Myears D W, Nohara R, Abendschein D R, Saffitz J E, Sobel B E, Bergmann S R
Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110.
J Am Coll Cardiol. 1988 May;11(5):1078-86. doi: 10.1016/s0735-1097(98)90068-7.
Coronary thrombolysis in patients frequently unmasks high grade residual stenosis. To determine whether beneficial effects of reperfusion are compromised by critical residual coronary stenosis, 14 dogs were instrumented with an external left anterior descending coronary artery balloon occluder, Doppler flow probe and adjustable screw clamp. In eight of the dogs, critical stenosis (abolition of reactive hyperemia after a 20 s occlusion; 95.7 +/- 1.0% cross-sectional area reduction) was induced before occlusion and maintained. In the control group (n = 6), no stenosis was induced. Each dog was subjected to 2 h of myocardial ischemia followed by balloon deflation and 24 h of reperfusion. Myocardial blood flow assessed with microspheres was similar during balloon inflation in both groups and indicative of profound ischemia. Transmural blood flow to the reperfused zone assessed 1 min after balloon deflation was significantly greater in control dogs without residual stenosis (383% of normal compared with 120% of normal in dogs with stenosis) (p less than 0.01). Compromise of transmural flow persisted in dogs with stenosis (85% compared with 121% of normal in control dogs after 1 h, p less than 0.05; and 49% compared with 68% after 24 h of reperfusion, p less than 0.05). Diminution of subendocardial blood flow after reperfusion was particularly marked. The extent of infarction was greater in the heart of dogs with residual stenosis. Thus, residual critical coronary stenosis compromises nutritional perfusion and salvage of reperfused myocardium after recanalization. These observations underscore the need for prompt identification of patients with high grade residual stenosis early after coronary thrombolysis and the potential value of angioplasty or coronary surgery in selected patients soon after initial recanalization.
对患者进行冠状动脉溶栓时,常常会发现存在高度残余狭窄。为了确定严重的残余冠状动脉狭窄是否会削弱再灌注的有益效果,对14只犬进行了如下操作:在左前降支冠状动脉外置一个球囊封堵器、多普勒血流探头和可调节螺旋夹。其中8只犬在闭塞前诱发并维持严重狭窄(闭塞20秒后反应性充血消失;横截面积减少95.7±1.0%)。对照组(n = 6)未诱发狭窄。每只犬均经历2小时心肌缺血,随后球囊放气并进行24小时再灌注。两组在球囊充盈期间用微球评估的心肌血流量相似,表明存在严重缺血。球囊放气1分钟后评估的再灌注区透壁血流量,在无残余狭窄的对照犬中显著更高(为正常的383%,而有狭窄的犬为正常的120%)(p<0.01)。有狭窄的犬透壁血流受损持续存在(再灌注1小时后为正常的85%,而对照犬为121%,p<0.05;再灌注24小时后为49%,对照犬为68%,p<0.05)。再灌注后心内膜下血流量的减少尤为明显。有残余狭窄的犬心脏梗死范围更大。因此,残余严重冠状动脉狭窄会损害营养灌注以及再灌注心肌的挽救。这些观察结果强调了在冠状动脉溶栓后早期迅速识别高度残余狭窄患者的必要性,以及在初始再通后不久对选定患者进行血管成形术或冠状动脉手术的潜在价值。