ArticleThe American journal of cardiology2024
Symptomatic Heart Failure and Clonal Hematopoiesis-Related Mutations in Patients With Acute Myeloid Leukemia.
Article in The American journal of cardiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Mutations in CHIP-associated genes at myeloid neoplasm diagnosis and risk of cardiovascular/cerebrovascular events.Annals of medicine · 2026Article
- Determining Risk Factors Associated with Cardiovascular Complications in Patients with Acute Leukemia: A Systematic Review.Cancers · 2025Review
- Beyond Thrombosis: Pulmonary Hypertension and Heart Failure in Patients With Myeloproliferative Neoplasms: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- Acute and Chronic Cardiovascular Adverse Events in Patients with Acute Myeloid Leukemia: A Systematic Review.Cancers · 2025Review
- Novel insights and clinical perception of the patients with acute leukemia transferred to ICU: a multi-center retrospective study spanning 10 years.Frontiers in medicine · 2025Article
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11 authors.
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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.
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