Komaru T, Isoyama S, Sekiguchi N, Akai K, Shiba N, Yasuda S, Funakoshi M, Shirato K, Zuguchi M, Nozaki E, Nishioka O, Tamaki K
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
J Am Coll Cardiol. 1996 Jan;27(1):30-7. doi: 10.1016/0735-1097(95)00441-6.
This study sought to investigate the effect of coronary angioplasty on chronic hypoperfusion-induced endothelial dysfunction in patients with coronary heart disease.
The endothelium is an important component for organ flow regulation. Ischemia with or without reperfusion is known to cause endothelial dysfunction. We tested the hypothesis that chronic hypoperfusion impairs endothelial function in the angiographically normal coronary artery segment distal to stenosis and that the impairment by chronic hypoperfusion is reduced by coronary angioplasty.
In 13 patients with stable angina pectoris, substance P (10, 30 and 100 pmol) and nitroglycerin (200 micrograms) were sequentially infused into the coronary artery in a cumulative manner on the day after coronary angioplasty. In 10 of these patients, vascular responses to these agents were again investigated 3 months after angioplasty. Changes in vascular diameter were evaluated in vessels located proximal and distal to the target lesion, both of which were angiographically normal, by performing computer-assisted quantitative coronary angiography. In five patients, the transstenotic pressure gradient was also measured with a pressure sensor-mounted guide wire before angioplasty.
On the day after angioplasty, the magnitude of dilation by substance P in distal segments was significantly less than that in proximal segments and inversely correlated with the transstenotic pressure gradient (p < 0.05) and lesion stenosis (p < 0.05). There was no difference in nitroglycerin-induced vasodilation between the two vessel segment groups. Three months later, the impaired response to substance P in the distal segment was restored to normal.
We conclude that chronic hypoperfusion impairs endothelium-dependent dilation of coronary artery distal to critical stenosis in patients with ischemic heart disease and that coronary angioplasty ameliorates the endothelial dysfunction within 3 months.
本研究旨在探讨冠状动脉血管成形术对冠心病患者慢性低灌注所致内皮功能障碍的影响。
内皮是器官血流调节的重要组成部分。已知有或无再灌注的缺血会导致内皮功能障碍。我们检验了这样一个假设，即慢性低灌注会损害狭窄远端血管造影正常的冠状动脉节段的内皮功能，并且冠状动脉血管成形术可减轻慢性低灌注所致的损害。
对13例稳定型心绞痛患者，在冠状动脉血管成形术后次日，依次以累积方式向冠状动脉内注入P物质（10、30和100 pmol）和硝酸甘油（200微克）。其中10例患者在血管成形术后3个月再次研究这些药物的血管反应。通过计算机辅助定量冠状动脉造影，评估目标病变近端和远端血管造影正常的血管直径变化。对5例患者，在血管成形术前还使用带压力传感器的导丝测量跨狭窄压力梯度。
血管成形术后次日，远端节段P物质所致的扩张幅度明显小于近端节段，且与跨狭窄压力梯度（p<0.05）和病变狭窄程度（p<0.05）呈负相关。两组血管节段硝酸甘油诱导的血管扩张无差异。3个月后，远端节段对P物质受损的反应恢复正常。
我们得出结论，慢性低灌注会损害缺血性心脏病患者严重狭窄远端冠状动脉的内皮依赖性扩张，并且冠状动脉血管成形术可在3个月内改善内皮功能障碍。
