{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,24]],"date-time":"2026-07-24T11:16:31Z","timestamp":1784891791852,"version":"3.55.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2025,5,20]]},"abstract":"<jats:sec id=\"jah310876-sec-0001\" xml:lang=\"en\">\n            <jats:title>Background<\/jats:title>\n            <jats:p xml:lang=\"en\">Cancer therapy\u2013related cardiac dysfunction frequently occurs in patients receiving anthracycline. Ivabradine reduces heart rate without affecting contractility and showed anti\u2010inflammatory, antioxidant, and antiapoptotic effects in experimental cardiotoxicity models. This study aims to evaluate the effect of ivabradine on cancer therapy\u2013related cardiac dysfunction in patients with lymphoma or sarcoma treated with anthracycline.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310876-sec-0002\" xml:lang=\"en\">\n            <jats:title>Methods<\/jats:title>\n            <jats:p xml:lang=\"en\">In a randomized, triple\u2010blind trial, patients starting anthracycline therapy received either ivabradine 5\u2009mg twice daily or placebo until 30\u2009days after completing treatment. The primary outcome was the incidence of cardiotoxicity measured as a \u226510% relative reduction in global longitudinal strain at 12\u2009months from baseline. Secondary outcomes included 12\u2010month clinical outcomes, a \u226510% decrease in the left ventricular ejection fraction to &lt;55%, diastolic dysfunction, and troponin T and N\u2010terminal pro\u2010B\u2010type natriuretic peptide levels.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310876-sec-0003\" xml:lang=\"en\">\n            <jats:title>Results<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              This study enrolled 107 patients (51 in the ivabradine group and 56 in the placebo group). The median dose of anthracycline was 300\u2009mg\/m\n              <jats:sup>2<\/jats:sup>\n              (250\u2013300\u2009mg\/m\n              <jats:sup>2<\/jats:sup>\n              ) in both groups. Cardiotoxicity measured as a \u226510% relative reduction in global longitudinal strain at 12\u2009months was reached in 57% versus 50% in the ivabradine and placebo groups (odds ratio, 1.32 [95% CI, 0.61\u20132.83];\n              <jats:italic toggle=\"no\">P<\/jats:italic>\n              =0.477). Fewer patients in the ivabradine group than in the placebo group had troponin T levels \u226514\u2009ng\/L (16 [39.0%] versus 23 [62.2%];\n              <jats:italic toggle=\"no\">P<\/jats:italic>\n              =0.041) at 6\u2009months, with this difference not maintained at the 12\u2010month follow\u2010up. In addition, there were no differences in the other secondary outcomes.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310876-sec-0004\" xml:lang=\"en\">\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p xml:lang=\"en\">A fixed 10\u2009mg\/day dose of ivabradine does not protect patients with cancer against anthracycline cardiotoxicity.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec id=\"jah310876-sec-1005\" xml:lang=\"en\">\n            <jats:title>Registration<\/jats:title>\n            <jats:p xml:lang=\"en\">\n              URL:\n              <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"uri\" xlink:href=\"https:\/\/clinicaltrials.gov\/\">https:\/\/clinicaltrials.gov\/<\/jats:ext-link>\n              ; Unique Identifier: NCT03650205.\n            <\/jats:p>\n          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