增强型体外反搏改善慢性稳定性心绞痛患者外周动脉血流介导的舒张功能：一项随机假手术对照研究。
Enhanced external counterpulsation improves peripheral artery flow-mediated dilation in patients with chronic angina: a randomized sham-controlled study.
机构信息
Department of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL 32611, USA.
出版信息
Circulation. 2010 Oct 19;122(16):1612-20. doi: 10.1161/CIRCULATIONAHA.109.923482. Epub 2010 Oct 4.
BACKGROUND
Mechanisms responsible for anti-ischemic benefits of enhanced external counterpulsation (EECP) remain unknown. This was the first randomized sham-controlled study to investigate the extracardiac effects of EECP on peripheral artery flow-mediated dilation.
METHODS AND RESULTS
Forty-two symptomatic patients with coronary artery disease were randomized (2:1 ratio) to thirty-five 1-hour sessions of either EECP (n=28) or sham EECP (n=14). Flow-mediated dilation of the brachial and femoral arteries was performed with the use of ultrasound. Plasma levels of nitrate and nitrite, 6-keto-prostaglandin F(1α), endothelin-1, asymmetrical dimethylarginine, tumor necrosis factor-α, monocyte chemoattractant protein-1, soluble vascular cell adhesion molecule, high-sensitivity C-reactive protein, and 8-isoprostane were measured. EECP increased brachial (+51% versus +2%) and femoral (+30% versus +3%) artery flow-mediated dilation, the nitric oxide turnover/production markers nitrate and nitrite (+36% versus +2%), and 6-keto-prostaglandin F(1α) (+71% versus +1%), whereas it decreased endothelin-1 (-25% versus +5%) and the nitric oxide synthase inhibitor asymmetrical dimethylarginine (-28% versus +0.2%) in treatment versus sham groups, respectively (all P<0.05). EECP decreased the proinflammatory cytokines tumor necrosis factor-α (-16% versus +12%), monocyte chemoattractant protein-1 (-13% versus +0.2%), soluble vascular cell adhesion molecule-1 (-6% versus +1%), high-sensitivity C-reactive protein (-32% versus +5%), and the lipid peroxidation marker 8-isoprostane (-21% versus +1.3%) in treatment versus sham groups, respectively (all P<0.05). EECP reduced angina classification (-62% versus 0%; P<0.001) in treatment versus sham groups, respectively.
CONCLUSIONS
Our findings provide novel mechanistic evidence that EECP has a beneficial effect on peripheral artery flow-mediated dilation and endothelial-derived vasoactive agents in patients with symptomatic coronary artery disease.
背景
增强型体外反搏（EECP）抗缺血的机制尚不清楚。这是第一项随机假对照研究，旨在调查 EECP 对周围动脉血流介导的扩张的心脏外效应。
方法和结果
42 例有症状的冠心病患者按 2:1 的比例随机分为 EECP 组（n=28）或假 EECP 组（n=14），各接受 35 次 1 小时的治疗。使用超声检测肱动脉和股动脉的血流介导的扩张。测量血浆硝酸盐和亚硝酸盐、6-酮-前列腺素 F1α、内皮素-1、非对称二甲基精氨酸、肿瘤坏死因子-α、单核细胞趋化蛋白-1、可溶性血管细胞黏附分子、高敏 C 反应蛋白和 8-异前列腺素的水平。EECP 增加肱动脉（+51% vs +2%）和股动脉（+30% vs +3%）血流介导的扩张，一氧化氮转化/产生标志物硝酸盐和亚硝酸盐（+36% vs +2%）和 6-酮-前列腺素 F1α（+71% vs +1%），而内皮素-1（-25% vs +5%）和一氧化氮合酶抑制剂非对称二甲基精氨酸（-28% vs +0.2%）分别减少（所有 P<0.05）。EECP 降低促炎细胞因子肿瘤坏死因子-α（-16% vs +12%）、单核细胞趋化蛋白-1（-13% vs +0.2%）、可溶性血管细胞黏附分子-1（-6% vs +1%）、高敏 C 反应蛋白（-32% vs +5%）和脂质过氧化标记物 8-异前列腺素（-21% vs +1.3%）（所有 P<0.05）。EECP 分别减少治疗组和对照组的心绞痛分级（-62% vs 0%；P<0.001）。
结论
我们的研究结果提供了新的机制证据，表明 EECP 对有症状的冠心病患者的周围动脉血流介导的扩张和内皮衍生的血管活性物质有有益作用。
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