Burcă Paula, Mihai B, Mihai Cătălina, Drug V L, Dranga Mihaela, Lăcătuşu Cristina, Prelipcean Cristina Cijevschi
Universitatea de Medicină şi Farmacie Gr.T. Popa, Facultatea de Medicinaă, Institutul de Gastroenterologie şi Hepatologie Iaşi.
Rev Med Chir Soc Med Nat Iasi. 2010 Apr-Jun;114(2):319-26.
Cirrhotic cardiomyopathy is a condition recently known in liver cirrhosis consisting of systolic dysfunction to stress factors, diastolic dysfunction and electrophysiological abnormalities in the absence of cardiac disease. The prevalence of cirrhotic cardiomyopathy remains unknown until now. It can be diagnosed by using a combination of electrocardiograph, 2-dimensional echocardiography, and various serum markers (brain natriuretic factor--BNP, proBNP, TnI). Pathogenic mechanisms underlying cirrhotic cardiomyopathy development include abnormal signaling betaadrenergic, cardiomyocites membrane fluidity changes, interstitial fibrosis, myocardial hypertrophy, altered transmembrane ion channels as intervention with negative inotropic effect of different substances whose concentration is increased in cirrhosis. Major stresses on the cardiovasculary system such as liver transplantations, infections, insertion of transjugular portosystemic stent-shunt (TIPSS) have been demonstrated to put in evidence the presence of cirrhotic cardiomyopathy. Heart failure is a significant cause of mortality after liver transplantation but the improvement of liver function determines cardiac abnormalities reversal. Current management recommendations include empirical, nonspecific and mainly supportive measures, no specific treatment can be recommended, and cardiac failure should be treated as in non-cirrhotic patients with sodium restriction, diuretics, and oxygen therapy when necessary. The exact prognosis remains unclear. The extent of cirrhotic cardiomyopathy generally correlates to the degree of liver insufficiency. Reversibility is possible (either pharmacological or after liver transplantation), but further studies are needed.
肝硬化性心肌病是一种最近才被认识到的肝硬化相关病症,其特征为在无心脏疾病的情况下,对应激因素出现收缩功能障碍、舒张功能障碍及电生理异常。迄今为止,肝硬化性心肌病的患病率仍不清楚。它可通过结合心电图、二维超声心动图及各种血清标志物(脑钠肽——BNP、proBNP、肌钙蛋白I)来诊断。肝硬化性心肌病发生的致病机制包括β肾上腺素能信号异常、心肌细胞膜流动性改变、间质纤维化、心肌肥大、跨膜离子通道改变以及不同物质的负性肌力作用干预,这些物质在肝硬化时浓度升高。诸如肝移植、感染、经颈静脉肝内门体分流术(TIPSS)置入等对心血管系统的主要应激因素已被证明可显示出肝硬化性心肌病的存在。心力衰竭是肝移植后死亡的重要原因,但肝功能的改善可使心脏异常逆转。目前的管理建议包括经验性、非特异性且主要是支持性措施,无法推荐特异性治疗,对于心力衰竭应如同非肝硬化患者一样进行治疗,必要时限制钠摄入、使用利尿剂及进行氧疗。确切的预后仍不明确。肝硬化性心肌病的程度通常与肝功能不全的程度相关。有可能实现可逆性(无论是通过药物治疗还是肝移植后),但仍需进一步研究。