"Typical" Q-wave infarction is manifested by prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event. Onset of infarction occurs often in the early morning hours, presumably in part because of the in-creased catecholamine-induced platelet aggregation and dimin-ished plasma concentrations of PAI-I after awakening. Onset is generally not directly associated with severe exertion.

Typical pain is intense, severe, unremitting for 30 to 60 minutes, crushing or squeezing in nature, retrosternal, and of-ten radiating down the ulnar aspect of left arm and into the neck, teeth, or jaw. Occasionally the pain is epigastric. Di-aphoresis, weakness, a sense of impending doom, profound restlessness, confusion, presyncope, hiccuping(presumably re-flecting irritation of the diaphragm), nausea and vomiting, and palpitations are common. Decreased systolic ventricular performance accounts for impaired perfusion of vital of vital or-gans and reflexly mediated compensatory responses to hypoten-sion such as restlessness and impaired mentation, pallor, cuta-neous vasoconstriction and sweating, tachycardia, and prerenal failure. Impaired left ventricular diastolic function leads to pul-monary vascular congestion with shortness of breath and tachypnea and pulmonary edema with orthophea. Impaired right ventricular diastolic function leads to systemic venous hy-pertension, edema, hepatomegaly, and further compromise of left ventricular cardiac output.

Myocardial infarction may be clinically silent (in as many as 1 per cent of patients), with the diagnosis established only retrospectively by ECG criteria. The patient may recall only an episode of "indigestion" or nothing. Stoicism, an unusually high pain threshold, disorders impairing function of the ner-vous system such as diabetes mellitus, or obtundation caused by medications or impaired cerebral perfusion may prevent recognition of typical chest pain.

Physical Findincs Typical of Acute Myocar-dial Infarc-tion.

Typical clinical findings can be summarized as follows:

General Appearance Pallor, diaphoresis, and restless-ness are present.

Vital Signs Heart rate is often increased secondary to sympathoadrenal discharge, ventricular ectopy, accelerated id-ioventric ular rhythm, ventricular tachycardia, atrial fibrilla-tion or flutter, or other supraventricular arrhythmias, especial-ly when atrial infarction or heart failure is present. Brad-yarrhythmias attributable to impaired sinus node function, AV nodal block, or infranodal block may be evident. The blood pressure is generally elevated initially with arterial vasocon-striction, in contrast to the case with acute pulmonary em-bolism, in which initial hypotension is frequent. However, with right ventricular infarction or severe left ventricular dys-function, hypotension occurs, The respiratory rate is usually increased in response to pulmonary congestion. Coughing, wheezing, and production of frothy sputum may occur. Fever is usually present within 24 to 48 hours and may exceed 39¡ãC.

Funduscopic Examination Manifestations of atheroselerotic vascular disease including copper wiring of arterioles, of hyperten-sion with arterial narrowing and hemorrhages, or of conditions predisposing to atherosclerosis such as diabetes with microa-neurysms may be seen, Funduscopic examination is particular-ly important to detect hemorrhage, which is a relative con-traindication to treatment with fibrinolytic agents.

Arterial and Venous Pulses Pulsus alternans, although rare, may reflect impaired left ventricular function, as may brevity of the carotid pulse secondary to decreased stroke volume, Jugular venous distention may accompany right ven-tricular infarction or right ventricular failure secondary to pro-found left ventricular dysfunction and pulmonary hyperten-sion.

Chest Rales secondary to pulmonary venous hyperten-sion are common with extensive left ventricular infarction; pleural effusions occur generally only with biventricular fail-ure.

Heart Lateral displacement of the apex impulse, dyski-nesis, a palpable $4, and a soft S1 may be indicative of dimin-ished contractility of the compromised left ventricle;paradoxi-cal split ring of S2 may reflect left bundle branch block or pro-longation of the pre-ejection period with delayed aortic valve closure despite decreased stroke volume;accentuated $4 and S may reflect diminished left ventricular complianee;a mitral re-gurgitation murmur indicative of either papillary muscle dys-function or rupture of annulus dilatation may be audible even if cardiac output is diminished markedly; a pericardial friction rub may be evident, premature ventricular beats, brief runs of ventricular tuchycardia, or accelerated idioventricular rhythm are common.

Abdomen Hepatojugular reflux may be elicited even when hepatomegaly is not marked

Extremities Peripheral cyanosis, edema, and pallor may indicate vasoconstriction, and diminished cardiac output may reflect right ventricular dysfunction or failure.

Neurologic Findings Patients with acute myocardial in-farction are prone to frank cerebrovascular insults as a result of ventricular mural thrombi and consequent embolization(with an incidence of approximately 1 per cent). Recrudescence of signs or symptoms of a prior cerebrovascular accident may oc-cur secondary to diminished cerebral perfusion. In contrast, the incidence of myocardial infarction in patients with cere-brovascular accidents in substantial.

The incidence of myocardial infarction appears to be greater and its prognosis worse in patients with depression. In-farction may precipitate reactive depression whether or not a drenergic blocking agents or other central nervous system (CNS)-active agents are administered.

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