CORONARY-ARTERY VASOCONSTRICTION ROUTINELY OCCURS AFTER PERCUTANEOUS TRANS-LUMINAL CORONARY ANGIOPLASTY - A QUANTITATIVE ARTERIOGRAPHIC ANALYSIS
CORONARY-ARTERY VASOCONSTRICTION ROUTINELY OCCURS AFTER PERCUTANEOUS TRANS-LUMINAL CORONARY ANGIOPLASTY - A QUANTITATIVE ARTERIOGRAPHIC ANALYSIS
复制标题
DOI：
10.1161/01.cir.78.6.1323
复制
发表时间：
1988-12-01
期刊：
影响因子：
37.8
通讯作者：
STADIUS, ML
中科院分区：
文献类型：
--
作者：
FISCHELL, TA;DERBY, G;STADIUS, ML
为了确定经皮冠状动脉腔内成形术 (PTCA) 是否通过拉伸和损伤（“麻痹”）动脉壁平滑肌来增加冠状动脉管腔直径，我们前瞻性地分析了 10 名患者在接受单纯单支血管 PTCA 后的前 30 分钟内自发变化，以及冠脉内硝酸甘油引起的节段冠状动脉直径变化。另外五名患者在整个手术过程中接受了静脉注射硝酸甘油，以确定硝酸甘油是否可以预防 PTCA 后的血管收缩。在研究时，所有患者均维持口服剂量的地尔硫卓和阿司匹林。在 PTCA 后 2、5、15 和 30 分钟进行冠状动脉造影，然后在 300 μg 静脉注射后 3 分钟进行冠状动脉造影。硝酸甘油。每次在以扩张段为中心、扩张段远端的冠状动脉段以及未用球囊导管或导丝操纵的对照血管中进行定量测量（计算机边缘检测）。 PTCA 后，在扩张节段和远端节段（10 例患者中的 10 例）观察到进行性血管收缩（定义为通过冠状动脉内注射硝酸甘油逆转的直径减小），但在对照节段中没有观察到。与 PTCA 术后 2 分钟和 5 分钟的血管收缩相比 (p < 0.001)，并与 30 分钟时的对照节段相比 (p < 0.005)，30 分钟扩张节段的血管收缩（平均 30±4%）具有统计学显着性。接受静脉注射硝酸甘油的 5 名患者在 PTCA 术后扩张段直径没有明显减小。总之，1）尽管使用阿司匹林和钙通道阻滞剂进行预处理，但 PTCA 后，在球囊扩张部位及其远端仍经常发生自发性冠状动脉收缩； 2) PTCA术后冠状动脉血管收缩可被冠状动脉内注射硝酸甘油迅速逆转，并且可以通过术中和术后持续静脉注射硝酸甘油来预防； 3）这些结果与PTCA通过动脉“麻痹”改善冠状动脉管腔尺寸的假设不相容； 4) 这些发现对于 PTCA 后血管突然闭合的病因学和预防具有重要意义。
To determine whether percutaneous transluminal coronary angioplasty (PTCA) increases coronary artery luminal dimensions by stretching and injuring ("paralyzing") the smooth muscle of the arterial wall, we prospectively analyzed spontaneous changes and then intracoronary nitroglycerin-induced changes in segmental coronary artery diameters during the first 30 minutes after uncomplicated single-vessel PTCA in 10 patients. Five additional patients received intravenous nitroglycerin throughout the procedure to determine whether nitroglycerin could prevent vasoconstriction after PTCA. All of the patients were maintained on oral doses of diltiazem and aspirin at the time of the study. Coronary arteriography was performed at 2, 5, 15, and 30 minutes after PTCA and then 3 minutes after 300 .mu.g i.c. nitroglycerin. Quantitative measurements (computerized edge-detection) were performed at each time, in coronary segments centered in the dilated segment, distal to the dilated segment, and in a control vessel not manipulated with the balloon catheter or guidewire. Progressive vasoconstriction (defined as a loss of diameter that was reversed by intracoronary nitroglycerin) was observed after PTCA in the dilated and distal segments (10 of 10 patients) but not in the control segment. The vasoconstriction in the dilated segment at 30 minutes (mean, 30 .+-. 4%) was statistically significant compared with vasoconstriction at 2 and 5 minutes after PTCA (p < 0.001) and compared with the control segment at 30 minutes (p < 0.005). There was no significant loss of diameter after PTCA in the dilated segment in the five patients who received intravenous nitroglycerin. In conclusion, 1) spontaneous coronary artery vasoconstriction after PTCA occurs routinely at and distal to the site of balloon dilatation despite pretreatment with aspirin and calcium channel blockers; 2) coronary artery vasocontriction after PTCA is rapidly reversed by intracoronary nitroglycerin and can be prevented by the continuous administration of intravenous nitroglycerin during and after the procedure; 3) these results are incompatible with the hypothesis that PTCA improves coronary luminal dimensions by arterial "paralysis"; and 4) these findings have implications concerning the etiology and prophylaxis of abrupt vessel closure after PTCA.