Coronary Reperfusion for the Treatment of Acute Myocardial Infarction: Postischemic Ventricular Dysfunction

Abstract

There has been recent interest in treating acute myocardial infarction with coronary reperfusion by fibrinolytic therapy. Experimental studies have shown that myocardial infarct size can be reduced by coronary reperfusion. However, return of cardiac function, high energy phosphate metabolism, and cardiac ultrastructure may be delayed within tissue which is salvaged by coronary reperfusion. This postischemic ventricular dysfunction is transient and has been termed the ‘stunned myocardium’ phenomenon. Although reperfused infarcts are hemorrhagic, the hemorrhage is confined well within tissue which is already necrotic and does not appear to exacerbate the extent of necrosis. Clinical trials designed to assess the benefits of reperfusion for the therapy of acute myocardial infarction should concentrate on long-term rather than short-term changes in cardiac function.

Myocardial reperfusion: a double-edged sword?

“…Reimer et al (5) have reported that reperfusion-induced myocardial hemorrhage, as noted on gross inspection and histologic examination, was always confined to and never extended outside areas of myocardial cell necrosis. We have observed (24,30) that dogs subjected to a 2-h coronary occlusion followed by prolonged reperfusion usually had visible hemorrhage within the infarct, that the hemorrhage was smaller than the zone of myocardial necrosis, and that a nonhemorrhagic rim of infarcted tissue surrounded the zone of hemorrhage. Similar observations have been made in patients in whom reperfusion was carried out by thrombolysis or coronary bypass surgery (31 (35).…”

“…While this increase is dramatic in irreversibly injured cells, it may also be seen transiently and to a lesser extent in reversibly injured tissue (24,25). This so-called "explosive" cell swelling of irreversibly injured cells (26) appears to be caused by an ischemia-induced sarcolemmal abnormality which causes a serious defect in regulation of cell volume and which is associated with marked increases in tissue water, sodium, chloride, and calcium.…”

Clinicopathological Characteristics of Left Ventricular Myocardium with Transient Asynergy.

“…Experimental animal studies have extensively demonstrated the relationships between the duration of ischemia and severity of myocardial ischemic lesions and the histologic and ultrastructural findings of "stunned myocardium". [2][3][4][5][6][7][8] However, little is known about the histopathologic substrates of "stunned myocardium" in humans, because the prognosis in patients with "stunned myocardium" and its sequelae appears to be good in the absence of superimposed ischemic lesions or other severe medical illnesses.…”

“…or over in size were not found macroscopically in the transverse sections. In experimental studies, a majority of the hematoxylin-eosin-stained sections of "stunned myocardium" show normal or nearly normal light microscopic features, [2][3][4] or, rarely, two or three hypereosinophilic myocytes are noted mainly in the subendocardium. 4) In Case 1, however, histological sections showed scattered necrotic foci in the subendocardium and trabeculae of the jeopardized zone.…”

“…1) The histological characteristics of "stunned myocardium" have been addressed extensively in experimental animal studies, [2][3][4][5][6][7][8] however, there are few reports in humans. The aim of this study was to demonstrate the histopathological substrates of left ventricular myocardium with transient asynergy in patients detected by echocardiography.…”