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Peer-reviewedCC BY 4.0Journal of Clinical Medicine

Heart Failure with Recovered Ejection Fraction: EGPA-Associated Cardiomyopathy Treated with Benralizumab

  1. 1Department of Heart Failure and Transplant, Mayo Clinic Florida, Jacksonville, FL 32224, USA
  2. 2Department of Neurology, Mayo Clinic Florida, Jacksonville, FL 32224, USA
  3. 3Department of Infectious Diseases, Mayo Clinic Florida, Jacksonville, FL 32224, USA

Abstract

Background: We report a case to demonstrate that targeted eosinophil depletion with Benralizumab (anti-IL-5 receptor α therapy) can induce the complete functional and structural reversal of advanced EGPA-associated cardiomyopathy. Case Presentation: A 56-year-old woman with a decade-long history of EGPA presented with progressive nonischemic dilated cardiomyopathy and a nadir ejection fraction of 25–30%. Cardiac MRI demonstrated diffuse nonischemic late gadolinium enhancement consistent with eosinophil-mediated myocardial injury. Despite the optimization of guideline-directed medical therapy, complete recovery was not achieved until benralizumab was initiated. Following biologic therapy, the ejection fraction recovered to 50% and severe mitral regurgitation regressed to mild. The exercise capacity was preserved throughout, with a peak VO2 of 117% and 111% of predicted before and after biologic therapy, respectively. The patient remains in NYHA Class I at the one-year follow-up. Discussion: We describe a case with EGPA-associated non-ischemic cardiomyopathy treated with benralizumab achieving the complete recovery of ventricular function and achieving the complete independence of steroid therapy. Conclusions: This case emphasizes the importance of identifying the inflammatory etiology of cardiomyopathy, optimizing GDMT systematically, and considering targeted biologic therapy directed at the underlying disease.

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BibTeX
@article{bangari2026heart,
  title = {{Heart Failure with Recovered Ejection Fraction: EGPA-Associated Cardiomyopathy Treated with Benralizumab}},
  author = {Laxmi Raj Bangari and Yugant Khand and Vidit Yadav and Aarti Desai and Andrea Muniz and Jose Ruiz and Jose Nativi-Nicolau and Juan Leoni and Parag Patel and Rohan Goswami},
  journal = {Journal of Clinical Medicine},
  year = {2026},
  month = oct,
  doi = {10.3390/jcm15208057},
  url = {https://www.mdpi.com/2077-0383/15/20/8057},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Heart Failure with Recovered Ejection Fraction: EGPA-Associated Cardiomyopathy Treated with Benralizumab
AU  - Laxmi Raj Bangari
AU  - Yugant Khand
AU  - Vidit Yadav
AU  - Aarti Desai
AU  - Andrea Muniz
AU  - Jose Ruiz
AU  - Jose Nativi-Nicolau
AU  - Juan Leoni
AU  - Parag Patel
AU  - Rohan Goswami
PY  - 2026
DA  - 2026/10/01
JO  - Journal of Clinical Medicine
DO  - 10.3390/jcm15208057
UR  - https://www.mdpi.com/2077-0383/15/20/8057
AB  - Background: We report a case to demonstrate that targeted eosinophil depletion with Benralizumab (anti-IL-5 receptor α therapy) can induce the complete functional and structural reversal of advanced EGPA-associated cardiomyopathy. Case Presentation: A 56-year-old woman with a decade-long history of EGPA presented with progressive nonischemic dilated cardiomyopathy and a nadir ejection fraction of 25–30%. Cardiac MRI demonstrated diffuse nonischemic late gadolinium enhancement consistent with eosinophil-mediated myocardial injury. Despite the optimization of guideline-directed medical therapy, complete recovery was not achieved until benralizumab was initiated. Following biologic therapy, the ejection fraction recovered to 50% and severe mitral regurgitation regressed to mild. The exercise capacity was preserved throughout, with a peak VO2 of 117% and 111% of predicted before and after biologic therapy, respectively. The patient remains in NYHA Class I at the one-year follow-up. Discussion: We describe a case with EGPA-associated non-ischemic cardiomyopathy treated with benralizumab achieving the complete recovery of ventricular function and achieving the complete independence of steroid therapy. Conclusions: This case emphasizes the importance of identifying the inflammatory etiology of cardiomyopathy, optimizing GDMT systematically, and considering targeted biologic therapy directed at the underlying disease.
SN  - 2077-0383
ER  -