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Symptomatic Heart Failure and Clonal Hematopoiesis-Related Mutations in Patients With Acute Myeloid Leukemia.

Author information

Affiliations

  • 1. Division of Cardiovascular Disease, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
      Authors
    • Kang Y 1
    • Lefebvre B 1
    • Pamies IM 1
    • Denduluri S 1
    • Scherrer-Crosbie M 1
    (5 authors)
  • 2. Division of Hematology and Oncology Disease, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania; Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
      Authors
    • Gill SI 2
    • McCurdy S 2
    • Luger S 2
    (3 authors)
  • 3. Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
      Authors
    • Doucette AG 3
    (1 author)
  • 4. Division of Cardiovascular Disease, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania; Division of Hematology and Oncology Disease, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
      Authors
    • Smith AM 4
    (1 author)
  • 5. Division of Cardiovascular Disease, Department of Medicine, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania; Abramson Cancer Center, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania.
      Authors
    • Carver J 5
    (1 author)

The American Journal of Cardiology, 06 Jul 2024, 226:9-17
https://doi.org/10.1016/j.amjcard.2024.06.033 PMID: 38972534 

Free full text available after 01 Sep 2025

Abstract 

Clonal hematopoiesis of indeterminate potential (CHIP) is a common risk factor for hematologic malignancies and cardiovascular diseases. This study aimed to investigate the association between CHIP-related mutations and symptomatic heart failure (HF) in patients diagnosed with acute myeloid leukemia (AML). A total of 563 patients with newly diagnosed AML who underwent DNA sequencing of bone marrow before treatment were retrospectively investigated. Cox proportional hazard regression models and Fine and Gray's subdistribution hazard regression models were used to assess the association between CHIP-related mutations and symptomatic HF. A total of 79.0% patients had at least 1 CHIP-related mutation; the most frequent mutations were DNMT3A, ASXL1, and TET2. A total of 51 patients (9.1%) developed symptomatic HF. The incidence of symptomatic HF was more frequent in patients with DNMT3A mutations (p <0.01), with a 1-year cumulative incidence of symptomatic HF in patients with DNMT3A mutations of 11.4%, compared with 3.9% in patients with wild-type DNMT3A (p <0.01). After adjustment for age and anthracyclines dose, DNMT3A mutations remained independently correlated with HF (hazard ratio 2.32, 95% confidence interval 1.26 to 4.29, p = 0.01). In conclusion, in patients with AML, the presence of DNMT3A mutations was associated with a twofold increased risk for symptomatic HF, irrespective of age and anthracyclines use.

Full text links 

Read article at publisher's site: https://doi.org/10.1016/j.amjcard.2024.06.033

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Funding 

Funders who supported this work.

NHLBI NIH HHS (1)

National Heart, Lung, and Blood Institute (1)

National Institutes of Health