5. a. men age 35 or over with family history of premature coronary artery disease

b. age 35 or over with two or more major cardiovascular risk factors, (dyslipidemias, hypertension, diabetes mellitus and cigarette smoking).

Of all patients with coronary artery insufficiency, the group of asymptomatic individuals with silent ischemia poses a major challenge in terms of detection and management. The implications of a diagnosis of silent ischemia in a previously “healthy” patient are far-reaching and extend beyond the medical realm into psychologic, emotional and socioeconomic areas.

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The greater incidence of anginal attacks in the morning hours may be indirect evidence of increased coronary artery tone. The sympathetic stimulation that takes place upon awakening and arising is an important mediator of the increase in blood pressure, heart and myocardial contractil­ity which occur in the morning causing an increase in oxygen consumption and changes in vasomotor tone.

Added factors in the etiology of painful and painless episodes are the transient alterations in coronary blood flow (inadequate supply), in contrast to a disproportionate in­crease in myocardial demand. Since approximately 75 per­cent of plaques are eccentric and pliable, the “free” vessel wall devoid of rigid atheromata experience changes in tone and contractility adding a dynamic component to a stable flow limiting lesion.

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1. d. local (cellular) metabolic changes e. decreased left ventricular compliance c. decreased left ventricular contractility b. increased left ventricular end-diastolic pressure a. electrocardiographic changes f angina.

The temporal sequence of events that characterize an ischemic cardiac episode is best described as a “cascade” of abnormalities which begins at a cellular level and amplifies its consequences to create regional tissue changes and eventually leads to organ dysfunction.

Interruption of adequate oxygen and fuel supply to a high metabolically active myocardial muscle fiber results in disruption of the energy dependent processes of relaxation and contraction. Local wall motion abnormalities occur within seconds following coronary occlusion. Impaired seg­mental diastolic and systolic functions are associated with metabolic changes which are more evident within 30-60 seconds. Changes in left ventricular function occur next, followed by electrocardiographic changes. Pain, when pres­ent, is a relatively late manifestation of coronary ischemia. As a general rule, for any given episode of myocardial ischemia, significant impairment of myocardial function is present before the pain mechanism is activated.

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CASE 2

A 66-year-old woman with a history of atherosclerotic heart disease, adult onset diabetes mellitus and hy­pertension presented for a scheduled follow-up visit. She gave a history of rare episodes of stable exertional angina. Her therapeutic regimen included glyburide, hydrochloro­thiazide, low salt, calorie restricted ADA diet and sublingual nitrates. During the preceding three months she required nitrates sporadically. Nonetheless, on certain occasions, predominantly during the morning hours, two nitroglycerin tablets were necessary to relieve her painful symptoms. No new or associated complaints were reported during these episodes. The last anginal attack occurred one week prior to her visit.

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