Silvestre Odilson M, Farias Alberto Q, Ramos Danusa S, Furtado Meive S, Rodrigues Ana C, Ximenes Rafael O, de Campos Mazo Daniel F, Yoshimura Zitelli Patricia M, Diniz Marcio A, Andrade José L, Strunz Celia, Friedmann Antônio A, Lee Samuel S, Carrilho Flair J, D'Albuquerque Luiz A C, Bacal Fernando
Heart Institute (InCor).
Department of Gastroenterology, Division of Gastroenterology and Hepatology.
Eur J Gastroenterol Hepatol. 2018 Aug;30(8):930-937. doi: 10.1097/MEG.0000000000001128.
Cirrhotic cardiomyopathy is characterized by an attenuated contractile response to stress. Long-term exposure of β-adrenergic receptors to persistently high levels of catecholamines has been implicated in its pathogenesis. We hypothesized that β-blockade with metoprolol could reverse the changes in heart function and morphology in cirrhotic cardiomyopathy.
In this prospective randomized trial, we included 78 patients aged between 18 and 60 years with abnormal cardiac output response under dobutamine stress echocardiography, without primary cardiac disease or a history of alcohol intake. Patients were assigned randomly to receive metoprolol or placebo for 6 months. The primary endpoint was the improvement in cardiac output response to stress, measured by an increase in the left ventricle stroke volume more than 30%.
Three (7.3%) patients in the metoprolol group and nine (24.3%) patients in the placebo group showed improved stroke volume (P=0.057). Diastolic dysfunction was found in two (4.8%) patients before and in five (15.6%) patients after therapy in the metoprolol group, and in 10 (27%) patients before and nine (31%) patients after therapy in the placebo group (P=0.67). After treatment, no echocardiography parameter of morphology was significantly different between metoprolol or placebo groups. No significant differences were observed in noradrenaline, plasma renin activity, and troponin levels between groups. Cirrhosis-related clinical events, including hospitalizations and mortality, were not significantly different between the two groups. Six months of therapy with β-blocker did not ameliorate heart function and morphology in patients with cirrhotic cardiomyopathy.
肝硬化性心肌病的特征是对应激的收缩反应减弱。β-肾上腺素能受体长期暴露于持续高水平的儿茶酚胺被认为与其发病机制有关。我们假设美托洛尔进行β受体阻滞可逆转肝硬化性心肌病患者的心脏功能和形态变化。
在这项前瞻性随机试验中，我们纳入了78例年龄在18至60岁之间、多巴酚丁胺负荷超声心动图检查时心输出量反应异常、无原发性心脏病或饮酒史的患者。患者被随机分配接受美托洛尔或安慰剂治疗6个月。主要终点是应激时心输出量反应的改善，通过左心室每搏输出量增加超过30%来衡量。
美托洛尔组有3例（7.3%）患者和安慰剂组有9例（24.3%）患者的每搏输出量有所改善（P=0.057）。美托洛尔组治疗前有2例（4.8%）患者存在舒张功能障碍，治疗后有5例（15.6%）患者存在舒张功能障碍；安慰剂组治疗前有10例（27%）患者存在舒张功能障碍，治疗后有9例（31%）患者存在舒张功能障碍（P=0.67）。治疗后，美托洛尔组和安慰剂组之间的超声心动图形态学参数无显著差异。两组之间去甲肾上腺素、血浆肾素活性和肌钙蛋白水平无显著差异。两组之间与肝硬化相关的临床事件，包括住院率和死亡率，无显著差异。β受体阻滞剂治疗6个月并未改善肝硬化性心肌病患者的心脏功能和形态。
