Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in overall ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional stuctural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used. When new CK-MB isoenzyme elevation is used as the gold standard, an incidence of approximately 20% to 30% is found. Autopsy data from patients who have died after a recent infarction are also consistent with this latter range. The pathophysiologic mechanism of infarct extension has been suggested by angiographic and postmortem studies. Flow to the region supplied by the infarct-related coronary artery is restored to a level sufficient to preserve part of the myocardium within the risk region. This blood supply can be provided by antegrade flow through the infarct-related vessel established by thrombolysis or thrombus retraction, or by flow through collateral channels. Later reduction or cessation of flow caused by rethrombosis or by a change in coronary hemodynamics produces enough ischemia to cause further necrosis. This pattern may repeat several times. Patients with infarct extension have greater incidences of congestive heart failure, arrhythmias, cardiogenic shock, and death. Infarct extension by increasing the amount of transmural necrosis may also lead to infarct expansion and its attendant complications. A number of risk factors for infarct extension have been proposed, but early postinfarction angina is most predictive of high risk. Thus, patients with early postinfarction angina should be considered for early revascularization procedures. More general therapeutic approaches such as treatment with β-blockers, calcium channel blockers, and nitrates have not definitively been shown to be of value in patients of any risk category. Recurrent infarction, or reinfarction, is defined as a new myocardial infarction occurring after the acute hospital phase of an earlier myocardial infarction. The new event may occur in regions either adjacent to or remote from the initial myocardial infarction. As in patients with infarct expansion and infarct extension, patients with reinfarction have increased morbidity and mortality. The incidence of reinfarction found in most studies is between 10% and 20%. Patients with either recurrent angina or a positive exercise stress test are at an increased risk of reinfarction. As with the risk of first myocardial infarction, hypertension, smoking, and elevated serum cholesterol have been identified as risk factors for reinfarction. Patients undergoing noncardiac surgery within 6 months of myocardial infarction also have a higher risk of reinfarction. Prevention of reinfarction should be aimed at reduction of known risk factors. In selected patients, revascularization procedures may be useful in preventing reinfarction. Treatment with daily aspirin and β-blockers has been shown to reduce the incidence of reinfarction and should be considered as routine postinfarction treatment in those patients without contraindication to such therapy.
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May 1, 1989
S G Richardson + 5
Open Access
