Tentolouris Costas, Tousoulis Dimitris, Antoniades Charalambos, Bosinakou Eirini, Kotsopoulou Maria, Trikas Athanasios, Toutouzas Pavlos, Stefanadis Christodoulos
Cardiology Units, Hippokration Hospital, Athens University Medical School, 69 S. Karagiorga, 16675 Athens, Greece.
Int J Cardiol. 2004 Apr;94(2-3):301-5. doi: 10.1016/j.ijcard.2003.08.002.
Proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) are important mediators of immune response, associated with endothelial dysfunction in patients with coronary artery disease (CAD) or heart failure. We compared endothelial function and levels of IL-6 and TNF-alpha between patients with ischemic heart failure, dilated cardiomyopathy, CAD and healthy controls.
The population consisted of 20 patients with dilated cardiomyopathy, 48 patients with ischemic cardiomyopathy, 26 patients with CAD and normal left ventricle function and 14 healthy controls. Forearm blood flow was measured using venous occlusion strain gauge plethysmography. Forearm vasodilatory response to reactive hyperemia (RH%) or to nitrate were considered as indexes of endothelium-dependent and endothelium-independent dilation, respectively.
Levels of IL-6 were significantly higher in ischemic cardiomyopathy compared to CAD patients (P<0.05) or controls (P<0.05) and in patients with dilated cardiomyopathy compared to controls (P<0.05). TNF-alpha levels were significantly higher in both groups with ischemic or dilated cardiomyopathy compared to CAD (P<0.05) or controls (P<0.05). RH% was significantly lower in ischemic and dilated cardiomyopathy compared to CAD (P<0.05) or controls (P<0.001) and higher in dilated than ischemic cardiomyopathy (P<0.05).
Impaired endothelial function and increased inflammatory process were found in both types of heart failure. A greater endothelial dysfunction was observed in patients with ischemic heart failure compared to those with dilated cardiomyopathy, implying that the underlying atherosclerosis may participate in this process.
促炎细胞因子，如肿瘤坏死因子α（TNF-α）和白细胞介素-6（IL-6）是免疫反应的重要介质，与冠状动脉疾病（CAD）或心力衰竭患者的内皮功能障碍有关。我们比较了缺血性心力衰竭、扩张型心肌病、CAD患者和健康对照者的内皮功能以及IL-6和TNF-α水平。
研究人群包括20例扩张型心肌病患者、48例缺血性心肌病患者、26例左心室功能正常的CAD患者和14名健康对照者。使用静脉阻塞应变计体积描记法测量前臂血流量。前臂对反应性充血（RH%）或硝酸盐的血管舒张反应分别被视为内皮依赖性和非内皮依赖性舒张的指标。
与CAD患者（P<0.05）或对照组（P<0.05）相比，缺血性心肌病患者的IL-6水平显著更高；与对照组（P<0.05）相比，扩张型心肌病患者的IL-6水平也显著更高。与CAD患者（P<0.05）或对照组（P<0.05）相比，缺血性或扩张型心肌病两组患者的TNF-α水平均显著更高。与CAD患者（P<0.05）或对照组（P<0.001）相比，缺血性和扩张型心肌病患者的RH%显著更低，且扩张型心肌病患者的RH%高于缺血性心肌病患者（P<0.05）。
在两种类型的心力衰竭中均发现内皮功能受损和炎症过程增加。与扩张型心肌病患者相比，缺血性心力衰竭患者的内皮功能障碍更严重，这意味着潜在的动脉粥样硬化可能参与了这一过程。
