Περίληψη:
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. © 2021 Bentham Science Publishers.
Συγγραφείς:
Dourakis, S.P.
Geladari, E.
Geladari, C.
Vallianou, N.
Λέξεις-κλειδιά:
albumin; biological marker; brain natriuretic peptide; calcitonin gene related peptide; calcium channel blocking agent; carbon monoxide; cyclic GMP dependent protein kinase; endocannabinoid; endothelial nitric oxide synthase; endothelin 3; lipopolysaccharide binding protein; nitric oxide; transforming growth factor beta receptor 1; troponin; vasculotropin, cardiomyopathy; diastolic blood pressure; echocardiography; electrocardiography; electrophysiology; heart left ventricle ejection fraction; heart output; heart rate; human; liver transplantation; pathophysiology; physiological stress; QT interval; QT prolongation; QTc interval; renin angiotensin aldosterone system; Review; systolic dysfunction; vasodilatation; cardiac muscle; cardiomyopathy; complication; heart failure; liver; liver cirrhosis; pathology, Cardiomyopathies; Heart Failure; Humans; Liver; Liver Cirrhosis; Myocardium
