O bstruction of a major branch of the left coronary artery in a previously normal ventricle is not usually associated with shock, experimentally or clinically. To examine the early hemodynamic alterations which may determine the course of ischemia when myocardial scar exists from previous infarction, 16 animals were successfully studied 9 wk after obstruction of the left circumflex artery. Acute ischemia during thrombus formation in the anterior descending artery of intact anesthetized dogs with scar was compared with animals undergoing the same procedure in the absence of scar (group 1). In the chronic animals, two types of hemodynamic responses were observed. Group 2 was characterized by heart failure usually persisting through 3 hr, and group 3 by a different ventricular volume response and rapidly developing shock. The weight of ischemic and scar areas were comparable and coronary blood flow (⁸⁵Kr method) to the ischemic site was reduced to a similar extent. Animals in groups 1 and 2 remained normotensive and had similar elevations of left ventricular enddiastolic volume (indicator dilution method) during the initial 60 min of ischemia. Group 2 had a significantly larger rise of end-diastolic pressure, presumably related to altered elastic properties associated with scar of subendocardial distribution.Group 3 had a stroke volume decline that was not significantly greater than group 2 and both groups had an initial rise of peripheral vascular resistance. Despite a nearly fourfold increase of left ventricular end-diastolic pressure, there was a significant decline of left ventricular end-diastolic volume in group 3. This preceded the onset of hypotension in group 3, with arterial pressure declining to a greater extent than stroke volume, usually culminating in cardiac standstill. Group 3 was distinguished by the presence of transmural scar, which was postulated to influence contiguous ischemic tissue in diastole so as to diminish ventricular volume. By analogy with the hemodynamics of acute pericardial tamponade, a reflex pathway activated in the myocardium in response to reduced end-diastolic volume has been suggested as a mechanism for the arterial hypotension.