Myocardial infarction
What is Myocardial infarction?
Myocardial infarction (MI) is commonly referred to as a heart attack. This describes the death (infarction) of a part of the heart muscle due to inadequate blood supply. The most frequent cause of MI is coronary artery disease (atherosclerotic heart disease).
Less often, MI may result from other causes of reduced myocardial blood flow, such as severe low blood pressure (hypotension) or prolonged spasm of a coronary artery (vasospasm).
Myocardial infarction may also result from conditions that drastically increase the heart's need for oxygen, such as severe hyperthyroidism. This section pertains primarily to MI caused by atherosclerotic coronary artery disease, a process in which fatty material is deposited in the walls of the coronary arteries supplying the heart muscle; this same process may also be occurring in arteries throughout the body. As the fatty deposits (plaques or atheromas) slowly increase in size over the years, this results in areas of narrowing (stenosis) inside the artery and reduced blood flow to the heart. The disease process produces no symptoms until stenosis becomes severe enough to result in an inadequate blood supply (ischemia) to meet the needs of the heart.
Myocardial ischemia that is mild to moderate in degree, and/or of brief duration, may cause chest pain (angina pectoris) but does not result in permanent tissue damage. Prolonged, severe myocardial ischemia results in tissue death which is a myocardial infarction.
The usual precipitating event for a Myocardial infarction is a rapid formation of a blood clot in an already narrowed coronary artery where plaque has ruptured. A clot may obstruct the artery where it forms, or it may be carried downstream until it obstructs a smaller artery. In either case, the portion of heart muscle supplied by the blocked artery is deprived of blood flow and undergoes infarction.
The location and size of a MI depend on the site(s) of arterial obstruction, and on whether there is overlapping blood supply from other coronary vessels (collateral circulation). The infarction may either involve the full thickness of the heart muscle (transmural) or a partial thickness (subendocardial).
How is it diagnosed?
History: An MI is usually preceded by a history of sudden chest pain.
The pain of a myocardial infarction is variable in character and location, but is often described as a steady crushing pain in the chest. If there is a pre-existing history of angina pectoris, the pain may be similar to it but more severe, and is not relieved by rest or by nitroglycerin (measures that usually relieves angina).
Other symptoms associated with the pain may include sweating, anxiety, light-headedness, nausea, vomiting, difficult breathing (dyspnea), and fainting (syncope). However, symptoms may be so mild that an individual may believe it's "gas" or "indigestion". An myocardial infarction can also occur without symptoms, referred to as a silent MI. This is usually discovered incidentally after the fact, when an EKG shows evidence of an old MI in an individual with no history of chest pain. Individuals with diabetes mellitus have an increased incidence of silent MI's, perhaps because the sensation of pain is diminished by a diabetes-related nerve disorder (diabetic neuropathy).
Physical exam may note a pale and sweaty expression. In a severe MI, there may be signs of circulatory shock including low blood pressure, a heart sound abnormality (gallop) and/or a pulse irregularity, or fluid in the lungs.
Tests: The diagnosis of an acute MI can usually be made by electrocardiography (EKG). The initial EKG usually shows abnormalities characteristic of an acute MI (elevated S-T segments). Repeated EKGs over the next few days then show a gradual evolution into a pattern characteristic of a completed MI, typified by Q waves. But a less severe heart attack, one in which only a partial thickness of the heart wall is involved (subendocardial), may not show the characteristic evolution, and may be difficult to differentiate from severe, unstable angina pectoris.
Cardiac enzymes are another important diagnostic test. Heart muscle contains several enzymes that are released into the blood when the muscle dies. Repeated blood tests over a period of several days show a rise in enzyme levels, followed by a decline. Since slightly different forms of the same enzymes are found in other tissues, specialized isoenzyme tests may be performed to differentiate between enzymes of the heart and other organs.
If the above tests are inconclusive, a type of radioisotope scan called infarct-avid imaging may be performed. A small quantity of a radioactive chemical is injected intravenously and accumulates selectively in recently infarcted myocardium. The radioactivity is detected, producing an image of the heart. An acute infarction shows up as a bright area ("hot spot") on the image.
