Defining the anatomic perfusion bed of an occluded coronary artery and the region at risk to infarction: A comparative study in the baboon, pig and dog

To assess selectively the effectiveness of therapeutic interventions to reduce infarct size, it is important to assess both ultimate infarct size as well as the size of the region of myocardium at risk to infarction. The anatomically defined perfusion bed of an occluded artery has generally been assumed to be synonymous with the region at risk of infarction. This assumption was tested by delineating the anatomic perfusion bed of an occluded artery with microvascular dyes and by examining the relation of the anatomic perfusion bed to the region of acute ischemic injury. In 8 baboons, 12 pigs and 15 dogs a major branch of the left anterior descending or left circumflex coronary artery was occluded. At 2 and 30 minutes after occlusion the eplcardial area of ischemic injury was determined by epicardial S-T segment mapping. The boundary of epicardial S-T segment elevation was resolved to within 1 mm and marked directly on the ventricular surface. The heart was then excised and the perfusion bed of the occluded artery was delineated by either (1) injecting different colored silicone rubber microvascular dyes into the previously occluded artery as well as the adjacent perfusion beds (direct method), or (2) injecting dye only into the adjacent perfusion beds (defect method).

Serial cross-sections of the left ventricle from the direct and defect dye-perfused hearts in all three species showed the perfusion bed of the occluded artery to be readily demarcated. Microscopic examination demonstrated no evidence of capillary anastomoses and minimal inter-digitation of capillaries at the perfusion bed boundaries. In dye-perfused hearts, the baboon and the pig showed no evidence of precapillary anastomoses between perfusion beds; however, the dog demonstrated numerous epicardial collateral channels. The epicardial area of the anatomic perfusion bed correlated closely with the epicardial area of S-T segment elevation at 2 minutes after occlusion in the baboon (r = 0.97), pig (r = 0.99) and dog (r = 0.96). The epicardial area of S-T segment elevation did not change through the 30 minute period of occlusion in the baboon and the pig, but in the dog it showed a progressive and variable reduction reflecting the gradual recruitment of existing collateral channels from adjacent perfusion beds.

It is concluded that the techniques of direct and defect dye delineation accurately define the anatomic perfusion bed of an occluded coronary artery. This anatomic perfusion bed corresponds to the region of myocardium undergoing acute ischemic injury and hence the region at risk to infarction immediately after coronary occlusion in the three species studied.