Evidence-based beta blocker use associated with lower heart failure readmission and mortality, but not all-cause readmission, among Medicare beneficiaries hospitalized for heart failure with reduced ejection fraction

PLoS One. 2020 Jul 9;15(7):e0233161. doi: 10.1371/journal.pone.0233161. eCollection 2020.

Abstract

The beta blockers carvedilol, bisoprolol, and sustained-release metoprolol succinate reduce readmissions and mortality among patients with heart failure with reduced ejection fraction (HFrEF), based upon clinical trial and registry studies. Results from these studies may not generalize to the typical patient with HFrEF. We conducted a retrospective cohort study of beneficiaries in the Medicare 5% sample hospitalized for HFrEF between 2007 and 2013 and were discharged alive. We compared the 30-day and 365-day heart failure (HF) readmission, all-cause readmission, and mortality rates between beneficiaries who filled a prescription for an evidence-based beta blocker and those who did not after being hospitalized for HFrEF. Out of 12,127 beneficiaries hospitalized for HFrEF, 20% were readmitted for HF, 62% were readmitted for any cause, and 27% died within 365 days. In competing risk models adjusted for demographics, healthcare utilization, and comorbidities, beta blocker use was associated with a lower risk of HF readmission between 8-365 days post discharge (hazard ratio 0.79 [95% confidence interval 0.76, 0.82]), but was not significantly associated with all-cause readmission (1.02 [0.97-1.07]). In Cox models adjusted for the same covariates, beta blocker use was associated with lower mortality 8-365 days post discharge (0.65 [0.60-0.71]). Results were similar when follow up was truncated at 30 days post discharge. Increasing the use of beta blockers following HFrEF hospitalization may not decrease all-cause readmissions among Medicare beneficiaries, but may reduce HF-specific readmissions and mortality.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Astrocytes / metabolism
  • Astrocytes / virology*
  • Astrocytoma / metabolism
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism
  • Cell Line
  • Cyclic AMP Response Element-Binding Protein / metabolism
  • Cysteine-Rich Protein 61 / genetics
  • Cysteine-Rich Protein 61 / metabolism*
  • Humans
  • Mice
  • Mice, Inbred C57BL
  • Phosphorylation
  • Serine Endopeptidases / metabolism
  • Up-Regulation
  • Viral Nonstructural Proteins / metabolism
  • Viral Proteins / metabolism
  • Virus Replication
  • Zika Virus / physiology*
  • Zika Virus Infection / metabolism
  • Zika Virus Infection / virology*

Substances

  • CCN1 protein, human
  • CCN1 protein, mouse
  • Cyclic AMP Response Element-Binding Protein
  • Cysteine-Rich Protein 61
  • Viral Nonstructural Proteins
  • Viral Proteins
  • Calcium-Calmodulin-Dependent Protein Kinase Type 2
  • NS3 protein, zika virus
  • Serine Endopeptidases

Grants and funding

The study was funded by Amgen Inc and NIH National Heart, Lung, and Blood Institute (5T32HL00745734). This research was supported by an academic collaboration between the University of Alabama at Birmingham and Amgen, Inc. The funders provided comments on the design and interpretation of this work. The academic authors conducted all analyses and maintained the rights to publish this manuscript.