Landesburg G, Zhou W, Aversano T
Department of Anesthesiology and Critical Care Medicine, Hebrew University-Hadassah Hospital, Jerusalem, Israel.
Anesth Analg. 1999 May;88(5):973-9. doi: 10.1097/00000539-199905000-00002.
It has been speculated but never proven that tachycardia-induced ischemia per se may lead to myocardial infarction. In 17 anesthetized dogs, the proximal left anterior descending (LAD) artery was cannulated and perfused via bypass from the left subclavian artery. Distal LAD pressure was reduced by a screw clamp to cause > or =20% decrease in wall thickening during pacing tachycardia but no decrease in resting heart rate (approximately 90 bpm). Dogs were randomly assigned to three groups: 1) control (n = 6) maintained at resting heart rate (approximately 90 bpm) and mean coronary pressure of 49+/-5 mm Hg for 4 h; 2) 4-h ischemia (n = 6), paced at 150 bpm and mean coronary pressure maintained at 59+/-6 mm Hg for 4 h; and 3) 1-h ischemia (n = 5), paced at 150 bpm and mean coronary pressure of 54+/-8 mm Hg for 1 h. Myocardial blood flow and infarct area were measured by radiolabeled microspheres and triphenyl-tetrazolium chloride staining, respectively. Despite the higher coronary pressure in the 4-h ischemia group (P = 0.02), patchy subendocardial necrosis occurred in all these dogs and in two of the 1-h ischemia dogs, and one control dog had minimal papillary muscle necrosis. Infarct area was largest in the 4-h ischemic group (15.5%+/-9.1%) compared with control and 1-h ischemia groups (0.09%+/-0.2% and 1.6%+/-2.1%, respectively) (P < 0.002). Relative (risk/ nonrisk areas) subendocardial flow was lower at the end of ischemia in the 4- and 1-h ischemia groups compared with the control group (0.3+/-0.1 and 0.4+/-0.1 vs 0.9+/-0.2; P = 0.008 and 0.01, respectively). Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to patchy subendocardial necrosis, despite anticoagulation and antiplatelet treatment.
Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to subendocardial infarction in dogs. These findings suggest a possible mechanism for postoperative myocardial infarction.
有人推测心动过速诱发的缺血本身可能导致心肌梗死，但从未得到证实。在17只麻醉犬中，通过左锁骨下动脉的旁路插管灌注左前降支（LAD）近端动脉。用螺旋夹降低LAD远端压力，使起搏心动过速时室壁增厚减少≥20%，但静息心率（约90次/分）无下降。犬被随机分为三组：1）对照组（n = 6），以静息心率（约90次/分）维持4小时，平均冠状动脉压力为49±5 mmHg；2）4小时缺血组（n = 6），以150次/分起搏，平均冠状动脉压力维持在59±6 mmHg 4小时；3）1小时缺血组（n = 5），以150次/分起搏，平均冠状动脉压力为54±8 mmHg 1小时。分别用放射性微球和氯化三苯基四氮唑染色测量心肌血流量和梗死面积。尽管4小时缺血组的冠状动脉压力较高（P = 0.02），但所有这些犬以及1小时缺血组的2只犬均出现斑片状心内膜下坏死，1只对照犬有轻微乳头肌坏死。与对照组和1小时缺血组相比（分别为0.09%±0.2%和1.6%±2.1%），4小时缺血组的梗死面积最大（15.5%±9.1%）（P < 0.002）。与对照组相比，4小时和1小时缺血组缺血结束时相对（危险/非危险区域）心内膜下血流较低（分别为0.3±0.1和0.4±0.1 vs 0.9±0.2；P = 0.008和0.01）。尽管进行了抗凝和抗血小板治疗，但在静息心率时无缺血的固定冠状动脉狭窄情况下，长时间心动过速诱发的缺血会导致斑片状心内膜下坏死。
在静息心率时无缺血的固定冠状动脉狭窄情况下，长时间心动过速诱发的缺血会导致犬心内膜下梗死。这些发现提示了术后心肌梗死的一种可能机制。
