Evidence map›Paper›PMID 41291975›Full record

ArticleCardio-oncology (London, England)2025

CPX-351 vs. conventional chemotherapy cardiotoxicity in high-risk AML: a post hoc phase III trial analysis.

Joshua D Mitchell, Michael Pfeiffer, John Boehmer, John Gorcsan, Shunsuke Eguchi, Yoshiyuki Orihara, Nalina Dronamraju, Sonja Dhani, Stefan Faderl, Tara L Lin and 3 more

Erratum issuedAbstract read
In one paragraph

Article in Cardio-oncology (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors.

Joshua D MitchellWashington University School of Medicine, 660 S. Euclid Ave, St Louis, MO, 63110, USA. jdmitchell@wustl.edu.ORCID http://orcid.org/0000-0001-7371-5742
Michael PfeifferHeart and Vascular Institute, Penn State Hershey Medical Center, Hershey, PA, USA.ORCID http://orcid.org/0000-0002-6472-7896
John BoehmerHeart and Vascular Institute, Penn State Hershey Medical Center, Hershey, PA, USA.
John GorcsanHeart and Vascular Institute, Penn State Hershey Medical Center, Hershey, PA, USA.
Shunsuke EguchiHeart and Vascular Institute, Penn State Hershey Medical Center, Hershey, PA, USA.ORCID http://orcid.org/0009-0007-6436-8110
Yoshiyuki OriharaHeart and Vascular Institute, Penn State Hershey Medical Center, Hershey, PA, USA.ORCID http://orcid.org/0000-0002-7438-8250
Nalina DronamrajuJazz Pharmaceuticals Plc, Dublin, Ireland.
Sonja DhaniJazz Pharmaceuticals Plc, Dublin, Ireland.
Stefan FaderlJazz Pharmaceuticals Plc, Dublin, Ireland.
Tara L LinDivision of Hematologic Malignancies & Cellular Therapeutics, University of Kansas, Kansas City, KS, USA.ORCID http://orcid.org/0000-0002-0242-6449
Geoffrey L UyDivision of Oncology, Washington University School of Medicine, St. Louis, MO, USA.
Jeffrey E LancetH. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Jorge E CortesGeorgia Cancer Center at Augusta University, Augusta, GA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCPX-351, a dual-drug liposomal encapsulation of daunorubicin and cytarabine in a synergistic 1:5 molar ratio, has demonstrated significantly improved overall survival in acute myeloid leukemia (AML) compared with 7 + 3, but its impact on cardiac function remains unclear. In a post hoc analysis of the pivotal clinical trial, we sought to determine the relative cardiotoxicity of CPX-351 vs. 7 + 3 in high-risk AML.

methodsWe evaluated cardiotoxicity in 102 patients with AML (CPX-351, n = 57; 7 + 3, n = 45) who had normal baseline left ventricular ejection fraction (LVEF) ≥ 53% and at least one post-baseline echocardiographic assessment. Cardiotoxicity was assessed through reported cardiac adverse events (AEs) and core lab assessment of echocardiograph changes in LVEF and/or left ventricular global longitudinal strain (GLS).

resultsA clinically significant change in LVEF (absolute change from baseline > 10% and LVEF <53%) and GLS (relative change from baseline > 12% and GLS < 18%) was less common with CPX-351 vs. 7 + 3 at follow-up 1 and/or 2 (8.8% vs. 20.0% and 21.1% vs. 44.4%, respectively). No CPX‑351-treated patients evaluated at final follow-up (follow-up 2) had decreased LVEF < 53% at follow-up 2, compared to 17.8% of 7 + 3-treated patients. The frequency of reported cardiac AEs was similar with CPX-351 (40.4%) and 7 + 3 (42.2%); most frequent were tachycardia in CPX-351-treated patients (CPX-351, 21.1%; 7 + 3, 8.9%) and atrial fibrillation/flutter in 7 + 3-treated patients (CPX-351, 7.0%; 7 + 3, 11.1%). 

conclusionIn addition to improving overall survival as demonstrated in the pivotal trial, CPX-351 may also be associated with less cardiotoxicity than 7 + 3 in high-risk AML patients.

Indexed as

7 + 3Acute myeloid leukemiaAnthracyclinesCardiotoxicityCPX-351Ejection fraction

Identifiers

PMID41291975
PMCPMC12797456

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.