Heart failure is a systemic disease based on its chronic inflammation status and because it affects other organs, including the kidneys, lungs, and liver. Acute decompensated heart failure (ADHF) is a more severe form of heart failure that causes an acute change in hemodynamics. ADHF negatively affects renal, hepatic, and pulmonary function and causes peripheral soft tissue edema.

Repeated hospital admissions for ADHF is one indicator of a poor clinical outcome in chronic heart failure patients [1,2]. The predictors of readmission and death have been investigated, and major risk factors are a low left ventricular ejection function (LVEF), low initial serum sodium level, increased serum creatinine, anemia, and low admission blood pressure [1,2].

These are markers of hemodynamic change, fluid and electrolyte imbalance, and reduced organ perfusion and function caused by depressed left and right ventricular function.

The predictors that indirectly reflect low cardiac function include hepatic congestion, which can be detected with liver function tests (LFTs), including serum bilirubin, alkaline phosphatase, and aminotransferases. These have been suggested as risk factors for future death, cardiovascular events, and readmission [3-6]. Furthermore, recent publications have reported that the type of death from heart failure can be discriminated using the bilirubin level: increased total bilirubin was associated with death from pump failure and not with sudden death [5].

Chronic hepatic congestion due to right ventricular dysfunction might increase the possibility of liver cirrhosis, so-called cardiac cirrhosis.

In a recent post hoc analysis, the prevalence of LFT abnormalities in ADHF was as much as 46% [2]. The liver and heart are connected intimately, similar to the relationship between the heart and kidney, usually called "cardiorenal syndrome," in patients with chronic and acute heart failure.

In this issue of Korean Journal of Internal Medicine, Chintanaboina et al. [7] reported an association between serum total bilirubin and readmission due to ADHF. They demonstrated that patients with a high serum bilirubin on admission had a high risk of readmission owing to decompensation, and that patients with a bilirubin >1.3 mg/dL or LVEF <35% were at higher risk.

This study once again confirmed the old story that hepatic congestion, which implies advanced heart failure, indicates a poor prognosis in acute and chronic heart failure patients [1-6,8].

Surprisingly, alleged poor risk predictors such as LVEF, serum creatinine, low serum sodium, and B-natriuretic peptide were not independent risk factors for readmission in a multiple regression analysis, as presented in Table 3.

Nevertheless, I feel that this small retrospective study had many confounding factors that could not be controlled. Therefore, a refined statistical method should have been applied, and this process should be described in more detail in this article.

Although it has substantial limitations, this study has value in that it confirms the correlation between total bilirubin and hospitalization in ADHF patients, who comprise a small portion of patients compared with those with chronic heart failure in terms of "bilirubin and heart failure prognosis."

Serum bilirubin is a potential indicator of risk stratification for rehospitalization, along with other prognostic markers such as low sodium and low initial blood pressure in ADHF. Moreover, it might help to guide the therapeutic options for ADHF.

Future studies should aim at improving the prognosis of ADHF patients with the guidance of liver function.