Liver Function in Heart Failure
Liver Function in Heart Failure
Abstract & Commentary
By Michael H. Crawford, MD, Editor
Source: Nikolaou M, et al. Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure. Eur Heart J 2013;34:742-749.
The incidence and predictive value of abnormal liver function tests (LFTs) in patients with acute decompensated heart failure is poorly understood. Thus, these investigators from the SURVIVE study report their experience in patients with acute decompensated heart failure due to systolic dysfunction treated with positive inotropic infusions. The SURVIVE trial compared levosimendan to dobutamine in hospitalized acute heart failure patients with left ventricular ejection fractions of < 30%. Cardiogenic shock, severe liver failure, chronic liver disease, and treatment with hepatotoxic drugs were exclusion criteria. SURVIVE showed no difference in all-cause mortality between the two groups, even though the levosimendan group exhibited greater decreases in BNP. In the 1134 with LFT measurements, > 25% had one or more abnormalities at baseline and most were modest elevations (1-2 times ULN). During therapy, the LFTs trended downward over 30 days. Multivariate predictors of abnormal alkaline phosphatase (AP) were ascites (hazard ratio [HR] = 1.8) and edema (1.7), whereas predictors of abnormal transaminase levels were acute myocardial infarction (HR = 3.1) and less worsening of heart failure after admission (0.4). Thirty-day mortality was significantly higher in those with elevated transaminases vs those with normal transaminases (18 vs 8%, P < 0.001). Mortality at 180 days was higher if AP or transaminases were elevated (34 and 32%) vs those with normal values (24 and 22%). The authors concluded that elevated transaminases are associated with signs of hypoperfusion and elevated AP are associated with signs of systemic congestion and elevated filling pressures. Also, elevated transaminases are associated with short-term mortality.
Commentary
This study is a retrospective subgroup analysis of a trial conducted for other purposes. Thus, it is subject to biases. Also, interesting data are not available such as other measures of hepatic function (bilirubin, albumin, and prothrombin time). In addition, there was no invasive hemodynamics or hepatic imaging done. Regardless, several interesting points were made. The authors make a clear case for measuring hepatic function parameters in all acute decompensated heart failure patients. The pattern of abnormalities may suggest the predominant hemodynamic abnormality (elevated AP with backward failure and elevated transaminases with forward failure). Also, elevated transaminases identify very high-risk patients for early mortality who need vigorous measures to increase organ perfusion. In addition, elevated liver function tests in general seem to identify higher-risk patients for 6-month mortality.
The potential mechanism of signs of cholestasis with congestion is interesting. Increased liver sinusoidal pressure probably collapses the bile ducts. Transaminase release is probably due to liver cell necrosis from ischemia due to reduced hepatic blood flow. My own clinical experience and reports from others suggest that prothrombin time is an early marker of liver injury in heart failure, and is probably due to poor perfusion that reduces liver protein production. Reduced biochemical production probably proceeds from cell necrosis. Unfortunately, prothrombin time was not measured in this study. There are obvious parallels between LFT abnormalities and renal dysfunction in heart failure, which also seems to be due to venous congestion and poor perfusion, and increases mortality. It may behoove us to pay more attention to cardiohepatic dysfunction as well.
The incidence and predictive value of abnormal liver function tests (LFTs) in patients with acute decompensated heart failure is poorly understood. Thus, these investigators from the SURVIVE study report their experience in patients with acute decompensated heart failure due to systolic dysfunction treated with positive inotropic infusionsSubscribe Now for Access
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