2nd Department of Internal Medicine and Research Laboratory, Medical School, National and Kapodistrian University of Athens, Hippokration Hospital, Athens, Greece.
Internal Medicine Department, Evaggelismos General Hospital, Athens, Greece.
Curr Cardiol Rev. 2021;17(1):78-84. doi: 10.2174/1573403X15666190509084519.
It is widely known that liver cirrhosis, regardless of the etiologies is accompanied by severe hemodynamic changes. The principal pathophysiological mechanisms are the hyperdynamic circulation with increased cardiac output, heart rate along with reduced systemic vascular resistance. Thus, counteractive mechanisms may develop that eventually lead to systolic as well as diastolic dysfunction and rhythm disturbances, in order to keep a steady homeostasis in the human body. Literally, blunted contractile responsiveness to physical or pharmacological stress, impaired diastolic relaxation and electrophysiological changes, primarily QT interval prolongation, do occur progressively in a cirrhotic patient with no known preexisting cardiac disease. This condition is identified as cirrhotic cardiomyopathy (CCM), an entity different from that seen in alcoholic cardiac muscle disease. For the past decades, clinicians did study and attempt to understand the pathophysiology and clinical significance of this process. Indeed, various factors have been identified acting at the molecular and cellular level. Electrocardiography, echocardiography and various serum biomarkers are the main tools that help healthcare practitioners to point to the correct diagnosis. Noteworthy, the subjects that suffer from cirrhotic cardiomyopathy may progress to heart failure during invasive procedures such as surgery, insertion of a transjugular intrahepatic portosystemic shunting (TIPS) and liver transplantation. Besides, several studies have illustrated that CCM is a contributing factor, or even a precipitant, of hepatorenal syndrome (HRS), a conceivable reversible kidney failure in patients with liver cirrhosis and ascites. The treatment is the same as it is in the patients with liver cirrhosis and heart failure and there is no particular treatment for cirrhotic cardiomyopathy. Hence, it is of utmost importance to clearly comprehend the pathophysiology of this disease in order to design more accurate diagnostic tools and definitive treatments in a way to prevent the complications of cirrhosis and overt heart failure. The objective of this review is to describe in a comprehensive way the pathological alterations that occur in the cardiovascular system of cirrhotic patients. It will also point the limitations that remain in the diagnosis and treatment strategies and more importantly, this review will alert the clinicians in the modern era to further observe and record additional pathological changes in this subset of patients.
众所周知，无论病因如何，肝硬化都伴随着严重的血流动力学变化。主要的病理生理机制是心输出量增加、心率加快和全身血管阻力降低的高动力循环。因此，可能会发展出对抗性机制，最终导致收缩和舒张功能障碍以及节律紊乱，以保持人体的稳定内环境。实际上，在没有已知先前存在的心脏病的肝硬化患者中，确实会逐渐出现对物理或药理学应激的收缩反应迟钝、舒张松弛受损和电生理变化，主要是 QT 间期延长。这种情况被确定为肝硬化心肌病 (CCM)，与酒精性心肌疾病中所见的不同。在过去的几十年中，临床医生确实研究并试图了解这一过程的病理生理学和临床意义。事实上，已经确定了各种作用于分子和细胞水平的因素。心电图、超声心动图和各种血清生物标志物是帮助医疗保健从业者做出正确诊断的主要工具。值得注意的是，患有肝硬化心肌病的患者在手术、经颈静脉肝内门体分流术 (TIPS) 和肝移植等侵入性操作过程中可能会进展为心力衰竭。此外，几项研究表明，CCM 是肝性肾衰竭 (HRS) 的一个促成因素，甚至是一个诱因，HRS 是肝硬化和腹水患者中可想象的可逆性肾衰竭。治疗方法与肝硬化和心力衰竭患者相同，并且没有针对肝硬化心肌病的特殊治疗方法。因此，了解这种疾病的病理生理学对于设计更准确的诊断工具和明确的治疗方法以预防肝硬化和明显心力衰竭的并发症至关重要。本综述的目的是全面描述肝硬化患者心血管系统发生的病理改变。它还将指出诊断和治疗策略中的局限性，更重要的是，本综述将提醒现代临床医生进一步观察和记录这组患者的其他病理变化。
