Heart Attack

What is a heart attack?

Your heart muscle needs oxygen to survive. A heart attack occurs when the blood flow that brings oxygen to the heart muscle is severely reduced or cut off completely (View an animation of blood flow). This happens because coronary arteries that supply the heart muscle with blood flow can slowly become narrrow from a buildup of fat, cholesterol and other substances that together are called plaque. This slow process is known as atherosclerosis . When a plaque in a heart artery breaks, a blood clot forms around the plaque. This blood clot can block the blood flow through the heart muscle. When the heart muscle is starved for oxygen and nutrients, it is called ischemia. When damage or death of part of the heart muscle occurs as a result of ischemia, it is called a heart attack or myocardial infarction (MI). About every 34 seconds, someone in the United States has a myocardial infarction (heart attack).

Signs and symptoms :

The onset of symptoms in myocardial infarction (MI) is usually gradual, over several minutes, and rarely instantaneous. Chest pain is the most common symptom of acute myocardial infarction and is often described as a sensation of tightness, pressure, or squeezing. Chest pain due to ischemia (a lack of blood and hence oxygen supply) of the heart muscle is termed angina pectoris. Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium,^[7][17] where it may mimic heartburn. Levine's sign, in which the patient localizes the chest pain by clenching their fist over the sternum, has classically been thought to be predictive of cardiac chest pain, although a prospective observational study showed that it had a poor positive predictive value.
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), weakness, light-headedness, nausea, vomiting, and palpitations. These symptoms are likely induced by a massive surge of catecholamines from the sympathetic nervous system which occurs in response to pain and the hemodynamic abnormalities that result from cardiac dysfunction. Loss of consciousness (due to inadequate cerebral perfusion and cardiogenic shock) and sudden death (frequently due to the development of ventricular fibrillation) can occur in myocardial infarctions.
Women and older patients report atypical symptoms more frequently than their male and younger counterparts. Women also report more numerous symptoms compared with men (2.6 on average vs 1.8 symptoms in men).^[  The most common symptoms of MI in women include dyspnea (shortness of breath), 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.
At least one-fourth of all myocardial infarctions are silent, without chest pain or other symptoms. 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 myocardial infarctions vary between 22 and 64%. A silent course is more common in the elderly, in patients with diabetes mellitus^[ and after heart transplantation, probably because the donor heart is not fully innervated by the nervous system of the recipient.^[24] In people with diabetes, differences in pain threshold, autonomic neuropathy, and psychological factors have been cited as possible explanations for the lack of symptoms.

Risk factors

Myocardial infarction results from atherosclerosis.^[  Smoking appears to be the cause of about 36% of coronary artery disease and obesity 20%. Lack of exercise has been linked to 7-12% of cases. Job stress appear to play a minor role accounting for about 3% of cases.
Risk factors for myocardial infarction include:

• Age
• Gender: At any given age men are more at risk than women, particularly before menopause,^[35] but because in general women live longer than men ischemic heart disease causes slightly more total deaths in women.
• Diabetes mellitus (type 1 or 2
• High blood pressure
• Dyslipidemia/hypercholesterolemia (abnormal levels of lipoproteins in the blood), particularly high low-density lipoprotein, low high-density lipoprotein and high triglycerides
• Tobacco smoking, including secondhand smoke
• Short term exposure to air pollution including: carbon monoxide, nitrogen dioxide, and sulfur dioxide but not ozone.^[38]
• Family history of ischaemic heart disease or myocardial infarction 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).
• Obesity (defined by a body mass index of more than 30 kg/m², or alternatively by waist circumference or waist-hip ratio).
• Lack of physical activity.
• Psychosocial factors including, low socio-economic status, social isolation, negative emotions and stress increase the risk of myocardial infarction and are associated with worse outcomes after myocardial infarction. 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.
• Alcohol — Studies show that prolonged exposure to high quantities of alcohol can increase the risk of heart attack.
• 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.
• Hyperhomocysteinemia (high homocysteine) in homocysteinuria is associated with premature atherosclerosis, whether elevated homocysteine in the normal range is causal is contentious.

Diagnosis

WHO criteria formulated in 1979 have classically been used to diagnose MI; a patient is diagnosed with myocardial infarction 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 such as creatine kinase-MB fraction and troponin

Prevention

The risk of a recurrent myocardial infarction 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 commenced on several long-term medications post-MI, with the aim of preventing secondary cardiovascular events such as further myocardial infarctions, congestive heart failure or cerebrovascular accident (CVA). Unless contraindicated, such medications may include:

• Antiplatelet drug therapy such as aspirin and/or clopidogrel should be continued to reduce the risk of plaque rupture and recurrent myocardial infarction. 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, however the risk of hemorrhage is increased.
• Beta blocker therapy such as metoprolol or carvedilol should be commenced. These have been particularly beneficial in high-risk patients such as those with left ventricular dysfunction and/or continuing cardiac ischaemia. β-Blockers decrease mortality and morbidity. They also improve symptoms of cardiac ischemia in NSTEMI.
• ACE inhibitor therapy should be commenced 24–48 hours post-MI in hemodynamically stable patients, particularly in patients 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 post-MI.
• Statin therapy has been shown to reduce mortality and morbidity post-MI. The effects of statins may be more than their LDL lowering effects. The general consensus is that statins have plaque stabilization and multiple other ("pleiotropic") effects that may prevent myocardial infarction in addition to their effects on blood lipids.
• The aldosterone antagonist agent eplerenone has been shown to further reduce risk of cardiovascular death post-MI in patients with heart failure and left ventricular dysfunction, when used in conjunction with standard therapies above. Spironolactone is another option that 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. In high-risk people there is no clear-cut decrease in potentially fatal arrhythmias due to omega-3 fatty acids. And they may increase risk in some groups.
• 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.

DRUGS :

Medications
With each passing minute after a heart attack, more heart tissue loses oxygen and deteriorates or dies. The main way to prevent heart damage is to restore blood flow quickly.
Medications given to treat a heart attack include:

• Aspirin. You may be given aspirin by emergency medical personnel soon after they arrive or as soon as you get to the hospital. Aspirin reduces blood clotting, thus helping maintain blood flow through a narrowed artery.
• Thrombolytics. These drugs, also called clotbusters, help dissolve a blood clot that's blocking blood flow to your heart. The earlier you receive a thrombolytic drug following a heart attack, the greater the chance you will survive and lessen the damage to your heart.
• Superaspirins. Doctors in the emergency room may give you other drugs that are somewhat similar to aspirin to help prevent new clots from forming. These include medications, such as clopidogrel (Plavix) and others, called platelet aggregation inhibitors.
• Other blood-thinning medications. You'll likely be given other medications, such as heparin, to make your blood less "sticky" and less likely to form more dangerous clots. Heparin is given intravenously or by an injection under your skin and is usually used during the first few days after a heart attack.
• Pain relievers. If your chest pain or associated pain is great, you may receive a pain reliever, such as morphine, to reduce your discomfort.
• Nitroglycerin. This medication, used to treat chest pain (angina), temporarily opens arterial blood vessels, improving blood flow to and from your heart.
• Beta blockers. These medications help relax your heart muscle, slow your heartbeat and decrease blood pressure making your heart's job easier. Beta blockers can limit the amount of heart muscle damage and prevent future heart attacks.
• Cholesterol-lowering medications. Examples include statins, niacin, fibrates and bile acid sequestrants. These drugs help lower levels of unwanted blood cholesterol and may be helpful if given soon after a heart attack to improve survival.