Reversible and irreversible changes in the dog heart during acute left ventricular failure due to experimental multifocal ischaemia.

Acute left ventricular (LV) failure was induced in closed-chest pentobarbital anaesthetized dogs (n = 15), by injection of 50 micron plastic microspheres into the main left coronary artery. There were marked reductions of cardiac output and peak LV dp/dt after the embolization, while LV end-diastolic pressure (LVEDP) increased markedly. Biopsies were taken 1, 2, 3, 4, 6, 8, 10, 36, 48 hours, 7 and 14 days after injection of microspheres. Histological examination of the left ventricle revealed multiple ischaemic lesions distributed throughout the are supplied by the left main coronary artery. Oilred O staining revealed deposition of fine lipid droplets in the ischaemic cardiac muscle cells bordering on the necrotic areas. Ultrastructurally the lipid-containing cells showed numerous vacuoles localized in association with the mitochondria. The vacuoles could be observed already 1 hour after embolization and increased in number up to 48 hours. At the end of the observation period at two weeks, the number of lipid droplets was markedly reduced and the heart regained its functional activity. It is concluded that the myocardial lesions induced by coronary embolization of plastic microspheres were associated with acute left ventricular pump failure and consist of multiple foci of damaged myocardium with a central core of necrotic tissue. In the periphery of these lesions there were myocytes with lipids and other signs of light and moderate ischaemic injury. Our suggestion is that these cells represent a region of intermediate injury of "border zone" cells that are a potentially salvageable myocardium.