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
findings 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 specific 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.
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: Left 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.
Cirrhosis is a chronic state of liver
caused by various aetiologies characterized by altered parenchyma and distorted
hepatic vascular architecture consequent to chronic tissue fibrosis and
regenerative nodules. Globally, cirrhosis has become an emergent cause of
mortality. Apart from the known complications of cirrhosis like 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.
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