Dupouy P, Geschwind H, Pelle G, Aptecar E, Hittinger L, El Ghalid A, Dubois-Randé J L
Unité de Recherche U.400 de 1'Institut National de la Santé et de la Recherche Médicale, Créteil, France.
J Am Coll Cardiol. 1996 May;27(6):1374-80. doi: 10.1016/0735-1097(96)00029-0.
The purpose of the present study was to assess whether brief, repeated coronary artery occlusions during balloon angioplasty induce a myocardial ischemic protective effect.
In animals, brief coronary artery occlusions preceding a more prolonged occlusion result in reduced infarct size. Whether myocardial protection against ischemia could also occur in humans during angioplasty remains controversial.
Thirteen patients with a proximal left anterior descending coronary artery stenosis with no angiographic collateral circulation underwent percutaneous transluminal coronary artery balloon angioplasty. Three 120-s balloon inflations separated by a 5-min equilibration period were performed. For each inflation, intracoronary ST segment modifications, septal wall thickening (M-mode echocardiography), left ventricular pressures and time derivatives were measured at baseline and at 30, 60 and 90 s after balloon inflation and 120 s after balloon deflation.
Intracoronary electrocardiographic analysis showed that the time course of the maximal ST segment elevation was identical at each inflation, as were wall motion changes assessed by the decrease in septal wall thickening. For the first and last inflations, peak positive dP/dt decreased significantly by 13 +/- 9% (mean +/- SD) and 14 +/- 13%, whereas peak negative dP/dt increased by 23 +/- 15% and 22 +/- 10%, respectively (all p < 0.01 from baseline values). The relaxation time constant, tau, was altered similarly during the different inflations, from 44 +/- 6 to 74 +/- 13 ms and from 57 +/- 13 to 77 +/- 13 ms (all p < 0.001) for the first and last inflations, respectively. Left ventricular end-diastolic pressure increased to the same level after each inflation. In contrast to other hemodynamic variables, tau and left ventricular end-diastolic pressure did not return to baseline values in between the inflations, which may be due to myocardial stunning.
In patients with proximal left anterior descending coronary artery stenosis and no evidence of collateral circulation, brief periods of ischemia, such as those used during routine coronary balloon angioplasty, do not provide any protection against myocardial ischemia.
本研究旨在评估在球囊血管成形术期间短暂、反复的冠状动脉闭塞是否会诱导心肌缺血保护作用。
在动物实验中，在较长时间的冠状动脉闭塞之前进行短暂的冠状动脉闭塞可使梗死面积减小。在血管成形术期间人类是否也能发生针对缺血的心肌保护作用仍存在争议。
13例左前降支近端冠状动脉狭窄且无血管造影显示有侧支循环的患者接受了经皮腔内冠状动脉球囊血管成形术。进行了3次每次持续120秒的球囊充盈，每次充盈之间间隔5分钟的平衡期。对于每次充盈，在基线时以及球囊充盈后30、60和90秒以及球囊放气后120秒测量冠状动脉内ST段改变、室间隔壁增厚（M型超声心动图）、左心室压力和时间导数。
冠状动脉内心电图分析显示，每次充盈时最大ST段抬高的时间进程相同，通过室间隔壁增厚减少评估的壁运动变化也相同。对于第一次和最后一次充盈，峰值正向dP/dt分别显著降低13±9%（平均值±标准差）和14±13%，而峰值负向dP/dt分别增加23±15%和22±10%（与基线值相比均p<0.01）。在不同的充盈过程中，松弛时间常数tau的变化类似，第一次和最后一次充盈时分别从44±6毫秒变为74±13毫秒以及从57±13毫秒变为77±13毫秒（均p<0.001）。每次充盈后左心室舒张末期压力升高到相同水平。与其他血流动力学变量不同，tau和左心室舒张末期压力在充盈之间未恢复到基线值，这可能是由于心肌顿抑。
在左前降支近端冠状动脉狭窄且无侧支循环证据的患者中，短暂的缺血期，如常规冠状动脉球囊血管成形术期间所采用的，不能提供任何针对心肌缺血的保护作用。
