抄録
In order to study the effects of residual stenosis on myocardial salvage, we created 99% coronary stenosis with or without contrast washout delay at reperfusion in six groups of dogs. In Group A (n=8), the artery was occluded for 1h before being fully reperfused. In Group B (n=9), the artery was occluded for 1h, then subjected to 6h of 99% stenosis without contrast washout delay. In Group C (n=8), the artery was occluded for 1h, followed by 1 week of 99% stenosis without contrast washout delay. In Group D (n=10). again the artery was occluded for 1h, then subjected to 6h of 99% stenosis with contrast washout delay. In Group E (n=8). the artery was occluded for 7h, then fully reperfused for 1 week. Finally, in Group F (n=8). the occlusion lasted for a full week. All dogs were sacrificed 1 week after occlusion. In Group A, myocardial creatine phosphokinase activity (CK) in the inner layer was 43.8±12.5% that of non-infarcted myocardium. Myocardial CK in Group B (46.5±7.4%) was little different but in Group C it dropped to 26.6±8.4%, suggesting that 99% residual stenosis is not deleterious if it is continued for 6h or less but that it will result in considerable depletion of myocardial CK, if it is sustained for 1 week. In Group D, myocardial CK dropped markedly to 11.3±3.7%, little different from that for either Group E (13.3±2.6%) or Group F (9.3±3.3%). This suggests that contrast washout de-lay following 99% stenosis is not beneficial to myocardial salvage. Infarct size, as determined using triphenyl tetrazolium chloride as a stain was smallest for Group A (6.8±3.6%) and largest for Group F (62.6±9.8%). Group B showed smaller infarct size (13.2±3.7%) than did either Group D (27.0±5.5%) or Group E (25.3±6.3%). From this. we came to the conclusion that 99% residual stenosis without contrast washout delay is not deleterious provided it is sustained for 6h or less.
