Evidence map›Paper›PMID 40694315›Full record

ArticleInternational journal of hematology2025

Cardiovascular toxicity from tyrosine kinase inhibitors in chronic myeloid leukemia with severe dilated cardiomyopathy.

Kenta Hayashino, Naoya Mochizuki, Akihiro Kawatsuki, Yuki Fujiwara, Hiroki Kobayashi, Tomoko Yamasaki, Takeru Asano, Shiro Kubonishi, Yasushi Hiramatsu

Abstract readCase Reports
PubMed Publisher
In one paragraph

Article in International journal of hematology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Kenta HayashinoDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan. ftyontyon8840@gmail.com.ORCID http://orcid.org/0000-0003-0092-1339
Naoya MochizukiDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Akihiro KawatsukiDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Yuki FujiwaraDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Hiroki KobayashiDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Tomoko YamasakiDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Takeru AsanoDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Shiro KubonishiDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.
Yasushi HiramatsuDepartment of Hematology and Oncology, Japanese Red Cross Society Himeji Hospital, 1-12-1, Shimoteno, Himeji-shi, Hyogo, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tyrosine kinase inhibitors (TKIs) have significantly improved the prognosis of patients with chronic myeloid leukemia (CML). However, few patients maintain remission after discontinuing TKIs, and most require long-term treatment. Prolonged use of TKIs is associated with an increased risk of cardiovascular events (CVEs), particularly in patients with pre-existing cardiovascular comorbidities. We present the case of a 37-year-old man with a decade-long history of severe dilated cardiomyopathy that responded inadequately to standard pharmacologic management, who was under consideration for heart transplantation. Following a diagnosis of CML, the patient experienced various CVEs with TKIs, including dasatinib, bosutinib, imatinib, and nilotinib. These agents were discontinued, and treatment was switched to asciminib, a novel agent that targets the myristoyl pocket of the BCR::ABL1 protein distinct from the ATP-binding site targeted by conventional TKIs. This treatment was well tolerated without any CVEs. Given its minimal off-target activity and lower reported incidence of CVEs, asciminib may offer a viable and safer therapeutic option for CML patients with advanced cardiovascular comorbidities, including those awaiting heart transplantation.

Indexed as

Cardiomyopathy, DilatedLeukemia, Myelogenous, Chronic, BCR-ABL PositiveProtein Kinase InhibitorsAdultAniline CompoundsCardiotoxicityHumansImatinib MesylateMaleNiacinamideNitrilesPyrazolesQuinolinesTyrosine Kinase InhibitorsAniline CompoundsasciminibbosutinibImatinib MesylateNiacinamideNitrilesProtein Kinase InhibitorsPyrazolesQuinolinesTyrosine Kinase InhibitorsCardiovascular events, asciminibChronic myeloid leukemiaDilated cardiomyopathyTyrosine kinase inhibitor

Identifiers

PMID40694315

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.