Pollutant Standards Index correlated with an 8% increased risk of out-of-hospital cardiac arrest on the day of exposure. Extremes of temperature are also associated. 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. Myocardial infarction can also occur as a late consequence of Kawasaki disease. Calcium deposits in the coronary arteries can be detected with CT scans. Calcium seen in coronary arteries can provide predictive information beyond that of classical risk factors. High blood levels of the amino acid homocysteine is associated with premature atherosclerosis; whether elevated homocysteine in the normal range is causal is controversial. In people without evident coronary artery disease, possible causes for the myocardial infarction are coronary spasm or coronary artery dissection. == Mechanism ==
Mechanism
Atherosclerosis can lead to a heart attack and how blocked blood flow in a coronary artery can lead to a heart attack. The most common cause of a myocardial infarction is the rupture of an atherosclerotic plaque on an artery supplying heart muscle. Plaques can become unstable, rupture, and additionally promote the formation of a blood clot that blocks the artery; this can occur in minutes. Blockage of an artery can lead to tissue death in tissue being supplied by that artery. 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. Atherosclerosis is characterized by progressive inflammation of the walls of the arteries. Other causes Atherosclerotic disease is not the only cause of myocardial infarction, but it may exacerbate or contribute to other causes. A myocardial infarction may result from a heart with a limited blood supply subject to increased oxygen demands, such as in fever, a fast heart rate, hyperthyroidism, too few red blood cells in the bloodstream, or low blood pressure. Damage or failure of procedures such as percutaneous coronary intervention (PCI) or coronary artery bypass grafts (CABG) may cause a myocardial infarction. Spasm of coronary arteries, such as Prinzmetal's angina may cause blockage. Cells in the area with the worst blood supply, just below the inner surface of the heart (endocardium), are most susceptible to damage. Ischemia first affects this region, the subendocardial region, and tissue begins to die within 15–30 minutes of loss of blood supply. The dead tissue is surrounded by a zone of potentially reversible ischemia that progresses to become a full-thickness transmural infarct. Injury to the myocardium also occurs during re-perfusion. This might manifest as ventricular arrhythmia. The re-perfusion injury is a consequence of the calcium and sodium uptake from the cardiac cells and the release of oxygen radicals during reperfusion. No-reflow phenomenon—when blood is still unable to be distributed to the affected myocardium despite clearing the occlusion—also contributes to myocardial injury. Topical endothelial swelling is one of many factors contributing to this phenomenon. == Diagnosis ==
Diagnosis
Criteria A myocardial infarction, according to established consensus, is defined by elevated cardiac biomarkers with a rising or falling trend and at least one of the following: • Symptoms relating to ischemia • Changes on an electrocardiogram (ECG), such as ST segment changes, new left bundle branch block, or pathologic Q waves • Changes in the motion of the heart wall on imaging • Demonstration of a thrombus on angiogram or at autopsy. Types A myocardial infarction is usually clinically classified as an ST-elevation MI (STEMI) or a non-ST elevation MI (NSTEMI). These are based on ST elevation, a portion of a heartbeat graphically recorded on an ECG. 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 or electrical cardioversion; it rises within 4–8 hours and returns to normal within 2–3 days. Electrocardiogram . Elevation of the ST segment can be seen in leads II, III and aVF. An electrocardiogram (ECGs) is a series of electrodes placed on a person's chest that measure electrical activity associated with contraction of the heart muscle. 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. Imaging Noninvasive imaging plays an important role in the diagnosis and characterisation of myocardial infarction. Myocardial perfusion imaging has no role in the acute diagnostic algorithm; however, it can confirm a clinical suspicion of Chronic Coronary Syndrome when the patient's history, physical examination (including cardiac examination) ECG, and cardiac biomarkers suggest coronary artery disease. Medical societies and professional guidelines recommend that the physician confirm a person is at high risk for Chronic Coronary Syndrome before conducting diagnostic non-invasive imaging tests to make a diagnosis, File:UOTW 36 - Ultrasound of the Week 2.webm|Pulmonary edema due to an MI as seen on ultrasound The chest pain in an MI may mimic heartburn. == Prevention ==
Prevention
There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted as secondary prevention after an initial myocardial infarction, Primary prevention Lifestyle Physical activity can reduce the risk of cardiovascular disease, and people at risk are advised to engage in 150 minutes of moderate or 75 minutes of vigorous intensity aerobic exercise a week. Vitamins and mineral supplements are of no proven benefit, and neither are plant stanols or sterols. Public health measures may also act at a population level to reduce the risk of myocardial infarction, for example by reducing unhealthy diets (excessive salt, saturated fat, and trans-fat) including food labeling and marketing requirements as well as requirements for catering and restaurants and stimulating physical activity. This may be part of regional cardiovascular disease prevention programs or through the health impact assessment of regional and local plans and policies. Most guidelines recommend combining different preventive strategies. A 2015 Cochrane Review found some evidence that such an approach might help with blood pressurebody mass index and waist circumference. However, there was insufficient evidence to show an effect on mortality or actual cardio-vascular events. Medication Statins, drugs that act to lower blood cholesterol, decrease the incidence and mortality rates of myocardial infarctions. They are often recommended in those at an elevated risk of cardiovascular diseases. 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. Secondary prevention There is a large crossover between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be adopted as secondary prevention after an initial myocardial infarct. and is recommended to start gradually after 1–2 weeks. Other medications include: Aspirin is continued indefinitely, as well as another antiplatelet agent such as clopidogrel or ticagrelor ("dual antiplatelet therapy" or DAPT) for up to twelve months. 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. possibly because other treatments for MI have improved. When beta blocker medication is given within the first 24–72 hours of a STEMI no lives are saved.