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Prepared By: LaniMyocardial infarction situations to tissue death 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 for biomarkers 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 state 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, thus causing death. It is also different from heart failure, in which the pumping action of the heart is impaired. Still, an MI may lead to heart failure.
Chest pain is the most common symptom of acute myocardial infarction and is often defined as a sensation of tightness, pressure, or squeezing. Pain radiates most often to the left arm, but may similarly radiate to the lower jaw, neck, right arm, back, and upper abdomen. The pain most expressive of an acute MI, with the highest likelihood ratio, is pain radiating to the right arm and shoulder. Equally, chest pain similar to a previous heart attack is also suggestive. The pain related 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 prognostic of cardiac chest pain, while a prospective observational study showed it had a poor positive predictive value. Pain that responds to nitroglycerin does not specify the presence or absence of a myocardial infarction.
Chest pain may be complemented by sweating, nausea or vomiting, and fainting, and these symptoms may also occur without any pain at all. Now 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 symptom, occurring when damage to the heart limits the output of the left ventricle, with gasping arising either from low oxygen in the blood, or pulmonary edema. Other less common symptoms include weakness, light-headedness, palpitations, and irregularities in heart rate or blood pressure. These symptoms are likely brought by a massive surge of catecholamines from the sympathetic nervous system, which occurs in response to pain and, where present, low blood pressure. 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. Cardiac arrest, and atypical indicators such as palpitations, occurs 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 occur devoid of any symptoms at all. These cases can be revealed 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 collective in the elderly, in those with diabetes mellitus and after heart transplantation. In people with diabetes, variances 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 maximum noticeable 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 reasons of myocardial infarction are shared with coronary artery disease, the primary cause of myocardial infarction, with other risk factors plus male sex, low levels of physical activity, a earlier family history, obesity, and alcohol use. Risk factors for myocardial disease are often comprised in risk factor stratification scores, such as the Framingham risk score. At any given age, men are more at risk than women for the growth of cardiovascular disease. 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 adjustable, with the most essential being tobacco smoking (including secondhand smoke). Smoking appears to be the cause of around 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.
There is varying indication about the significance of saturated fat in the development of myocardial infarctions. Eating polyunsaturated fat instead of saturated fats has been shown in studies to be linked 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 ingesting 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) increases the risk of a heart attack.
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.
Cardiac rehabilitation benefits many who have experienced myocardial infarction, even if there has been considerable heart damage and resultant left ventricular failure. It should start soon after release from the hospital. The program may include routine advice, exercise, social support, as well as references about driving, flying, sport participation, stress management, and sexual intercourse.
There is a large border between the lifestyle and activity recommendations to prevent a myocardial infarction, and those that may be implemented as secondary prevention after an initial myocardial infarction, because of shared risk factors and an aim to reduce atherosclerosis affecting heart vessels.
Physical activity can reduce the risk of cardiovascular disease, and people at risk are advised to engage in 150 minutes of adequate or 75 minutes of dynamic intensity aerobic exercise a week. Keeping a healthy weight, drinking alcohol within the recommended limits, and quitting smoking reduce the risk of cardiovascular disease.
Replacing polyunsaturated fats such as olive oil and rapeseed oil instead of saturated fats may reduce the risk of myocardial infarction, although there is not universal agreement. Dietary modifications are recommended by some national authorities, with references including 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.
Public health measures may also act at a population level to reduce the risk of myocardial infarction, for example by 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.
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.
Aspirin has been studied broadly 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 extreme 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.
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. Recommendations include stopping smoking, a gradual return to exercise, eating a healthy diet, low in saturated fat and low in cholesterol, and drinking alcohol within recommended limits, exercising, and trying to achieve a healthy weight. Exercise is both safe and effective even if people have had stents or heart failure, and is recommended to start gradually after 1–2 weeks. Counselling should be provided relating to medications used, and for warning signs of depression. Previous studies suggested a benefit from omega-3 fatty acid supplementation but this has not been confirmed.
Following a heart attack, nitrates, when taken for two days, and ACE-inhibitors decrease the risk of death. 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. 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. 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 medication causes a temporary decrease in the heart’s ability to pump blood.
ACE inhibitor therapy should be started within 24 hours, and continued indefinitely at the highest tolerated dose. This is provided there is no evidence of worsening kidney failure, high potassium, low blood pressure, or known narrowing of the renal arteries. Those who cannot tolerate ACE inhibitors may be treated with an angiotensin II receptor antagonist.
Statin therapy has been shown to reduce mortality and subsequent cardiac events, and should be commenced with the aim of lowering LDL cholesterol. Other medications, such as ezetimibe, may also be added with this goal in mind.
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.
A defibrillator, an electric device connected to the heart and surgically inserted under the skin, may be recommended. This is particularly if there are any ongoing signs of heart failure, with a low left ventricular ejection fraction and a New York Heart Association grade II or III after 40 days of the infarction. Defibrillators detect potentially fatal arrhythmia and deliver an electrical shock to the person to depolarize a critical mass of the heart muscle.
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