ABSTRACT
Cardiac dysfunction in patients with cirrhosis and potential clinical implications have long been known, but the pathophysiology and potential targets for therapeutic intervention are still under investigation and are only now becoming understood. The pathophysiological changes result in systolic dysfunction, diastolic dysfunction, and electrophysiological changes. Here, we aim to review cirrhotic cardiomyopathy from a cellular and physiological model and how these patients develop overt heart failure in the setting of stress, such as infection, ascites, and procedures including transjugular intrahepatic portosystemic shunt, portocaval shunts, and orthotopic liver transplantation. We will also review the most current, although limited, available therapeutic modalities.
Subject(s)
Cardiomyopathies/etiology , Liver Cirrhosis/complications , Cardiomyopathies/pathology , Cardiomyopathies/physiopathology , Humans , Liver Cirrhosis/pathology , Liver Cirrhosis/physiopathologyABSTRACT
Chronic heart failure (CHF) and chronic kidney disease (CKD) are serious medical conditions with significant morbidity and mortality. Emerging evidence indicates that the function of these two organ systems are affected by each other in a complex interplay. Most patients with CKD suffer frequently from cardiac abnormalities including left ventricular hypertrophy (LVH), left ventricular dilatation (LVD), left ventricular (LV) diastolic and/or systolic dysfunction. Although previously thought that LV systolic dysfunction was an absolute contraindication to renal transplantation, several observational studies have shown this not to be true and that transplantation can lead to significant improvement in LV systolic function. Furthermore, correction of the uremic state by renal transplantation leads to improvement of LVD and possibly regression of LVH. In fact, the reduction of LVH postkidney transplantation was shown to be dependent on adequate renal function and hypertension control. Diabetes mellitus does not seem to be a confounding factor in the improvement of uremic cardiomyopathy with renal transplantation.
