Cirrhotic Cardiomyopathy: The Interplay Between Liver and Cardiac Muscle. How Does the Cardiovascular System React When the Liver is Diseased?

Abstract

: It is widely known that liver cirrhosis, regardless of the etiologies is accompanied by severe hemodynamic changes. The principal pathophysiological mechanisms are the hyper-dynamic 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 trans-jugular 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 outmost 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.

Risk factors and diagnostic value of urinary N-terminal pro-brain natriuretic peptide for verification of heart failure in human immunodeficiency virus-infected patients

“…У ВИЧ-инфицированных больных высокая частота встречаемости вирусных гепатитов В и С является ФР развития циррозов печени вирусной этиологии. В нашем исследовании наличие цирроза печени стало ФР развития ХСН у ВИЧ-инфицированных больных, что согласуется с новой концепцией формирования "цирротической кардиомиопатии", основными патофизиологическими механизмами которой являются гипердинамическое кровообращение с повышенным сердечным выбросом, частотой сердечных сокращений наряду со снижением си-стемного сосудистого сопротивления, что в конечном итоге приводит к систолической, а также ДД ЛЖ и нарушениям ритма [15].…”

Cirrhotic Cardiomyopathy: The Interplay Between Liver and Heart

“…Systolic dysfunction, in general, refers to an emptying problem of the left ventricle (LV), described by a decreased ejection fraction (EF), usually as a result of an impaired myocardial contractile function [44,45]. Systolic dysfunction in CCM, according to the world conference of gastroenterology 2005 criteria, is defined as left ventricular ejection fraction (LVEF) <55% at rest and/or blunted contractile response to stress [46].…”

Cardiovascular manifestation of end-stage liver disease and perioperative echocardiography for liver transplantation: anesthesiologist’s view

“…Relative arterial underfilling also stimulates baroreceptors and causes expansion of plasma volume with activation of the neurohumoral axis, including the renin-angiotensin-aldosterone system (RAAS), sympathetic nerve system (SNS), and arginine vasopressin [ 18 ]. Prolonged alterations in hemodynamic status and subsequent structural and functional changes in the heart could contribute to the development of CCM [ 19 ].…”