Key result
The presence of β1-adrenoceptor autoantibodies in patients with first STEMI was an independent predictor of major adverse cardiovascular events (HR 1.802; 95% CI 1.301-2.496; P<0.001).
Why the study?
Does the presence of autoantibodies against β1-adrenoceptor and cardiac troponin-I predict left ventricular remodeling and MACEs in patients with first STEMI?
Cohort (n=491)
Yes
Does the presence of autoantibodies against β1-adrenoceptor and cardiac troponin-I predict left ventricular remodeling and MACEs in patients with first STEMI?
Hazard Ratio: 1.802 (95% CI 1.301–2.496)
p-value: p=< 0.001
In patients with first STEMI, autoantibodies against β1-adrenoceptor and cardiac troponin-I are prevalent and independently predict left ventricular remodeling, with β1-aab also predicting MACEs.
May support post-STEMI risk stratification; leaves open whether autoantibodies are causal or actionable targets.
AIMS: The prevalence and potential role of autoantibodies against the β1-adrenoceptor autoantibody (β1-aab) and cardiac troponin-I (anti-cTnI) in patients with ST-elevation myocardial infarction (STEMI) are unknown. The aim of this study is to test whether β1-aab and anti-cTnI are prevalent in STEMI patients and to investigate their prognostic value for left ventricular remodeling and clinical outcomes in STEMI patients. METHODS: This study included 491 patients with first STEMI at two centers. Serum samples were obtained. β1-aab and anti-cTnI were detected by enzyme-linked immunoabsorbent assay. Echocardiographic assessments were performed at admission and following 1 year. The major adverse cardiovascular events (MACEs) were evaluated during a median follow-up period of 37 months. RESULTS: The positive rates of β1-aab and anti-cTnI in STEMI patients were 39.1 and 19.1%, respectively. The extent of left ventricular remodeling correlated with the presence of β1-aab and/or anti-cTnI (double positive > single positive > double negative). Logistic regression revealed that both β1-aab [odds ratio (OR) 2.298, 95% confidence interval (CI) 1.561-3.384, P < 0.001] and anti-cTnI (OR 2.389, 95% CI 1.460-3.909, P = 0.001) were predictive of left ventricular remodeling. Cox proportional-hazard regression revealed that β1-aab, but not anti-cTnI, was strongly predictive of MACEs (hazard ratio 1.802, 95% CI 1.301-2.496, P < 0.001). CONCLUSION: β1-aab and anti-cTnI were prevalent in STEMI patients. Both β1-aab and anti-cTnI were independent predictors of left ventricular remodeling, whereas only β1-aab was an independent predictor of MACEs. Our findings suggest that β1-aab and anti-cTnI may actively participate in the process of left ventricular remodeling after STEMI.
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Fan et al. (2015) conducted a cohort in ST-elevation myocardial infarction (STEMI) (n=491). β1-adrenoceptor autoantibody (β1-aab) vs. Absence of β1-aab was evaluated on Major adverse cardiovascular events (MACEs) (HR 1.802, 95% CI 1.301-2.496, p=< 0.001). The presence of β1-adrenoceptor autoantibodies in patients with first STEMI was an independent predictor of major adverse cardiovascular events (HR 1.802; 95% CI 1.301-2.496; P<0.001).
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