Vassanelli C, Menegatti G, Zanolla L, Molinari J, Zanotto G, Zardini P
Division of Cardiology, University of Verona, Italy.
Coron Artery Dis. 1994 Dec;5(12):979-86. doi: 10.1097/00019501-199412000-00004.
Abnormal endothelium-dependent vasomotion has frequently been observed early after coronary angioplasty. The aim of this study was to investigate endothelium-mediated coronary vasomotion caused by increasing intracoronary infusions of acetylcholine into epicardial coronary arteries 3-6 months after coronary angioplasty in patients without restenosis (50% luminal diameter reduction).
Intracoronary acetylcholine was infused during follow-up coronary angiography followed by an intracoronary bolus of 250 g nitroglycerin in 18 patients who had undergone successful angioplasty of 21 isolated coronary artery lesions. Using an automated edge-detection program, coronary artery measurements were performed in the proximal reference segment, in the proximal part of the angioplasty site, at the site of previous maximal stenosis, in the distal part of the angioplasty site, and in the distal reference segment.
In the segments of the coronary artery not manipulated by balloon catheter, acetylcholine did not produce significant luminal diameter changes (+2 +/- 23% in the proximal segment and -3 +/- 27% in the distal segment at 10(-4) mol/l). All the angioplasty vessel segments, excluding the proximal reference segments, showed an abnormal dose-related reactivity to the acetylcholine. Maximal vasoconstriction was observed at 10(-4) mol/l and was 4.9 +/- 11.1% in the proximal reference segment, 9.3 +/- 19.1% in the proximal angioplasty site (P = 0.0314), 20.3 +/- 24.1% at the site of previous maximal stenosis (P = 0.0005), 10.7 +/- 16.8% at the distal angioplasty site (P = 0.0098), and 9.3 +/- 14.1% in the distal reference segment (P = 0.0032). The maximal response of the angioplasty site to acetylcholine and to nitroglycerin did not correlate either with the time to follow-up or with the follow-up stenosis. Nitroglycerin-induced vasodilation was significant in all segments, but was lower in the lesion-related segments. Acetylcholine evoked the same effect on both the vessels that were manipulated and those that were not.
Three to 6 months after coronary angioplasty, endothelium-dependent vasodilation was impaired not only at the site of previous maximal stenosis, but also in segments directly injured by balloon inflation. In contrast, endothelium-independent vasodilation by nitroglycerin is maintained in all segments. These observations suggest that the endothelium is still functionally impaired in the area of balloon dilation.
冠状动脉血管成形术后早期常观察到内皮依赖性血管运动异常。本研究的目的是调查在冠状动脉血管成形术后3 - 6个月，对无再狭窄（管腔直径减少50%）的患者向心外膜冠状动脉内递增注入乙酰胆碱所引起的内皮介导的冠状动脉血管运动。
在18例成功对21处孤立冠状动脉病变进行血管成形术的患者的随访冠状动脉血管造影期间，向冠状动脉内注入乙酰胆碱，随后注入250μg硝酸甘油团注。使用自动边缘检测程序，在近端参考节段、血管成形术部位的近端、先前最大狭窄部位、血管成形术部位的远端以及远端参考节段进行冠状动脉测量。
在未被球囊导管操作的冠状动脉节段，乙酰胆碱未引起显著的管腔直径变化（在10⁻⁴mol/L时，近端节段为 +2 ± 23%，远端节段为 -3 ± 27%）。除近端参考节段外，所有血管成形术血管节段对乙酰胆碱均表现出异常的剂量相关反应性。在10⁻⁴mol/L时观察到最大血管收缩，在近端参考节段为4.9 ± 11.1%，在血管成形术近端部位为9.3 ± 19.1%（P = 0.0314），在先前最大狭窄部位为20.3 ± 24.1%（P = 0.0005），在血管成形术远端部位为10.7 ± 16.8%（P = 0.0098），在远端参考节段为9.3 ± 14.1%（P = 0.0032）。血管成形术部位对乙酰胆碱和硝酸甘油的最大反应与随访时间或随访时的狭窄程度均无相关性。硝酸甘油诱导的血管舒张在所有节段均显著，但在病变相关节段较低。乙酰胆碱对被操作和未被操作的血管产生相同的作用。
冠状动脉血管成形术后3至6个月，内皮依赖性血管舒张不仅在先前最大狭窄部位受损，而且在因球囊扩张直接受损的节段也受损。相比之下，硝酸甘油介导的非内皮依赖性血管舒张在所有节段均得以维持。这些观察结果表明，在球囊扩张区域内皮功能仍受损。
