title: Effect of the blood supply to the normal noninfarcted myocardium on the incidence and severity of early post-occlusion arrhythmias in dogs.
abstract: This work was initiated by the discrepancy existing between the traditional experimental infarction model with occlusion of one single major coronary artery in the otherwise healthy myocardium and the clinical situation in which two or more major coronary arteries are stenosed at the same time. A model mimicking this latter clinical situation was elaborated as follows: In anaesthetized, open-chest dogs the haemodynamic, electrophysiological and blood flow changes due to 5 min occlusion of the left anterior descending coronary artery (LAD) were studied in the absence and presence of a critical constriction of the left circumflex coronary artery (LCX). Control LAD occlusion resulted in enhanced ST-segment elevation and inhomogeneity of electrical activation, depressed left ventricular contractility (LVdP/dt) and local myocardial contractility, as well as in a decline of myocardial blood flow (MBF) in the ischaemic area supplied by LAD. These changes were accompanied by no or slight extrasystolic activity. In the presence of critical stenosis of LCX, occlusion of the LAD aggravated myocardial ischaemia, i.e. ST-segment elevation and diminution of MBF were more marked, mainly in the subepicardium of the ischaemic area. The incidence and severity of arrhythmias significantly increased. Even ventricular fibrillation occurred in one third of the animals, both during LAD occlusion and after its release. Thus, acute LAD occlusion in the presence of a stenosed LCX produced a more severe myocardial ischaemia associated with more severe arrhythmias than occlusion of LAD alone. This model is more relevant to the clinical situation in which multivessel coronary artery disease is common.
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D003326:Coronary Circulation; D004285:Dogs; D004562:Electrocardiography; D006439:Hemodynamics; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D014693:Ventricular Fibrillation / Q000503:physiopathology