The present study inspected the correlation linking the ALBI score and in-hospital mortality in HF patients. We elucidated that: (1) the ALBI score is an independent prognosticator of in-hospital death; (2) the predictive significance of NT-proBNP + ALBI is superior to NT-proBNP, and ALBI score can enhance the estimation potential of the initial NT-proBNP model in patients with HF.
Various studies have assessed the prognostic clinical significance using distinct liver function test (LFT) indices in HF patients. Post-hoc evaluation of the EVEREST study posited that the low baseline albumin and increased bilirubin, were associated with clinical outcome.16 PROTECT study found the escalating AST and ALT on day 3, and diminishing albumin on day 4 are independent predictors of 180-day outcomes of HF patients.17 More and more studies have realized that the reserve of liver function is not only a single parameter, but also other factors with joint variables exist, so at present, the joint scoring system is mostly used to judge the liver function reserve of patients, including Child-Pugh classification(CP), MELD score and ALBI score.9,18,19 The CP constitutes some weaknesses, such as subjective parameters (ascites and encephalopathy), and interrelated indices (serum albumin and ascites), and it was not statistically established.20 MELD score system is an independent prediction index of adverse outcomes in HF patients.21–25 However, for the ALBI score, there is limited research. To our best knowledge, no study has explored the prediction value of the ALBI score for the in-hospital mortality in HF patients. In our study, we elucidated that the ALBI score was correlated with in-hospital mortality for HF patients. With ALBI score as a continuous variable, we established that the risk of in-hospital mortality increased by 8.2% per 0.1 score increase in ALBI (OR = 1.082, 95% CI:1.052 ~ 1.113, p < 0.001). As illustrated in Table 2, ALBI score was still associated with in-hospital mortality when treated as a categorical variable (OR = 1.670, 95% CI:1.231 ~ 2.265, p = 0.001). Previous reports have verified that NT-proBNP is linked to adverse events in HF patients, whether in hospital or discharged.26–27 NT-proBNP is excreted by the kidney, and its circulating concentrations must be interpreted based on renal clearance.28 The patients with HF usually suffer a renal dysfunction,3–5 NT-proBNP may be abnormally elevated in this group of patients, which limits its clinical utility in this setting. 28–29 The ALBI score has no such restrictions, compared to the classic indicator NT-proBNP, ALBI score has not less than its predictive value (C- statistic: z = 0.0938, p = 0.9253). Furthermore, ALBI score can enhance the predictive significance of NT-proBNP (C- statistic: z = 1.990, p = .0467; IDI = 0.0082, p < 0.001; NRI = 0.4012, p < 0.001).
Although the detailed pathophysiological correlation linking liver dysfunction to HF requires detailed assessments, numerous likely mechanisms can be postulated. Severe congestive HF is linked to two different kinds of liver conditions: acute hepatocellular necrosis that is caused by compromised blood supply as well as jaundice, which is correlated with the passive congestion.30 Compromised blood supply due to diminished cardiac output has a connection with acute hepatocellular necrosis with distinct escalations in serum aminotransferases.31 The passive hepatic congestion is associated with the elevated central venous pressure, resulting in increments in the levels of liver enzymes, as well as indirect and direct circulating bilirubin. Kato et al studied liver metabolism of HF in a rat model and established that congestive HF is linked to atypical metabolism in tissues adjacent to the heart.32 In the congestive HF rats, hepatic protein blood concentrations, including albumin, transferrin, retinol-binding protein, and transthyretin were reduced and correlated with elevated levels of circulatory proinflammatory cytokines (TNF-α and IL-1β). Because of heart which has poor capacity of energy storage, and it need a continuous energy supply, all the above studies support the possibility that liver dysfunction may lead to impaired cardiac energy supply, which may lead to a poor prognosis.32,33 The ALBI score was initially created from Japanese hepatocellular carcinoma (HCC) patients to estimate the extent of liver dysfunction.9 However, it has also been widely used in patients without HCC. 33–36Notably, one study posited that the ALBI score was related to liver function as assayed by the indocyanine green injection test. 37 These results support that the ALBI score can reflect residual liver function reserve, even in patients without HCC.
Our findings have some clinical significance. First, observing ALBI in HF patients may be significant in establishing HF patients with elevated risk of in-hospital adverse events. Moreover, the predictive significance of ALBI score is as good as that achieved by NT-proBNP. If the patient is combined with kidney dysfunction, which NT-proBNP is limited for clinical utility, ALBI score may be useful for this setting. At last, if we consider the patient's cardiac function and liver dysfunction together, it may bring some help to clinicians.
The current study has several limitations. First, it constituted a retrospective and observational design; therefore, possible confounders and selection bias were not absolutely adjusted. Secondly, we did not examine all the LFTs individually, as some biosignatures were missing in our dataset. For example, in the FINRISK study, moderate to high levels of serum γ-glutamyltransferase were markedly correlated with incident HF among 38076 people.38 In addition, higher alkaline phosphatase was linked to a dismal prognosis in patients with AHF.39 Thirdly, the study population constituted part of the Asians, therefore, the results of the study may need to be further serious in other populations.