ArticleJACC. CardioOncology2020
Acute Effects of Ibrutinib on Ventricular Arrhythmia in Spontaneously Hypertensive Rats.
Article in JACC. CardioOncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Vasohibin 1 acts as a key regulator of arrhythmogenesis in pressure-overload-induced cardiac hypertrophy.Acta pharmacologica Sinica · 2026Article
- Cardiotoxicity of small-molecule kinase inhibitors in cancer therapy.Experimental hematology & oncology · 2025Review
- Advancements in research on the cardiovascular toxicity caused by TEC family kinases inhibitors.Frontiers in pharmacology · 2025Review
- Cardiovascular Considerations During Cancer Therapy: Gaps in Evidence andJACC. CardioOncology · 2024Review
- Effects and mechanisms of dexmedetomidine preconditioning on isoproterenol-induced ventricular arrhythmias.Scientific reports · 2024Article
- Impaired Cardiac AMPK (5'-Adenosine Monophosphate-Activated Protein Kinase) and CaJournal of the American Heart Association · 2024Article
- Arrhythmogenic Ventricular Remodeling by Next-Generation Bruton's Tyrosine Kinase Inhibitor Acalabrutinib.International journal of molecular sciences · 2024Article
- Chronic Lymphocytic Leukemia: Management of Adverse Events in the Era of Targeted Agents.Cancers · 2024Review
- A real-world pharmacovigilance study of amivantamab-related cardiovascular adverse events based on the FDA adverse event reporting system (FAERS) database.Scientific reports · 2024Article
- Advancements in understanding cardiotoxicity of EGFR- TKIs in non-small cell lung cancer treatment and beyond.Frontiers in pharmacology · 2024Review
- Epidemiology, clinical characteristics and potential mechanism of ibrutinib-induced ventricular arrhythmias.Frontiers in pharmacology · 2024Review
- Tyrosine kinase inhibitor-associated ventricular arrhythmias: a case series and review of literature.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2023Review
- Role of PARP and TRPM2 in VEGF Inhibitor-Induced Vascular Dysfunction.Journal of the American Heart Association · 2023Article
- Cardiovascular Toxicities of Ibrutinib: A Pharmacovigilance Study Based on the United States Food and Drug Administration Adverse Event Reporting System Database.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Ibrutinib-Associated Cardiotoxicity: From the Pharmaceutical to the Clinical.Drug design, development and therapy · 2022Review
- Bruton's tyrosine kinase Inhibitors and Cardiotoxicity: More Than Just Atrial Fibrillation.Current oncology reports · 2021Review
- Deciphering the Electrophysiological Mechanisms for Ibrutinib-Induced Ventricular Arrhythmias.JACC. CardioOncology · 2020Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe Bruton's Tyrosine Kinase Inhibitor ibrutinib is associated with ventricular arrhythmia (VA) and sudden death. However, the pro-arrhythmic electrophysiological dysregulation that results from ibrutinib with age and cardiovascular disease is unknown.
objectivesThis study sought to investigate the acute effects of ibrutinib on left ventricular (LV) VA vulnerability, cytosolic calcium dynamics, and membrane electrophysiology in old and young spontaneous hypertensive rats (SHRs).
methodsLangendorff-perfused hearts of young (10 to 14 weeks) and old (10 to 14 months) SHRs were treated with ibrutinib (0.1 μmol/l) or vehicle for 30 min. Simultaneously, LV epicardial action potential and cytosolic calcium transients were optically mapped following an incremental pacing protocol. Calcium and action potential dynamics parameters were analyzed. VA vulnerability was assessed by electrically inducing ventricular fibrillations (VFs) in each heart. Western blot analysis was performed on LV tissues.
resultsIbrutinib treatment resulted in higher vulnerability to VF in old SHR hearts (27.5 ± 7.5% vs. 5.7 ± 3.7%; p = 0.026) but not in young SHR hearts (8.0 ± 4.9% vs. 0%; p = 0.193). In old SHR hearts, following ibrutinib treatment, action potential duration (APD) alternans (p = 0.008) and APD alternans spatial discordance (p = 0.027) were more prominent. Moreover, calcium transient duration 50 was longer (p = 0.032), calcium amplitude alternans ratio was significantly lower (p = 0.001), and time-to-peak of calcium amplitude was shorter (p = 0.037). In young SHR hearts, there were no differences in calcium and APD dynamics.
conclusionsIbrutinib-induced VA is associated with old age in SHR. Acute dysregulation of calcium and repolarization dynamics play important roles in ibrutinib-induced VF.
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