ENDOTHELIUM-DEPENDENT DILATION OF THE CORONARY MICROVASCULATURE IS IMPAIRED IN DILATED CARDIOMYOPATHY
ENDOTHELIUM-DEPENDENT DILATION OF THE CORONARY MICROVASCULATURE IS IMPAIRED IN DILATED CARDIOMYOPATHY
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DOI：
10.1161/01.cir.81.3.772
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发表时间：
1990-03-01
期刊：
影响因子：
37.8
通讯作者：
GANZ, P
中科院分区：
文献类型：
--
作者：
TREASURE, CB;VITA, JA;GANZ, P
扩张型心肌病患者冠状动脉微血管的扩张储备减少。虽然血管外压力增加、心动过速和心肌质量增加可以解释某些损害，但最近的证据表明可能存在内在微血管疾病。我们检验了微血管内皮依赖性舒张功能受损可能是一种促成机制的假设。我们将内皮依赖性扩张剂乙酰胆碱（Ach）（10-8至10-6 M）和平滑肌血管扩张剂腺苷（AD）（10-6至10-4 M）注入8例扩张型心肌病患者（平均射血分数，28%）和7例对照（非典型胸痛）的冠状动脉左前降支。在恒定动脉压下，用多普勒速度导管（通过血管造影校正横截面积）测量冠状动脉血流（CBF），评估小血管阻力。对照组患者脑血流量增加232 s ±。40%（平均值±）SEM），而心肌病患者的CBF没有显著变化（41 . ±. 24%）（p < 0.0001，对照vs心肌病）。对于AD，对照组患者的CBF增加422 . ±. 56%，心肌病患者CBF增加268 ±。43%（p = 0.13）。通过标准化每个患者的Ach剂量反应至其最大AD血流反应，获得了归因于内皮依赖性血管舒张的冠状动脉血流储备比例的指数。在七个对照组患者接受乙酰胆碱和AD，56。用内皮依赖性血管扩张剂Ach获得最大AD血流反应的23 ± 9%，而在同时接受Ach和AD的7名心肌病患者中，仅获得23 ± 9%。最大AD反应达到14%（p < 0.01）。因此，扩张型心肌病患者的冠状动脉微血管内皮依赖性血管舒张功能受损。内皮功能障碍与心肌衰竭之间可能存在一定的病理联系。
Dilator reserve of the coronary microvasculature is diminished in patients with dilated cardiomyopathy. Although increased extravascular compressive forces, tachycardia, and increased myocardial mass can explain some impairment, recent evidence suggests the possibility of intrinsic microvascular disease. We tested the hypothesis that impairment of endothelium-dependent dilation of the microvasculature could be a contributing mechanism. We infused the endothelium-dependent dilator acetylcholine (Ach) (10-8 to 10-6 M) and the smooth muscle vasodilator adenosine (AD) (10-6 to 10-4 M) into the left anterior descending coronary artery in eight patients with dilated cardiomyopathy (mean ejection fraction, 28%) and seven controls (atypical chest pain). Small vessel resistance was assessed by measuring coronary blood flow (CBF) at constant arterial pressure with a Doppler velocity catheter (corrected for cross-sectional area by angiography). With Ach, control patients increased CBF 232s .+-. 40% (mean .+-. SEM), whereas CBF did not significantly change in cardiomyopathy patients (41 .+-. 24%) (p < 0.0001, control vs cardiomyopathy). With AD, control patients increased CBF 422 .+-. 56% and cardiomyopathy patients increased CBF 268 .+-. 43% (p = 0.13). An index of the proportion of coronary flow reserve attributable to endothelium-dependent vasodilation was obtained by standardizing each patient''s Ach dose response to his maximal AD flow response. In seven control patients receiving both Ach and AD, 56 .+-. 9% of the maximal AD flow response was attained with the endothelium-dependent vasodilator Ach, whereas in seven cardiomyopathy patients receiving both Ach and AD, only 23 .+-. 14% of the maximal AD response was attained (p < 0.01). Thus, endothelium-dependent vasodilator function is impaired in the corornary micorvasculature of patients with dilated cardiomyopathy. There might be pathogenetic links between dysfunction of the endothelium and myocardial failure.