Endocardial injury and the pathogenesis of mural thrombosis in the left ventricle.

To define the interactions between blood and endocardium damaged by lactic acid, the left ventricles of 48 isolated continuously perfused and beating hearts were exposed for 0-4 hours to Krebs Henseleit buffer (KHB) with or without 33 mumol.ml-1 of lactic acid (pH 6.4). After excising its apex, the left ventricle was flushed with KHB, followed by 10 ml of lightly heparinised blood, and then by a further 10 ml of KHB. Lactic acid caused endothelial cell membrane rupture, intercellular separation, and exfoliation with exposure of the basal lamina and underlying connective tissue. Whereas multilayered platelet aggregations formed on exposed basal lamina, fibrin deposition and incorporation of blood cells were only observed in the larger thrombi which formed on exposed collagen. These findings indicate that a metabolite which accumulates in ischaemic myocardium can cause endocardial injury which would predispose to the mural thrombosis which can complicate myocardial infarction.