Dilated Cardiomyopathy
Dilated Cardiomyopathy
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DOI：
10.1093/med/1.1.med-9780198520771-div1-289
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发表时间：
2005
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影响因子：
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通讯作者：
H. Schultheiss;D. Fairweather;A. Caforio;F. Escher;R. Hershberger;S. Lipshultz;Peter P. Liu;A. Matsumori;A. Mazzanti;J. Mcmurray;S. Priori
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作者：
H. Schultheiss;D. Fairweather;A. Caforio;F. Escher;R. Hershberger;S. Lipshultz;Peter P. Liu;A. Matsumori;A. Mazzanti;J. Mcmurray;S. Priori
扩张型心肌病患者冠状动脉微血管的扩张器储备减少。尽管血管外压力增加、心动过速和心肌质量增加可以解释一些损害，但最近的证据表明存在内在微血管疾病的可能性。我们验证了微血管内皮依赖性扩张功能受损可能是其作用机制的假说。对8例扩张型心肌病患者(平均射血分数为28%)和7例对照组(不典型胸痛)的冠状动脉左前降支分别注入血管内皮依赖性扩张剂乙酰胆碱(Ach)(10-8~10-6M)和血管平滑肌扩张剂腺苷(AD)(10-6~10‘M)。小血管阻力通过使用多普勒速度导管测量恒定动脉压下的冠脉血流量(CBF)来评估(通过血管造影校正横截面积)。使用Ach后，对照组患者的CBF232±40%(平均值+扫描电子显微镜)增加，而心肌病患者的CBF232±40%增加(41±24%)(p<；0.0001，对照组与心肌病组相比)。AD患者对照组CBF422±56%，心肌病组CBF268±43%(P=0.13)。通过标准化每个患者的Ach剂量反应与其最大AD血流反应，获得可归因于内皮依赖性血管扩张的冠状动脉血流储备比例的指数。在7例同时接受Ach和AD治疗的对照组患者中，内皮依赖性血管扩张剂Ach可获得56±9%的最大AD血流反应，而在7例同时接受Ach和AD治疗的心肌病患者中，仅获得最大AD反应的23±14%(p<；0.01)。因此，扩张型心肌病患者的冠脉微血管内皮依赖性血管扩张功能受损。内皮功能障碍与心力衰竭之间可能存在致病联系。(1990年版；第81期：772-779期)
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`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 232+40%1 (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%o 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 coronary microvasculature of patients with dilated cardiomyopathy. There might be pathogenetic links between dysfunction of the endothelium and myocardial failure. (Circulation 1990;81:772-779)