Abstract

Myocardial infarction is a pathological process established by a compromise in the blood supply to an area of myocardium of such severity that even with prolonged rest adequate oxygen connot be obtained. In the United States there are approximately 600,000 to 800,000 persons each year suffering attacks from this disease.1 Even though in recent years greater facilitation in diagnosis and tremendous strides in therapy have reduced mortality during the first attack in private patients to 5 per cent or less,2 the overall annual mortality is 200,000.1 A large number of the deaths occur during the most productive years of life ; many of those who survive suffer disabling complications. The figures for mortality and disabling complications can be decreased by a careful differential diagnosis of patients presenting chest pains and other symptoms characteristic of myocardial infarction and by individualization of therapeutic procedures. Diagnosis The diagnosis of acute myocardial infarction is based on the history, the clinical findings, and an evaluation of the electrocardiographic changes. There are many nonspecific signs which may be used as adjuncts. A tentative diagnosis of myocardial infarction may be suggested in a patient presenting a severe, oppressive pain over the lower sternum or more extensively over the precordium or anterior chest which lasts for 30 minutes or longer and which is not relieved by rest or nitrites.3 Radiation of this pain to neck, shoulders, or arms confirms the likely origin in the heart. The pain builds up slowly and steadly to a plateau of maximal intensity. Anxiety and fear of impending doom mount rapidly as the pain continues. After several hours the pericardial inflammation resulting from ventricular necrosis may introduce a sharp, stabbing component to the pain. It is typically aggravated by respiration, emotion, swallowing, and may have a throbbing element synchronous with the heartbeat.4 Complications as shock and congestion of the lungs from acute left ventricular failure may increase the complexity of the symptoms ;4 however, a rapid fall in blood pressure within twenty-four hours or even a more gradual fall in the next few days is interpreted as an important confirmatory sign.1 Fever, leukocytosis, and elevation of the erythrocyte sedimentation rate are clinical signs which support the diagnosis. Serial changes in the electrocardiogram are of great value, but not essential, for the diagnosis.4 The electrocardiogram is considered characteristic of acute myocardial infarction when elevation of the RS-T segment and a deep Q wave are present in one or more leads, with progressive change from RS-T elevation to T-wave inversion in serial records.� At 45ubmitted in the 1957 Essay Contest of the American College of Chest Physicians.

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