WAVEFRONT PHENOMENON OF MYOCARDIAL ISCHEMIC CELL-DEATH .2. TRANSMURAL PROGRESSION OF NECROSIS WITHIN THE FRAMEWORK OF ISCHEMIC BED SIZE (MYOCARDIUM AT RISK) AND COLLATERAL FLOW

  • 1 January 1979
    • journal article
    • research article
    • Vol. 40  (6) , 633-644
Abstract
The evolution of myocardial ischemic cell death within the framework of the anatomical boundaries of the ischemic bed at risk and the magnitude and transmural distribution of collateral blood flow was quantitated. Myocardial ischemia was produced by proximal left circumflex coronary artery (LCC) occlusions in open-chest dogs. Infarcts reprefused at 40 min, 3 h or 6 h were compared with permanent infarcts. All dogs were sacrificed at 4 days. Re8ional myocardial blood flow was measured with 9 .mu.m tracer microspheres before, and 20 min after, LCC occlusion. The location and size of the ischemic LCC bed at risk was determined by a dye injection technique. Infarct size was quantitated from serial histologic sections. Necrosis involved 28, 70 and 72% of the ischemic bed at risk in infarcts reprefused at 40 min, 3 h and 6 h, respectively vs. 79% following permanent LCC ligation. Viable and potentially salvageable subepicardial muscle persisted for at least 3 h after the onset of ischemia. Most of the salvageable myocardium was in the subepicardium. In all groups, the lateral borders necrosis were sharp in the subendocardial zone and were determined by the anatomical boundaries of the ischemic LCC bed at risk. LCC bed size ranged from 29-48% of the left ventricle and contributed to variation in infarct size. Infarct size, as a percentage of bed size, was determined by the transmural extent of necrosis within that bed (r [correlation coefficient] = -0.97). This transmural extent of necrosis was related to subepicardial collateral flow after 3 h (r = 0.92) and 6 or 96 h (r = 0.85) but not after 40 min (r = 0.26) of ischemia. Irreversible injury of ischemic myocardium developed as a transmural wavefront, occurring 1st in the subendocardial myocardium but ultimately becoming nearly transmural. Eventual transmural necrosis and overall infarct size were determined by, and can be predicted from, flow measurements obtained shortly after coronary occlusion.