Abnormal Liver Function in Relation to Hemodynamic Profile in Heart Failure Patients
Received 7 May 2009; received in revised form 10 June 2009; accepted 3 August 2009. published online 27 September 2009.
Abstract
Background
We studied the relation between liver function abnormalities and hemodynamic profile in patients with heart failure (HF).
Methods and Results
In 323 HF patients, liver function was determined by aspartate and alanine aminotransferase (AST, ALT), alkaline phosphatase, γ-glutamyl transpeptidase (GGT), lactate dehydrogenase, and direct and total bilirubin (Bili dir, Bili tot). Central venous pressure (CVP) and cardiac index (CI) were determined invasively. Follow-up consisted of time to all-cause mortality. Mean age was 53 ± 15 years, and 60% were male. In multivariable analysis, all liver function tests related to CVP, but higher CVP was predominantly related to GGT (r = 0.336, P < .001) and Bili dir (r = 0.370, P < .001). Only elevated AST (r =−0.177, P < .01), ALT (r = −0.130, P < .05), and Bili tot (r = −0.158, P < .01) were associated with both low CI and elevated CVP. The prognostic value of abnormal liver function tests was related to their interaction with CI and CVP.
Conclusions
Elevated liver function tests mainly indicate higher CVP, whereas only the presence of elevated AST, ALT, or Bili dir may indicate a low CI. The absence of prognostic information in the presence of invasive hemodynamic measurements suggests that abnormal liver function tests in HF reflect a poor hemodynamic status.
1Department of Cardiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
2Department of Epidemiology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
3Department of Internal Medicine, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands
Reprint requests: A.A. Voors, MD, PhD, Department of Cardiology, University Medical Center Groningen, Hanzeplein 1, 9700 RB Groningen, The Netherlands. Tel: (+31) 503612355.
The authors have no conflicts of interest.
K. Damman is supported by the Netherlands Heart Foundation (grant 2006B157). A.A. Voors and D.J. van Veldhuisen are Clinical Established Investigators of the Netherlands Heart Foundation (grants 2006T37 and D97-017, respectively).
ABSTRACT