Key result
The combination of high β1-AA and sST2 levels was independently associated with a significantly increased risk of all-cause mortality (HR 3.348) in patients with acutely decompensated heart failure.
Why the study?
Limited studies have investigated the correlation between β1 adrenergic receptor autoantibody and soluble suppression of tumorigenicity-2 expression in patients with acutely decompensated heart failure.
Cohort (n=192)
No
Elevated plasma β1-AA and sST2 levels are positively correlated in patients with acutely decompensated heart failure, and their combination independently predicts higher all-cause mortality.
Answers are grounded in this paper and cite their sources.
β1-AA–sST2 correlation in ADHF is hypothesis-generating; leaves open prognostic utility pending larger prospective validation.
Background Both 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). Objective To explore the correlation between β1-AA and sST2, and evaluate their prognostic value in patients with ADHF. Methods Patients 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. Results There 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). Conclusion The 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.
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Sun et al. (2022) conducted a cohort in Acutely Decompensated Heart Failure (ADHF) (n=192). High β1-AA and sST2 levels vs. Low β1-AA and sST2 levels was evaluated on All-cause mortality (HR 3.348, 95% CI 1.440-7.784, p=0.005). The combination of high β1-AA and sST2 levels was independently associated with a significantly increased risk of all-cause mortality (HR 3.348) in patients with acutely decompensated heart failure.
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