Endocardial alterations in myocardial infarction

Abstract

Transmural infarcts of the ventrolateral wall of canine left ventricle were produced by ligation of the ventral interventricular (anterior descending) branch of the left coronary artery. Endocardium from these infarcted hearts was sampled at sites corresponding to the infarct center and periphery, and to uninfarcted (normal) area at 24 and 48 hours after ligation, and examined by correlative scanning and transmission electron microscopy and by light microscopy. Endocardial samples from sham-ligated hearts were included as a further control. Striking alterations were observed in the endocardium that lined infarcted myocardium. There was endothelial desquamation coextensive with leukocytic invasion. Leukocytes appeared to initiate sloughing by separating the endothelial cells from their basal lamina and partially from one another. The latter cells desquamated in sheets, leaving behind a denuded basal lamina. Although altered in form, the individual endothelial cells seemed to remain largely intact. Denuded subendothelial surfaces only rarely contained thrombi. In areas where the cardiac endothelium was altered, the subjacent subendocardium, myocardium, and usually the remainder of the endocardium also showed leukocytic exudate. Samples from uninfarcted regions showed an intact, leukocyte-free endocardium, as did the sham-ligated controls. The appearance of abnormal endocardium was qualitatively similar wherever found, whether in different areas of the same heart or from one heart to another, and regardless of age of infarct. In 48-hour infarcts, almost all of the central and most of the peripheral samples exhibited the changes described. The data suggested a similar pattern for hearts with 24-hour infarcts. By locating biopsy sites in frozen cardiac sections processed for histologic staining and 201-thallium autoradiography, the electron microscopy results were shown to correlate with the intramural histopathologic topography of the infarcts. The alterations described here represent the endocardial manifestation of the inflammatory stage of transmural infarcts, known to be well developed in 1- and 2-day-old lesions.