Abstract
BackgroundBoth β1 adrenergic receptor autoantibody (β1-AA) and soluble suppression of tumorigenicity-2 (sST2) take a role in the pathological remodeling of heart failure. However, limited studies investigated the correlation between the expression of β1-AA and sST2 in patients with acutely decompensated heart failure (ADHF).ObjectiveTo explore the correlation between β1-AA and sST2, and evaluate their prognostic value in patients with ADHF.MethodsPatients who were admitted for ADHF were included. The N-terminal pro-brain natriuretic peptide (NT-proBNP), sST2, and β1-AA in blood samples were tested at hospital admission and then followed up for assessing the outcomes. Pearson correlation analysis was used to explore the correlation between β1-AA and sST2. The effects of β1-AA, sST2, or the combination of them on the all-cause mortality of patients with ADHF were assessed by Multivariate Cox regression analysis.ResultsThere were 96 patients with ADHF and 96 control populations enrolled. The β1-AA was significantly higher in ADHF than in the control group (0.321 ± 0.06 vs. 0.229 ± 0.04, P = 0.000). Pearson correlation analysis showed that β1-AA was positively correlated with sST2 (r = 0.593), NT-proBNP (r = 0.557), Procalcitonin (r = 0.176), and left ventricular end-diastolic diameter (r = 0.315), but negatively correlated with triglycerides (r = −0.323), and left ventricular ejection fraction (r = −0.430) (all P < 0.05) in ADHF. Patients with ADHF, complicated with both high β1-AA and sST2, showed the highest all-cause mortality during an average of 25.5 months of follow-up. Multivariate Cox regression showed the combination of both high β1-AA and sST2 independently correlated with the all-cause mortality after adjustment for other risk factors (hazard ratio 3.348, 95% CI 1.440 to 7.784, P = 0.005). After adding with β1-AA and sST2, the area under the curves for the prognostic all-cause mortality could increase from 0.642 to 0.748 (P = 0.011).ConclusionThe β1-AA is positively correlated with sST2 in patients with ADHF. Elevated plasma β1-AA and sST2 level in patients with ADHF are associated with poorer prognoses.
Highlights
Heart failure (HF) is a terminal stage of heart disease characterized by high mortality, which becomes more and more prevalent and brings a huge burden to health care [1]
Pearson correlation analysis showed that β1 adrenergic receptor autoantibody (β1-AA) was positively correlated with suppression of tumorigenicity-2 (sST2) (r = 0.593), NT-proBNP (r = 0.557), Procalcitonin (r = 0.176), and left ventricular end-diastolic diameter (r = 0.315), but negatively correlated with triglycerides (r = −0.323), and left ventricular ejection fraction (r = −0.430) in Acutely decompensated HF (ADHF)
Multivariate Cox regression showed the combination of both high β1-AA and sST2 independently correlated with the all-cause mortality after adjustment for other risk factors
Summary
Heart failure (HF) is a terminal stage of heart disease characterized by high mortality, which becomes more and more prevalent and brings a huge burden to health care [1]. The β1 adrenergic receptor (β1-AR) is a G proteincoupled receptor that triggers physiological or pathological responses via activating the signaling cascade of adenylate cyclase, cyclic adenosine 3’,5’-monophosphate, and protein kinase A This signaling pathway regulates intracellular calcium concentration and determines cardiomyocyte contractility [3]. Studies on clinical heart failure found that the β 1-AA can be antagonized by β-blockers and can be eliminated through immunoadsorption, which reverses the pathological remodeling and improves cardiac function [9, 10]. Both β1 adrenergic receptor autoantibody (β1-AA) and soluble suppression of tumorigenicity-2 (sST2) take a role in the pathological remodeling of heart failure. Limited studies investigated the correlation between the expression of β1-AA and sST2 in patients with acutely decompensated heart failure (ADHF)
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