Cardiac hepatopathy, hepatic injury caused by cardiac dysfunction, is a common entity but has been characterized incompletely, particularly the relationship between hemodynamics and histology. We aimed to describe the clinical, biochemical, hemodynamic, and histologic characteristics of this disorder. Eighty-three patients from 2 tertiary referral centers were studied. Patients were divided into 3 groups based on the duration of cardiac dysfunction: (1) acute (n = 12); (2) chronic (n = 53); and (3) acute on chronic (n = 18). Results showed that serum aminotransferase levels were increased typically, particularly in the acute group (median aspartate aminotransferase level was 30.2 times the upper limit of normal [range, 1-100]; P < .0001 vs. the chronic group). The most salient hemodynamic features were elevated right atrial (14 mm Hg [range, 1-29]), and hepatic venous pressures (wedged: 18 mm Hg [range, 5-35]; free: 15 mm Hg [range, 2-30]). The hepatic venous pressure gradient was normal in most (81%), correlated moderately with the aminotransferase levels (aspartate aminotransferase level: r = .59; P < .0001), and associated with the presence of centrilobular necrosis and inflammation, periportal necrosis, and stainable hepatic iron (P < .05 for all comparisons), but not fibrosis. Sinusoidal dilatation was associated with higher right atrial (P = .047) and free hepatic venous pressures (P = .06). Although cirrhosis was rare (n = 1), centrilobular fibrosis was common (74%) and not associated with any hemodynamic measurement. In conclusion, cardiac hepatopathy has diverse clinical, hemodynamic, and histologic manifestations that vary with the temporal course of cardiac dysfunction. Hepatic fibrosis is common, but does not correlate with systemic or hepatic hemodynamics.

Background. Orthotopic liver transplantation (OLT) stresses the cardiovascular system, and cardiac complications after OLT are common. Methods. Hundred ninety-seven patients (≥40 years) who had OLT from 2002 to 2007 were reviewed to identify predictors of cardiac complications within 6 months after transplantation. Results. Median age was 56 years (40–75 years); 69% men. Reasons for OLT were hepatitis C virus (HCV) 45.5%, alcohol 22%, hepatocellular carcinoma (HCC) 8%, primary biliary cirrhosis 10%, and others 14.5%. Eighty-two patients suffered one or more cardiac complications within 6 months after OLT (pulmonary edema=61 [overt heart failure=7], arrhythmia=13, pulmonary hypertension=7, pericardial effusion=2, and right atrial thrombus=1). Cardiac causes were the leading cause of death (n=5; 23.8% of all mortality). By multivariate analysis, after adjusting for age and sex, independent predictors were adverse intraoperative cardiovascular events (adjusted odds ratio; 95% confidence interval: 5.89, 1.82–19.14), history of cardiac disease (2.42, 0.89–6.6), and i-MELD (integrated model for end-stage liver disease) score (1.08, 1.02–1.14), whereas adverse intraoperative cardiovascular events (5.73, 1.96–16.78) and i-MELD (1.07, 1.01–1.13) predicted pulmonary edema. None of the following variables predicted complications: age, sex, OLT indication, body mass index, blood pressure, alcohol and smoking history, pre-OLT investigations (chest X-ray, electrocardiogram, echocardiography, coronary angiography, pulmonary arterial pressure, and 2-methoxy isobutyl isonitrile scan), immunosuppressive treatment, or intraoperative variables (transfusion amount, cadaveric vs. living graft or cold ischemia and rewarming times). Conclusions. Cardiac complications after OLT are common and were the leading cause of death after surgery. Adverse intraoperative cardiovascular events, previous cardiac disease, and advanced liver disease as quantified by i-MELD score predicted postoperative cardiac complications.

Cardiovascular abnormalities accompany both portal hypertension and cirrhosis. These consist of hyperdynamic circulation, defined as reduced mean arterial pressure and systemic vascular resistance, and increased cardiac output. Despite the baseline increased cardiac output, ventricular inotropic and chronotropic responses to stimuli are blunted, a condition known as cirrhotic cardiomyopathy. Both conditions may play an initiating or aggravating pathogenic role in many of the complications of liver failure or portal hypertension including ascites, variceal bleeding, hepatorenal syndrome and increased postoperative mortality after major surgery or liver transplantation. This review briefly examines the major mechanisms that may underlie these cardiovascular abnormalities, concentrating on nitric oxide, endogenous cannabinoids, central neural activation and adrenergic receptor changes. Future work should address the complex interrelationships between these systems.