Venous congestion in advanced heart failure (HF) patients is frequently accompanied by dysfunction of several peripheral organs (liver, kidneys), and is associated with unfavorable prognosis. However, there are few data regarding the correlation between the degree of venous congestion and the type and range of hepatic function abnormalities.

150 patients with advanced HF on optimal medical therapy, in care unit of Chronic Heart Failure, continuing to have symptoms and signs of congestion despite that the daily furosemide dose was =250mg in each patient. We evaluate those patients clinically, biologically and with echocardiography.

Mean age of patients was 62.7±10.8years, whereas 30% of them suffered from idiopathic dilated cardiomyopathy. Mean values of New York Heart Association functional class, were 3.5±0.5, of left ventricular ejection fraction 27.5±7.9%, of right atrial pressure (RAP) 15±5mmHg of pulmonary capillary wedge pressure (PCWP) 23.6±5,7mmHg and of cardiac index 1.8±0.6Lt/min/m². Serum values of BNP not evaluated, serum creatinine 2.9±4,9mg/dl, bilirubin 1.8±2,1mg/dl, aspartate (AST) 34±27IU/L, alanine aminotransferase (ALT) 43±122 IU/L, alkaline phospatase 95±81IU/L and gamma-glutamyl transferase (gamma-gt) 122±75IU/L.

No correlation between RAP, PCWP and liver function enzymes was demonstrated.

Patients with severe systematic venous congestion (RAP values up to 30mmHg) could present with normal values of hepatic enzymes. Contrary, in patients with significant dysfunction of liver biochemistry the values of RAP and PCWP could be within normal range. Indices of cholestasis or liver cell lysis were also irrelevant to the degree of congestion. Interestingly, right ventricular systolic function (sTDi) was demonstrated to correlate with serum creatinine (r=0.517, p=0.049) and the value of direct bilirubin (r=0.754, p=0.031).

The type and range of hepatic biochemistry abnormalities which is noted with congestion seems to be independent of intracardiac filling pressures, possibly indicating a systematic/inflammatory rather than a mechanistic mechanism of their generation.