ADDRESSING THE RACIAL DISPARITY OF ANGIOTENSIN INHIBITOR ASSOCIATED REDUCTION IN HFREF HOSPITALIZATIONS: DISTINGUISHING BETWEEN RACE AND ANCESTRY
Recommended Citation
Littleton S, Luzum JA, Dorsch M, Lanfear D, Liu B. ADDRESSING THE RACIAL DISPARITY OF ANGIOTENSIN INHIBITOR ASSOCIATED REDUCTION IN HFREF HOSPITALIZATIONS: DISTINGUISHING BETWEEN RACE AND ANCESTRY. Clin Pharmacol Ther 2024; 115:S11.
Document Type
Conference Proceeding
Publication Date
2-14-2024
Publication Title
Clin Pharmacol Ther
Abstract
BACKGROUND: Angiotensin inhibitors are vital for heart failure (HF) treatment and reducing HF-related hospitalizations. Despite this, HF hospitalization rates in the US remain high, with unexplained racial disparities between Black and White HF patients. This work aimed to investigate the influence of genomic ancestry and self-identified race on the racial disparities in angiotensin inhibitor-associated reductions in HF hospitalizations. METHODS: The work included 977 patients from a registry at Henry Ford Health System (HFPGR) and 810 patients from the GUIDE-IT clinical trial, all with heart failure reduced ejection fraction (HFrEF). At Henry Ford, 492 self-identified Black and 485 self-identified White patients were followed for an average of 3.0 years. Additionally, 381 patients had >80% African genomic ancestry, while 471 had <5%. In GUIDE-IT, 322 self-identified Black patients and 488 self-identified White patients were followed for an average of 1.2 years. Angiotensin inhibitor exposure was calculated from pharmacy claims, and African genomic ancestry was determined by a genome-wide array in Henry Ford patients. Fine and Gray time-dependent Cox proportional hazards models were used to assess the association of drug exposure with the first recorded HF hospitalization by self-identified race in both Henry Ford and GUIDE-IT patients or by the proportion of African ancestry in Henry Ford patients. A P-value of <0.05 was considered statistically significant for main effects, and <0.1 for interactions. Both models were evaluated unadjusted and adjusted for baseline risk factors (eg. age, sex, ejection fraction) and angiotensin inhibitor propensity score. RESULTS: Results are presented in the Figure. CONCLUSION: In summary, these results demonstrated no significant difference in angiotensin inhibitor-associated reduction in HFrEF hospitalizations by self-identified race or genomic ancestry. Black patients and those with >80% African ancestry did not show increased risk, while White patients and those with <5% African ancestry had a slightly elevated risk. Overall, no racial disparities in angiotensin inhibitor-associated reductions in HFrEF hospitalizations were observed in these patient cohorts. This suggests the need for future research to explore the social context of self-identified race, including social determinants of health.
Volume
115
First Page
S11
