Parissis John T, Karavidas Apostolos, Bistola Vassiliki, Arapi Sophia, Paraskevaidis Ioannis A, Farmakis Dimitrios, Korres Dimitrios, Filippatos Gerasimos, Matsakas Evaggelos, Kremastinos Dimitrios T
Second Department of Cardiology, Attikon University Hospital, Rimini 1, 12461 Chaidari, Athens, Greece.
Atherosclerosis. 2008 Mar;197(1):278-82. doi: 10.1016/j.atherosclerosis.2007.04.023. Epub 2007 Jun 12.
Endothelial activation and dysfunction may be an important contributor to chronic heart failure (CHF) progression. We sought to investigate whether the calcium sensitizer levosimendan affects beneficially endothelial function and attenuates the deleterious effects of soluble adhesion molecules in patients with advanced CHF.
Twenty-six advanced CHF patients (mean New York Heart Association class, 2.6+/-0.3; ischemic/dilated, 18/8; mean left ventricular ejection fraction <35%) hospitalized due to syndrome worsening, were randomized (2:1) to receive either a 24-h levosimendan infusion of 0.1 microg/kg/min (n=17) or placebo (n=9). Endothelial function estimated by endothelial-dependent flow-mediated dilatation of the brachial artery (FMD), as well as plasma soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1), were assessed before and 48 h after therapy.
Baseline characteristics and medications were well balanced in the two treatment groups. A significant improvement of FMD (6.4+/-4.4% from 4.8+/-3.0%; p<0.05) with concomitant reduction of plasma concentrations of sICAM-1 (231+/-75 pg/ml from 339+/-157 pg/ml; p<0.05) and sVCAM-1 (1134+/-508 pg/ml from 1386+/-602 pg/ml; p<0.05) were observed only in levosimendan treated patients.
Levosimendan could be an effective treatment in improving the endothelial function and reducing the detrimental adhesion molecule activation in advanced CHF patients.
内皮细胞激活和功能障碍可能是慢性心力衰竭（CHF）进展的重要因素。我们试图研究钙增敏剂左西孟旦是否对晚期CHF患者的内皮功能有有益影响，并减轻可溶性黏附分子的有害作用。
26例因症状恶化住院的晚期CHF患者（纽约心脏协会平均分级为2.6±0.3；缺血性/扩张性心肌病，18/8；平均左心室射血分数<35%），随机（2:1）接受24小时静脉输注左西孟旦，剂量为0.1μg/kg/min（n = 17）或安慰剂（n = 9）。在治疗前和治疗后48小时评估通过肱动脉内皮依赖性血流介导的血管舒张（FMD）估计的内皮功能，以及血浆可溶性细胞间黏附分子-1（sICAM-1）和可溶性血管细胞黏附分子-1（sVCAM-1）。
两个治疗组的基线特征和用药情况均衡良好。仅在接受左西孟旦治疗的患者中观察到FMD有显著改善（从4.8±3.0%提高到6.4±4.4%；p<0.05），同时血浆sICAM-1浓度降低（从339±157 pg/ml降至231±75 pg/ml；p<0.05），sVCAM-1浓度降低（从1386±602 pg/ml降至1134±508 pg/ml；p<0.05）。
左西孟旦可能是改善晚期CHF患者内皮功能和减少有害黏附分子激活的有效治疗方法。
