Abstract 11877: Beta-blocker Dose Stratifies Both Mortality Risk and Circulating Procollagen Levels In African-Americans With Heart Failure
Introduction: While African Americans (AAs) have the highest prevalence of heart failure (HF) and HF mortality, insufficient data exists regarding the impact of HF medication on mortality in AAs. This study aimed to identify medication use practices associated with survival in a predominantly AA HF population.
Methods: HF patients were prospectively recruited from, and followed within, the University of Illinois Health System from 11/2001 to 11/2015, when vital status was determined. Data were extracted from electronic health records and Social Security Death Index. Beta-blocker (BB), ACE-I, and ARB doses were categorized as high, medium, or low based on published HF trials. Associations between dose and all-cause mortality were assessed using a Cox proportional hazard model, adjusting for enrollment age, sex, race, ischemic or non-ischemic etiology, NYHA functional class, and concomitant HF medication use. Using linear regression (adjusted for the same covariates), doses were also compared with plasma procollagen N-terminal peptide type III (PIIINP) levels, a previously shown marker for cardiac fibrosis.
Results: In total, 352 patients (75% AA, 50% female, 63% HFrEF: LVEF < 45%) consented to participate, with 84 dying by the end of data recording. Of those, 95% used BBs, 90% ACE-I/ARBs, and 19% ARAs. ACE-I/ARB dose was not associated with mortality (HR: 0.86, 95% CI: 0.62-1.17, P = 0.33). In contrast, increased BB dose was associated with reduced risk of death (HR: 0.64, 95% CI: 0.47-0.86, P = 0.003; Figure 1). This effect remained consistent when stratified by HFrEF or HFpEF. Higher BB (but not ACE/ARB) dose was also associated with lower circulating levels of PIIINP (N = 149 patients, P = 0.05), which still trended after further adjustment for BP and HR.
Conclusions: These findings suggest that aggressive titration of BB dose, unlike ACE-I/ARB dose, may confer a mortality benefit in AA patients with HFrEF or HFpEF which may be mediated through decreased cardiac fibrosis.
Author Disclosures: J.D. Duarte: None. M.J. Arwood: None. I. Liko: None. I. Mansour: None. M. Kansal: None. T. Stamos: None. L.H. Cavallari: None. A.A. Desai: None.
- © 2016 by American Heart Association, Inc.