Zeiher A M, Schächinger V, Weitzel S H, Wollschläger H, Just H
Department of Cardiology, University of Freiburg, FRG.
Circulation. 1991 May;83(5):1519-25. doi: 10.1161/01.cir.83.5.1519.
Experimental studies have demonstrated that intracoronary platelet aggregation and thrombus formation may induce marked vasoconstriction of epicardial arteries with endothelial injury.
To examine the effects of intracoronary thrombus formation on coronary vasomotor tone of human epicardial arteries in vivo, we studied 15 patients who developed intracoronary thrombi adherent to the guide wire during balloon dilatation. Epicardial artery luminal area was evaluated by quantitative coronary angiography proximal and distal to the site of intracoronary thrombus formation and in a reference vessel before and after thrombus formation as well as after intracoronary injection of 0.2-0.3 mg nitroglycerin. All artery segments distal to the site of thrombus formation showed vasoconstriction with a luminal area reduction of -27.4 +/- 17.1% (p less than 0.001), whereas proximal vessel segments and reference vessels not manipulated during percutaneous transluminal coronary angioplasty did not demonstrate any significant luminal area changes during thrombus formation. Angiographic measurements after advancing the guide wire with the adherent thrombus (performed in six of the 15 patients) revealed in all patients that vasoconstriction did develop at a new site distal to the thrombus persistence of the initial vasoconstriction now residing proximal to the thrombus. Thus, there was a sequential association between thrombus formation and subsequent distal vasoconstriction. Intracoronary injection of nitroglycerin abolished the thrombus-induced vasoconstriction. No significant luminal area changes were observed in 20 patients without angiographic evidence of intracoronary thrombus formation.
Intracoronary thrombus formation during percutaneous transluminal coronary angioplasty causes focal vasoconstriction of epicardial arteries in patients with coronary artery disease. Although caution must be advised in the extrapolation of this phenomenon, which was observed in a manipulated artery during coronary angioplasty, the vasoconstrictor response to intracoronary thrombus formation in vivo may play an important role in the dynamic mechanisms of acute coronary heart disease syndromes.
实验研究表明，冠状动脉内血小板聚集和血栓形成可导致伴有内皮损伤的心外膜动脉显著血管收缩。
为了研究冠状动脉内血栓形成对人体心外膜动脉血管舒缩张力的影响，我们对15例在球囊扩张过程中导丝上形成冠状动脉内血栓的患者进行了研究。通过定量冠状动脉造影评估冠状动脉内血栓形成部位近端和远端的心外膜动脉管腔面积，以及在血栓形成前、形成后以及冠状动脉内注射0.2 - 0.3mg硝酸甘油后在参照血管中的管腔面积。所有血栓形成部位远端的动脉节段均出现血管收缩，管腔面积减少-27.4±17.1%（p<0.001），而经皮腔内冠状动脉成形术期间未操作的近端血管节段和参照血管在血栓形成过程中未显示任何显著的管腔面积变化。在15例患者中的6例推进带有附着血栓的导丝后进行血管造影测量，结果显示所有患者在血栓远端的新部位均出现血管收缩，初始血管收缩现位于血栓近端。因此，血栓形成与随后的远端血管收缩之间存在相继关联。冠状动脉内注射硝酸甘油可消除血栓诱导的血管收缩。在20例无冠状动脉内血栓形成血管造影证据的患者中未观察到显著的管腔面积变化。
经皮腔内冠状动脉成形术期间冠状动脉内血栓形成可导致冠心病患者的心外膜动脉局部血管收缩。尽管在推断这一在冠状动脉成形术期间操作的动脉中观察到的现象时必须谨慎，但体内对冠状动脉内血栓形成的血管收缩反应可能在急性冠心病综合征的动态机制中起重要作用。
