Vizir V A, Berezin A E
Klin Med (Mosk). 2000;78(7):36-9.
The aim of the study was to investigate the effect of angiotensin-converting enzyme inhibitor enalapril and non-peptide blocker of AT1 receptors losartan on endothelial function of the shoulder artery in patients with congestive cardiac insufficiency. The examination covered 96 patients (mean age 46.71 +/- 4.13) with stable effort angina (functional class II-III) and circulatory insufficiency (NYHA functional class II-III) having end-diastolic left-ventricular volume > 160 ml, left ventricular ejection fraction < 35%, sinus rhythm, cardiothoracal index > 0.55 units. Patients with fibrillar tachyarrhythmia, high grade blocks, pacemaker migration, artificial pacemaker, myocardial infarction were not included in the trial. The patients were randomized into 3 groups 32 patients each. In addition to basic therapy patients of group 1 received long-acting nitrates, digoxin, aspirin and furosemide; group 2--enalapril in daily dose 10 mg; group 3--losartan in daily dose 25 mg. A course of treatment lasted 12 weeks. Endothelial function was assessed by high resolution echography, dopplerography performed before and after temporary occlusion of the shoulder artery and sublingual nitroglycerin. In patients with cardiac insufficiency, accelerated blood flow in the shoulder artery after its temporary occlusion promoted realization of the vasoconstrictory reaction. This was verified as endothelial dysfunction. In the course of the treatment all the patients achieved insignificant increase of the shoulder artery initial diameter. After sublingual intake of nitroglycerin vasodilation was also insignificant. 12-week enalapril and losartan prevented vasoconstriction in the shoulder artery in response to quicker circulation following arterial occlusion. However, higher maximal flow speed did not correspond to the increment in the artery diameter after the occlusion in any group. The flow-induced vasodilation was more pronounced in the enalapril group. Losartan group had a trend to an increase in the inner diameter of the shoulder artery. It is shown that enalapril and losartan in congestive cardiac insufficiency improves endothelium-dependent vasodilation caused by nitroglycerin. Enalapril demonstrated stronger ability than losartan to reverse endothelial dysfunction in patients with cardiac insufficiency resultant from ischemic heart disease.
本研究旨在探讨血管紧张素转换酶抑制剂依那普利和AT1受体非肽类阻滞剂氯沙坦对充血性心力衰竭患者肱动脉内皮功能的影响。研究对象为96例（平均年龄46.71±4.13岁）稳定性劳力型心绞痛（心功能Ⅱ-Ⅲ级）和循环功能不全（纽约心脏病协会心功能Ⅱ-Ⅲ级）患者，其左心室舒张末期容积>160ml，左心室射血分数<35%，窦性心律，心胸指数>0.55单位。有室性快速心律失常、高度房室传导阻滞、起搏器移位、人工起搏器、心肌梗死的患者未纳入试验。患者被随机分为3组，每组32例。除基础治疗外，第1组患者接受长效硝酸盐、地高辛、阿司匹林和呋塞米治疗；第2组患者每日服用10mg依那普利；第3组患者每日服用25mg氯沙坦。疗程持续12周。通过高分辨率超声心动图、肱动脉临时阻断前后及舌下含服硝酸甘油后的多普勒超声评估内皮功能。在心力衰竭患者中，肱动脉临时阻断后血流加速促进了血管收缩反应的发生。这被证实为内皮功能障碍。在治疗过程中，所有患者肱动脉初始直径均有轻微增加。舌下含服硝酸甘油后血管舒张也不明显。12周的依那普利和氯沙坦治疗可预防肱动脉因动脉阻断后循环加快而出现的血管收缩。然而，任何一组中较高的最大流速均与阻断后动脉直径的增加不相符。依那普利组中血流诱导的血管舒张更为明显。氯沙坦组肱动脉内径有增加趋势。结果表明，依那普利和氯沙坦可改善充血性心力衰竭患者中由硝酸甘油引起的内皮依赖性血管舒张。在因缺血性心脏病导致心力衰竭的患者中，依那普利逆转内皮功能障碍的能力比氯沙坦更强。
