Cirrhotic cardiomyopathy: A cardiologist’s perspective

Abstract

Cardiac dysfunction is frequently observed in patients with cirrhosis, and has long been linked to the direct toxic effect of alcohol. Cirrhotic cardiomyopathy (CCM) has recently been identified as an entity regardless of the cirrhosis etiology. Increased cardiac output due to hyperdynamic circulation is a pathophysiological hallmark of the disease. The underlying mechanisms involved in pathogenesis of CCM are complex and involve various neurohumoral and cellular pathways, including the impaired β-receptor and calcium signaling, altered cardiomyocyte membrane physiology, elevated sympathetic nervous tone and increased activity of vasodilatory pathways predominantly through the actions of nitric oxide, carbon monoxide and endocannabinoids. The main clinical features of CCM include attenuated systolic contractility in response to physiologic or pharmacologic strain, diastolic dysfunction, electrical conductance abnormalities and chronotropic incompetence. Particularly the diastolic dysfunction with impaired ventricular relaxation and ventricular filling is a prominent feature of CCM. The underlying mechanism of diastolic dysfunction in cirrhosis is likely due to the increased myocardial wall stiffness caused by myocardial hypertrophy, fibrosis and subendothelial edema, subsequently resulting in high filling pressures of the left ventricle and atrium. Currently, no specific treatment exists for CCM. The liver transplantation is the only established effective therapy for patients with end-stage liver disease and associated cardiac failure. Liver transplantation has been shown to reverse systolic and diastolic dysfunction and the prolonged QT interval after transplantation. Here, we review the pathophysiological basis and clinical features of cirrhotic cardiomyopathy, and discuss currently available limited therapeutic options.

Consensus conference on TIPS management: Techniques, indications, contraindications

“…The disease is generally unapparent at rest and becomes manifest under pharmacogical or physical stress as infection, haemorrhage, large volume paracentesis, and exercise. Left ventricular (diastolic) dysfunction may be a significant factor in the development of ascites and hepatorenal syndrome [65,66,68,77,78] as well as pulmonary arterial hypertension (PAH, defined as mPAP ≥25 mmHg). This condition is not infrequent in cirrhotic patients with portal hypertension (up to 16% in transplant candidates).…”

Ocena kardiologiczna pacjentów z niewydolnością wątroby w ramach kwalifikacji do operacji przeszczepienia wątroby

“…Do naj- E/E' -stosunek maksymalnej prędkości wczesnej (rozkurczowej) fali napływu mitralnego (mierzonej za pomocą doplera pulsacyjnego) do wczesnorozkurczowej prędkości ruchu pierścienia mitralnego (mierzonej za pomocą tkankowego badania doplerowskiego) stosowany jako wskaźnik podwyższonego ciśnienia napełniania lewej komory; VO2peak -szczytowe pochłanianie tlenu; VE/VCO2slope -współczynnik regresji linowej zależności wentylacji minutowej od ilości wydalanego dwutlenku węgla; EKG -badanie elektrokardiograficzne; 6MWT ( częstszych odchyleń opisywanych w populacji pacjentów z marskością należą przerost mięśnia sercowego, powięk-szenie lewego przedsionka (LA, left atrium) i lewej komory (LV, left ventricle) serca [4]. U pacjentów z niewydolnością wątroby powiększenie LA ma charakter wieloczynnikowy i nie zawsze odzwierciedla podwyższone ciśnienie napeł-niania LV.…”

Introductory Chapter: Last Crossroad

“…The typical hemodynamic signs of alcoholic cirrhosis are hyperdynamic circulation with high cardiac output, decreased peripheral resistance and arterial pressure. Depression or desensitization of β-adrenergic receptors impairs chronotropic and inotropic responses of the heart and can be the early sign of cirrhotic CMP [12]. The second mechanism is downregulation of intracellular calcium kinetics.…”