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Impaired Ca handling in ventricular cardiomyocytes has been identified as a causative factor for complications in the dystrophic heart, and restoration of normal Ca handling in myocytes has emerged as a promising new therapeutic strategy. In the present study, we explored the hypothesis that ivabradine, a drug clinically approved for the treatment of heart failure and stable angina pectoris, improves Ca handling in dystrophic cardiomyocytes and thereby enhances contractile performance in the dystrophic heart. Therefore, ventricular cardiomyocytes were isolated from the hearts of adult dystrophin\u2010deficient DMD<jats:sup>mdx<\/jats:sup> rats, and the effects of acutely applied ivabradine on intracellular Ca transients were tested. In addition, the drug's acute impact on cardiac function in DMD<jats:sup>mdx<\/jats:sup> rats was assessed by transthoracic echocardiography. We found that administration of ivabradine to DMD<jats:sup>mdx<\/jats:sup> rats significantly improved cardiac function. Moreover, the amplitude of electrically induced intracellular Ca transients in ventricular cardiomyocytes isolated from DMD<jats:sup>mdx<\/jats:sup> rats was increased by the drug. We conclude that ivabradine enhances Ca release from the sarcoplasmic reticulum in dystrophic cardiomyocytes and thereby improves contractile performance in the dystrophic heart.<\/jats:p>","DOI":"10.14814\/phy2.15664","type":"journal-article","created":{"date-parts":[[2023,4,10]],"date-time":"2023-04-10T03:27:37Z","timestamp":1681097257000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Ivabradine acutely improves cardiac Ca handling and function in a rat model of Duchenne muscular dystrophy"],"prefix":"10.14814","volume":"11","author":[{"given":"Petra Lujza","family":"Szabo","sequence":"first","affiliation":[{"name":"Ludwig Boltzmann Institute for Cardiovascular Research at the Center for Biomedical Research and Translational Surgery Medical University of Vienna  Vienna 1090 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