Significance of epicardial Q waves as an acute marker of myocardial necrosis in dogs.

This study examines the significance of epicardial Q waves as a marker of myocardial cell necrosis. Ischaemia was produced in dogs by two methods: coronary artery occlusion sustained for 24 h (Group 1) and occlusion for 1 h followed by reperfusion (Group 2). Q waves did not appear until after 3 h of sustained occlusion, but were present within 40 min of reperfusion. In both groups, Q waves were not transient but persisted for at least 24 h. CPK levels were determined at 24 h in specimens from each lead site. In Group 1, Q sites had 66.6 +/- 5.9% (mean +/- SEM) less CPK than R wave sites (P less than 0.005). In Group 2, Q sites had only 28.2 +/- 4.5% less CPK than R sites. These results suggest that the extent of necrosis was greater at Q sites with sustained occlusion than with reperfusion. A similar relationship existed for the levels of ATP and CP determined at Q and R sites at 24 h. Histological examination by light and electron microscopy confirmed that in both groups, Q sites corresponded to areas of necrosis, while R sites indicated normal myocardium. However, the type of necrosis depended on the pathogenesis. Our results demonstrated that epicardial Q waves were a reliable marker of cell death, but that the morphological picture and extent of cell death depended on the mechanism and manner of injury. These conclusions were tested in a final series (Group 3) in which propranolol was given before and with release of the occlusion (0.5 mg.kg-1 at each time). In 47 sites at risk, in five dogs only two Q waves appeared. In each of these two, cell death was confirmed by evidence of CPK depletion and morphological alteration. In the remaining sites, no CPK depletion occurred. Histological examination revealed only infrequent small islands of subendocardial necrosis. The results confirm the validity of the epicardial electrocardiographic findings and illustrate the role of propranolol in preventing reperfusion necrosis.