myocardial infarction

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myocardial infarction:

see under infarctioninfarction,
blockage of blood circulation to a localized area or organ of the body resulting in tissue death. Infarctions commonly occur in the spleen, kidney, lungs, brain, and heart.
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Myocardial Infarction


a form of necrosis of the heart muscle caused by an acute insufficiency of blood flow through the coronary arteries nourishing the heart tissues. The coronary insufficiency may be caused either by a sudden interruption of the blood flow through a coronary artery or by a disparity between the oxygen demand of the myocardium and the capacity of the coronary arteries to satisfy it. The anatomical basis of myocardial infarction is in 98 percent of the cases atherosclerosis of the coronary arteries. A sudden acute interruption of coronary circulation resulting in myocardial infarction may follow (1) the narrowing (stenosis) of a coronary artery from pronounced atherosclerosis or the formation of a large atherosclerotic plaque, (2) the occlusion of the lumen of the blood vessel by a thrombus, or (3) a sudden increase in the load on the myocardium and the consequently greater need for oxygen. Young persons may suffer myocardial infarction because of neurohumoral disturbances during spasm of the myocardial blood vessels against a background of only moderate atherosclerosis.

Myocardial infarction generally arises after thrombosis of the coronary vessels. A thrombus in a coronary vessel may result from either systemic disorders (decreased amount of anticoagulants, such as heparin and fibrinolysin, in the blood, reduced capability of a compensatory increase in these substances, increased amount of clotting factors) or local changes (development of rough spots on the intima of a blood vessel, disintegration or ulceration of an atherosclerotic plaque, eddies in the blood flow, slowing of the blood flow). Myocardial infarction often follows an increase in the patient’s ordinary activity. The heart needs more oxygen and nutrients because of the increased load. However, coronary arteries altered by atherosclerosis cannot respond with an adequate increase in the blood flow; this results in myocardial ischemia and sometimes in infarction.

Myocardial infarction was first described in 1909 by the Russian scientists V.P. Obraztsov and N.D. Strazhesko. It affects almost exclusively the walls of the left ventricle, posterior or (most often) anterior. Extensive infarctions extend to most of the anterior or posterior wall and, in 10 to 20 percent of the cases, to the interventricular septum. The necrotic tissues are gradually resorbed and a connective-tissue scar develops on the site in six or seven weeks. The wall at the site of an infarction may become thin; if the infarction is extensive, a cardiac aneurysm may form. Myocardial infarction generally occurs in males over 40 years of age. Smoking, diabetes mellitus, overweight, and a sedentary way of life are predisposing factors.

An infarction is manifested most often by a severe attack of angina pectoris—retrosternal pains radiating to the left arm, back, and shoulder blade. These pains usually cannot be relieved by the ordinary vasodilators (Validol, nitroglycerin) or sometimes even by narcotics. In some cases the initial symptom is a choking sensation without other pain. A gastralgic condition, manifested by pain in the upper part of the stomach, has also been noted. An elevated temperature, an increased leukocyte count, and an accelerated ESR (erythrocyte sedimentation rate) after a few days are characteristic. There is a rise in the levels of certain enzymes in the blood (transaminase, aldolases, the first isoenzyme of lactate dehydrogenase). The precise diagnosis is based on the electrocardiogram.

The severity of the course of myocardial infarction is largely determined by the presence of complications, the most serious being cardiogenic shock. In cardiogenic shock blood pressure falls sharply (below 90/60 mm Hg), cold sweats appear, and there is pronounced general weakness. In almost 90 percent of the cases myocardial infarction is complicated by an abnormal heart beat (arrhythmia). The exclusion of the necrotic part of the myocardium from contractile activity may lead to cardiac insufficiency. In some cases this decrease in the contractile capacity of the heart is compensated by the surviving portions of the myocardium; in other cases signs of cardiac insufficiency appear (dyspnea, suffocation, pulmonary congestion, edema, tachycardia). A rare complication is thromboembolism, which is caused by the transport of part of a thrombus from the heart cavity to various vascular regions.

Treatment of myocardial infarction involves early hospitalization, specialized emergency care, and strict bed rest; the administration of anticoagulants and fibrinolytic agents; pain relievers, such as nitrous oxide and neuroleptic agents; electric impulse therapy to control disturbances of rhythm; and cardiac glycosides and diuretics for cardiac insufficiency.

After recovering from a myocardial infarction, the patient must follow a sparing regimen for five to seven months, relaxing this care only gradually. Work involving great physical exertion or emotional stress is thereafter forbidden. Walking, light physical work (in a kitchen garden or flower garden, housework) and exercise therapy are recommended. Four meals a day (not too heavy) that are rich in vitamins and limited in (but not exclusive of) animal fats, meat broths, concentrated coffee, and tea are recommended.


Chazov, E.I. Trombozy i embolii v klinike vnutrennikh boleznei. Moscow, 1966.
Miasnikov, A.L. Gipertonicheskaia bolezn’ i ateroskleroz. Moscow, 1965.
Shestakov, S.V. Grudnaia zhaba i infarkt miokarda. Moscow, 1962. (Bibliography.)
Voprosy morfologii i patogeneza infarkta. Editor in chief, A.I. Strukov.Moscow, 1959.


References in periodicals archive ?
As per the study protocol, only those patients coming within 12 hours of onset of typical symptoms of acute myocardial infarction were included in the study.
Given that his symptoms were associated with conditions at rest in the morning, coronary artery spasm should also be considered as a possible trigger for the myocardial infarction; however, we did not perform a spasm provocation test.
The antiplatelet mechanism of aspirin is to make arachidonic acid lose its ability to transform into prostaglandin endoperoxide and hindering the formation of prostaglandin E2 and thromboxane A2 through inhibiting the activity of cyclooxygenase in platelets.17 However, a study shows that aspirin resistance exists in a few patients although aspirin has a good therapeutic effect in the treatment of acute myocardial infarction,18 that is, acute thrombosis may occur even after taking aspirin, and the incidence of adverse reactions increases with the increase of dosage.
Rapid bedside whole blood cardiac specific troponin-T immunoassay for diagnosis of acute myocardial infarction. Am Heart J.
During the follow-up period, after the adjustment for several confounding factors, such as sex, age, hypertension, heart failure, dyslipidemia, hemodialysis, and statin usage, the adjusted hazard ratios (HRs) for the risk of subsequent MACEs during hospitalization for IE in treatment cohort did not attain statistical significance; 1.18 (95% confidence interval [CI], 0.53-2.66) for myocardial infarction and 1.29 (95% CI, 0.87-1.91) for ischemic stroke [Table 2].
The presence of two primary risk factors suggest a risk for myocardial infarction by four times, whereas if there are three primary risk factors, the risk is by 10 times higher [4].
A well-developed coronary collateral limits ischemia, reduces the size of myocardial infarction, preserves left ventricle function, and has a favourable impact on the prognosis of patients with coronary artery
This case reminds us of importance of having a high index of suspicion, especially in elderly diabetic patients where benign self-limiting condition like hiccups can be the only presenting symptoms of a serious underlying pathology like ST elevation myocardial infarction.
Survival Rates of Patients after Myocardial Infarction Depending on Age and Diabetes Mellitus.
The results obtained by our group suggest, however, that mitochondrial genome mutations can also be associated with myocardial infarction. We have previously demonstrated that mtDNA mutations were present in cells from atherosclerotic aortas and arteries [10-14].
KEY WORDS: Post myocardial infarction; ventricular septal defect; and repair.

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