How is myocardial infarction treated?
An myocardial infarction is a medical emergency requiring immediate hospitalization in a coronary care unit (CCU).
Treatment includes bedrest, oxygen, narcotics for pain relief, anti-arrhythmic drugs, if needed, anticoagulants and anti-platelet drugs to inhibit clotting, and drugs (beta blockers) to reduce the heart's need for oxygen and arrhythmic control. Calcium channel blockers help prevent infarct extension in subendocardial MI's. Other drugs (ACE inhibitors) have recently been shown to improve survival in stable myocardial infarction individuals with reduced left heart function. In such individuals, ACE inhibitors help prevent congestive heart failure.
However, these drugs also lower blood pressure, so they are not used in individuals who are clinically unstable. Anticoagulants and anti-platelet drugs help prevent further thrombosis, but do not remove clots that have already formed. Recently-formed clots may be removed by administration of a drug to dissolve clots (thrombolytic agent). If given early in the course of an myocardial infarction, thrombolytic agents can limit the size of the infarct, preserve heart function, and reduce the risk of mortality. Thrombolytic therapy is most effective if given within the first six hours, but may still be beneficial up to twelve hours after the onset of pain.
Congestive heart failure, if present, usually responds to diuretics. Vasodilators may also be helpful in reducing the heart's workload.
For cardiogenic shock, vasopressors are required to maintain blood pressure. Circulatory support may also be given by means of intra-aortic balloon counterpulsation. Myocardial rupture, a rare but desperate situation, requires surgical repair. In selected cases, when a massive MI is accompanied by heart failure so severe as to cause shock or when symptoms continue, emergency coronary bypass surgery or coronary balloon angioplasty may be performed. In these individuals, immediate bypass or angioplasty does improve prognosis for survival. After a small uncomplicated MI, bedrest is continued for one to three days. After two to three days, the individual can be transferred to a less intensively monitored setting, and after a week, the individual may be allowed to go home.
Physical activity is gradually increased over the next three to six weeks. After six weeks, if no complications have occurred and if cardiac stress tests show no residual ischemia, most individuals can return to normal activity. After a large or complicated myocardial infarction, the period of hospitalization and recovery is longer, and activity limitations may be permanent. Blood thinners may be prescribed for three to six months in addition to anti-platelet drugs to reduce the risk of clotting in the heart and embolization. In addition to cardiac stress testing to detect residual ischemia, echocardiography may be performed to evaluate ventricular function.
Individuals with residual or recurrent angina after an MI, or with painless ischemia on cardiac stress testing, may benefit from coronary bypass surgery or coronary balloon angioplasty. Coronary arteriography is performed to determine the feasibility of these procedures. Those who are not candidates for these procedures are treated medically, the same as for angina. After medical treatment has been optimized, or after surgery or angioplasty, cardiac stress tests are again performed. A cardiac rehabilitation program may facilitate the individual's return to the best possible level of functioning.
Postmyocardial infarction syndrome is also treated with nonsteroidal anti-inflammatory drugs (NSAIDs). If these do not relieve symptoms, a brief course of steroids may be given. Persistent arrhythmias are treated with antiarrhythmic drugs. In some cases, the management of arrhythmias or heart block may require an artificial pacemaker.
To minimize the progression of coronary artery disease, modification of risk factors is essential. This can be done through a correct diet, adequate exercise, and cessation of smoking. In some cases, medication may be required for hypertension, diabetes, and/or high cholesterol levels. In addition, a small daily dose of an antiplatelet drug helps to inhibit clotting. These measures are continued indefinitely.
Medications
Zocor (Simvastatin), Altace (Ramipril), Mevacor (Lovastatin), Coumadin (Warfarin), Pravachol (Pravastatin), Tenormin (Atenolol)
What might complicate it?
