Hanet C, Evrard P, Jacquet L, Goenen M, Robert A
Division of Cardiology, University of Louvain, Brussels, Belgium.
Circulation. 1993 Nov;88(5 Pt 2):II257-62.
Increasing blood flow through conduit arteries induces vasodilation through endothelium-dependent mechanisms. In humans, flow-mediated dilation of angiographically normal epicardial coronary arteries has been observed during tachycardia, this response being impaired in the presence of atherosclerosis.
To evaluate whether the endothelium-dependent physiological vasodilatory response of epicardial coronary arteries to tachycardia is preserved in heart transplant recipients, 22 patients with angiographically smooth coronary arteries were studied with quantitative angiography. A total of 14 patients had undergone cardiac transplantation more than 1 year (mean, 28 +/- 18 months) before the study, and 8 patients were nontransplant patients with atypical chest pain and normal exercise tests (control group). Angiograms of the left coronary artery were obtained on 35-mm cinefilms at 3-minute intervals in basal conditions, during pacing-induced tachycardia (150 beats per minute), and after intracoronary injection of 1.5 mg of isosorbide dinitrate. During tachycardia, the mean luminal diameter of the midsegment of the left anterior descending coronary artery increased by 8.9 +/- 6.1% from 2.64 +/- 0.56 to 2.88 +/- 0.62 mm (P < .001) in transplant recipients and by 7.5 +/- 5.0% from 2.37 +/- 0.54 to 2.53 +/- 0.50 mm (P < .025) in the control group (transplant vs control patients, NS). A further coronary dilation was observed in all patients after isosorbide dinitrate, up to 124.8 +/- 8.1% of basal lumen diameter in transplant recipients and up to 129.1 +/- 16.1% of basal diameter in the control group.
The vasodilator response of epicardial coronary arteries to tachycardia is preserved in heart transplant recipients. This suggests that the functional response of the endothelium to an increase in coronary blood flow remains normal in these patients.
通过传导动脉增加血流量可通过内皮依赖性机制诱导血管舒张。在人类中,心动过速期间已观察到造影正常的心外膜冠状动脉的血流介导的扩张,在存在动脉粥样硬化时这种反应受损。
为了评估心外膜冠状动脉对心动过速的内皮依赖性生理血管舒张反应在心脏移植受者中是否保留,对22例造影显示冠状动脉光滑的患者进行了定量血管造影研究。共有14例患者在研究前1年以上(平均28±18个月)接受了心脏移植,8例患者为非移植患者,有非典型胸痛且运动试验正常(对照组)。在基础状态下、起搏诱导的心动过速期间(每分钟150次心跳)以及冠状动脉内注射1.5毫克硝酸异山梨酯后,每隔3分钟在35毫米电影胶片上获取左冠状动脉的血管造影图像。在心动过速期间,心脏移植受者左前降支冠状动脉中段的平均管腔直径从2.64±0.56毫米增加到2.88±0.62毫米,增加了8.9±6.1%(P<.001),对照组从2.37±0.54毫米增加到2.53±0.50毫米,增加了7.5±5.0%(P<.025)(移植患者与对照患者相比,无显著性差异)。所有患者在注射硝酸异山梨酯后均观察到进一步的冠状动脉扩张,心脏移植受者可达基础管腔直径的124.8±8.1%,对照组可达基础直径的129.1±16.1%。
心脏移植受者心外膜冠状动脉对心动过速的血管舒张反应得以保留。这表明这些患者内皮对冠状动脉血流量增加的功能反应仍然正常。