Citation: Naqvi IH, Mahmood K, Talib A and Rizvi NZ. Looking Beyond Liver! Cirrhotic Cardiomyopathy: Pathophysiology, Clinical Presentation and Management Strategies. J Gastroenterol Liver Dis. 2017; 2(1): 1009. J Gastroenterol Liver Dis - Volume 2 Issue 1 - 2017 Submit your Manuscript | www.austinpublishinggroup.com Naqvi et al. © All rights are reserved Journal of Gastroenterology, Liver & Pancreatic Diseases Open Access Abstract Cardiac dysfunction in cirrhosis of liver remains dormant due to hyperdynamic circulatory state even with the severe stage of cirrhosis. This in actuality is worsening of the cardiac functions. The decline in diastolic functions, inotropic and chronotropic functions and cardiac hypertrophy all occur simultaneously in the setting of an absent organic cardiac disease. The Cirrhotic cardiomyopathy has pertinent indings in its loop comprising of impaired contractile reaction to stress stimuli and electrophysiological abnormalities along with prolonged QT interval. The disruption in β-adrenergic receptor signalling, altered composition of cardiomyocyte membrane lipids plus biophysical properties, ion channel defects and enhanced cardiodepressant factors attributed to hormones are the pathogenic assailants. The hindrance to diagnose cirrhotic cardiomyopathy mainly lies in unavailability of a stark speciic diagnostic test nevertheless; an echocardiogram is favourably used to follow deteriorating diastolic functions and the E/e′ ratio thus giving insight to the progression of disease. The severity of cirrhosis is linked in parallel with ensuing cirrhotic cardiomyopathy which substantially impairs arterial blood volume. So, in case of any hemodynamic stress, a heart bearing cirrhotic cardiomyopathy retorts with diminished cardiac response which may cause renal hypoperfusion leading to renal failure. The management is mainly symptomatic where only the liver transplantation could play an imperative role in correction of the cardiac functions. Keywords: Cirrhotic cardiomyopathy; Cardiac dysfunction; Left ventricular diastolic dysfunction; Arterial blood volume; Hepatorenal syndrome ascites, hepatic encephalopathy, upper GI bleeding and Coagulopathy, cardiac involvement in the form of Cirrhotic Cardiomyopathy (CCM) has recently gained attention as the commonest cause of post liver transplant mortality [3]. Cardiac dysfunction was established in cirrhosis of liver half a century ago when cardiovascular changes like hyperdynamic circulation, high cardiac output, reduced peripheral vascular resistance and reduced blood pressure were described [4,5]. Consequent pathological evidence of cardiac dysfunction in cirrhosis of liver was cardiac hypertrophy, edema of cardiomyocyte without valvular heart disease, coronary artery disease and hypertension [6]. Initially, it was believed that the cardiac dysfunction is directly consequent to alcohol toxicity and was termed as latent alcoholic cardiomyopathy [7]. he decreased hemodynamic retort to either of the physiologic (exercise) or pharmacologic strain even with an elevated basal cardiac output which was witnessed in a few trials on human and animal models of non-alcoholic cirrhosis [8,9]. his review spotlights on deinition, pathophysiology, clinical signiicance, diagnosis and management of CCM. Deinition of CCM CCM is deined as impaired cardiac functions without any organic cardiac disorder pertaining to diminished cardiac contractility when stimulated (physiological / pharmacological) and adapted relaxation Abbreviations CCM: Cirrhotic Cardiomyopathy; QTc: Corrected QT interval; SNS: Sympathetic Nervous System; RAAS: Renin Angiotensin Aldosterone System; CAIDS: Cirrhosis-Associated Immune Dysfunction Syndrome; NO: Nitric Oxide; CO: Carbon monoxide; LV: Let Ventricle; SVR: Systemic Vascular Resistance; BDL: Bile Duct Ligation; PWCP: Pulmonary Wedge Capillary Pressure; PRAL: Plasma Renin Activity; TGF β: Transforming Growth Factor Β; IVRT: Increased Isovolumic Relaxation Time; DT: Deceleration Times; TDI: Tissue Doppler Imaging; CAMP: Cyclic Adenosine Monophosphate; PKA: Protein Kinase; ECS: Endocanabinoid System; iNOS: inducible Nitric Oxide Synthase; L-NMMA: N Omegamonomethyl-larginine; NGL: Nitro-arginine Methyl Ester; HO: Haem Oxygenase; CGMP: Cyclic Guanosine Monophosphate; MAPKs: Mitogen-Activated Protein Kinase; HRS: Hepatorenal Syndrome; ANP: Atrial Natriuretic Peptide; BNP: B Type Natriuretic Peptide; GLS: Global Longitudinal Strains Introduction Cirrhosis is a chronic state of liver caused by various aetiologies characterized by altered parenchyma and distorted hepatic vascular architecture consequent to chronic tissue ibrosis and regenerative nodules [1,2]. Globally, cirrhosis has become an emergent cause of mortality. Apart from the known complications of cirrhosis like Review Article Looking Beyond Liver! Cirrhotic Cardiomyopathy: Pathophysiology, Clinical Presentation and Management Strategies Naqvi IH 1 *, Mahmood K 1 , Talib A 1 and Rizvi NZ 2 1 Department of Medicine, Dow University of Health Sciences, Pakistan 2 Lifeline Medical Centre, Pakistan *Corresponding author: Naqvi IH, Department of Medicine, DOW University of Health sciences, Karachi, Pakistan, C 12 Marahaba Galaxy, Block M North Nazimabad Karachi, Pakistan Received: October 09, 2016; Accepted: January 23, 2017; Published: January 24, 2017