# Impact of Medication Dose Optimization on Heart Failure Outcomes in African-American Female Patients: A Safety-Net Hospital Experience

**Authors:** Ricardo A Rodriguez Mejia, Eric Acker, Tark Abou-elmgd, Thirumala Keerthi Chandrika Kammaripalle, Humza Rana

PMC · DOI: 10.7759/cureus.87443 · Cureus · 2025-07-07

## TL;DR

This study shows that optimizing heart failure medications can reduce readmissions and deaths in African-American women, especially when prioritizing certain drug combinations.

## Contribution

The study identifies specific medication prioritization strategies to improve outcomes in African-American female heart failure patients in safety-net hospitals.

## Key findings

- Each one-point increase in GDMT composite reduced 30-day and 90-day readmission risks by 15%.
- Optimizing RAS inhibitors and beta blockers reduced readmission risk significantly.
- Medium-dose MRAs and beta blockers were strongly associated with reduced mortality.

## Abstract

Heart failure among African-American female patients represents a significant public health challenge, with hospitalization rates being much higher than those of White female patients. The high prevalence of comorbidities in this population often necessitates the selective implementation of guideline-directed medical therapy (GDMT). This study examines which medication classes should be prioritized to improve outcomes in this vulnerable population.

We conducted a retrospective study of 283 African-American female patients with heart failure admitted to Cape Fear Valley Medical Center, a safety-net hospital serving low- to medium-income patients in North Carolina, between 2021 and 2022. We analyzed the relationships between GDMT regimens and clinical outcomes using multivariable logistic regression. A GDMT composite, ranging from zero to nine, was developed to measure overall medication optimization.

Among the 283 patients studied, 141 (50%) experienced a 30-day readmission, 161 (57%) a 90-day readmission, and 65 (23%) died within a year. Medication utilization was suboptimal: 28 patients (10%) received the goal doses of renin-angiotensin system (RAS) inhibitors, 37 (13%) were administered goal doses of beta blockers, 11 (4%) received medium/goal doses of mineralocorticoid receptor antagonists (MRAs), and 31 (11%) were given sodium-glucose cotransporter 2 (SGLT2) inhibitors at goal doses. The mean GDMT composite was 2.4±1.8, with only 23 patients (8%) achieving a composite of greater than or equal to five. Each one-point increase in GDMT composite reduced 30-day (OR=0.85, p=0.02) and 90-day (OR=0.86, p=0.03) readmission risks. A higher GDMT composite was associated with decreased mortality in the unadjusted analysis (OR=0.86, p=0.07), with mortality rates declining from 28% (11/39) with a GDMT composite of zero to 10% (1/10) with a composite of greater than or equal to eight. Concurrent optimization of RAS inhibitors and beta blockers reduced readmission risk (OR=0.70, p=0.04). Low-dose MRA lowered 30-day readmission (OR=0.27, p<0.01) and medium-dose beta blockers reduced one-year mortality (OR=0.13, p=0.03), as did medium doses of MRA (OR=0.01, p<0.01). Key clinical predictors included lower ejection fraction (OR=0.95, p<0.01), previous hospitalizations (OR=3.37, p<0.01), and chronic kidney disease (OR=2.49, p=0.03).

In a safety-net hospital setting, strategic prioritization of specific GDMT components improved outcomes among African-American female patients with heart failure and multiple comorbidities. Each one-point increase in the GDMT composite was associated with a 15% reduction in readmission risk and a trend toward lower mortality. Beta blockers should be prioritized for mortality reduction, MRAs for both mortality and readmission reduction, and RAS inhibitors with beta blockers for reducing readmissions. These findings inform medication strategies for clinicians serving similar vulnerable populations.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252), chronic kidney disease (MONDO:0005300)

## Full-text entities

- **Genes:** REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}
- **Diseases:** died (MESH:D003643), Heart Failure (MESH:D006333), chronic kidney disease (MESH:D051436)
- **Chemicals:** SGLT2) inhibitors (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

14 references — full list in the complete paper: https://tomesphere.com/paper/PMC12327919/full.md

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Source: https://tomesphere.com/paper/PMC12327919