Beta-Blocker Use in Hypertension and Heart Failure (A Secondary Analysis of the Systolic Blood Pressure Intervention Trial)

Daniel N. Silverman, Jeanne du Fay de Lavallaz, Timothy B. Plante, Margaret M. Infeld, Parag Goyal, Stephen P. Juraschek, Geoff B. Dougherty, Peter W. Callas, Markus Meyer

Research output: Contribution to journalArticlepeer-review

Abstract

Given the concern that beta-blocker use may be associated with an increased risk for heart failure (HF) in populations with normal left ventricular systolic function, we evaluated the association between beta-blocker use and incident HF events, as well as loop diuretic initiation in the Systolic Blood Pressure Intervention Trial (SPRINT). SPRINT demonstrated that a blood pressure target of <120 mm Hg reduced cardiovascular outcomes compared with <140 mm Hg in adults with at least one cardiovascular risk factor and without HF. The lower rate of the composite primary outcome in the 120 mm Hg group was primarily driven by a reduction in HF events. Subjects on a beta blocker for the entire trial duration were compared with subjects who never received a beta blocker after 1:1 propensity score matching. A competing risk survival analysis by beta-blocker status was performed to estimate the effect of the drug on incident HF and was then repeated for a secondary end point of cardiovascular disease death. Among the 3,284 propensity score–matched subjects, beta-blocker exposure was associated with an increased HF risk (hazard ratio 5.86; 95% confidence interval 2.73 to 13.04; p <0.001). A sensitivity analysis of propensity score–matched cohorts with a history of coronary artery disease or atrial fibrillation revealed the same association (hazard ratio 3.49; 95% confidence interval 1.15 to 10.06; p = 0.028). In conclusion, beta-blocker exposure in this secondary analysis was associated with increased incident HF in subjects with hypertension without HF at baseline.

Original languageEnglish (US)
Pages (from-to)58-64
Number of pages7
JournalAmerican Journal of Cardiology
Volume165
DOIs
StatePublished - Feb 15 2022

Bibliographical note

Funding Information:
This work was supported by grant R01 HL-122744 to Dr. Meyer from the National Institutes of Health (Bethesda, MD, USA) and grant K23 HL135273 to Dr. Juraschek from the National Institutes of Health (Bethesda, MD, USA).

Publisher Copyright:
© 2021

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural

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