Among the most common acute complications of a MI are heart rhythm abnormalities (arrhythmias). Even a small MI may result in life-threatening arrhythmias such as ventricular fibrillation, particularly during the first 24 to 48 hours. Other acute complications include extension of the infarct to involve more of the heart muscle. Extension of an infarct results from continuing clotting in the coronary artery. For example, a partial-thickness (subendocardial) infarction may extend to become full-thickness (transmural). Congestive heart failure may occur; in its severe form, cardiogenic shock may result. Heart failure and cardiogenic shock occur when a large area of the ventricle is damaged, including damage from previous MI's, so that the heart's pumping capacity is impaired. Inflammation of the covering of the heart (pericarditis) may occur during the first few days after an acute MI, and usually subsides within three to five days.
Myocardial rupture may occur within the first week after an acute myocardial infarction rupture of a papillary muscle results in acute mitral insufficiency. Rupture of the interventricular septum or of the outer wall of the ventricle can also occur. Free wall rupture may occur either suddenly (usually resulting in immediate death) or gradually. Blood clots attached to the inner heart wall (mural thrombi) are a common complication of large anterior MIs. A mural thrombus may embolize into the arterial circulation, usually within the first six weeks after an MI Emboli originating in the heart may occlude arteries elsewhere in the body, including the brain (resulting in transient ischemic attack or stroke) or the extremities.
A minority of individuals may develop postmyocardial infarction syndrome (Dressler's syndrome) up to three months after an myocardial infarction. This syndrome consists of fever, pericarditis, and sometimes pleuritis. It differs from the pericarditis that occurs during the acute phase of an MI. It is an autoimmune reaction and may come and go for months. A large MI may result in an area of scar tissue that bulges outward as the surrounding myocardium contracts (ventricular aneurysm). Infarcted heart muscle is replaced by scar tissue, and does not regenerate. This increases the work the heart must do to pump blood and may result in persistent heart failure.
Ventricular aneurysms may be associated with persistent arrhythmias, and also frequently contain mural thrombi. Ventricular aneurysms usually require surgical removal. After a MI has healed, the scarred myocardium is painless. Residual or recurrent angina pectoris suggests that additional myocardium is getting insufficient blood supply (ischemia). After a subendocardial infarction, ischemia may result from continued obstruction or re-obstruction of the same coronary vessel. These individuals are at risk for having a subendocardial infarct become a transmural one.
Predicted outcome
In the acute phase of an MI, prognosis for survival depends on the individual's age and general health, the size of the infarct, the promptness of treatment, the type of treatment, and the development of complications. Small MIs have a good prognosis, if serious arrhythmias are prevented during the first few days. Massive MIs, involving more than 50% of the left ventricle, and accompanied by heart failure or cardiogenic shock have a high mortality rate. Prompt restoration of blood supply (revascularization) by coronary thrombolysis, coronary bypass, or balloon angioplasty early in the course of an acute MI can limit the size of the infarct and improve the prognosis.
After hospital discharge, prognosis for functional recovery and long term survival depends on the extent of residual ischemia (as determined by cardiac stress testing) the extent of left ventricular impairment (as revealed by echocardiography or angiocardiography), and the presence or absence of persistent ventricular arrhythmias. If residual ischemia is present, prognosis also depends on whether or not revascularization is feasible.
Ability to return to work depends on the functional classification after treatment as determined by stress testing and on the individual's occupation. Individuals with good ventricular function and no residual ischemia can usually return to normal activity. If return to previous occupation is not possible, restriction to lighter and/or part-time work may be feasible. A rehabilitation program may help the individual attain the best possible level of functioning.
Alternatives
Other diseases that can mimic the symptoms of a heart attack are a hiatal hernia, perforated stomach ulcer, acute inflammation of the gallbladder or pancreas, or acute pericarditis.
TYPE OF REHABILITATION
Cardiac therapy, three times a week, for a period of eight to twelve weeks.
Appropriate specialists
Cardiologist, physiatrist, and thoracic surgeon.
Last updated 4 April 2018