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The authors summarize mechanistic plausibility via If current inhibition, preclinical findings, and early clinical trials suggesting reduced troponin elevation and strain changes, while highlighting later higher-quality evidence (including an IPAC triple-blind trial) showing no major differences. Mixed results and uncertainty across cancer types, dosing, and timing are emphasized.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/ivabradine-for-anthracycline-induced-cardiotoxicity-emerging-promise-and-current-evidence/435632/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/ivabradine-for-anthracycline-induced-cardiotoxicity-emerging-promise-and-current-evidence/435632.png","ImageObject",300,407,{"name":92,"@type":93},"dhado","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-11-03","2026-09-29",true,{"@type":102,"interactionType":103,"userInteractionCount":24},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"Why is anthracycline cardiotoxicity clinically challenging?","Question",{"text":112,"@type":113},"It is cumulative and dose-dependent, progressing from subclinical left-ventricular dysfunction to overt heart failure, which limits optimal therapy.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"What is the proposed mechanism of ivabradine for cardioprotection?",{"text":117,"@type":113},"Ivabradine selectively inhibits the If (“funny”) current in the sino-atrial node to reduce heart rate, potentially improving diastolic perfusion and myocardial oxygen balance without harming contractility or systemic blood pressure.",{"name":119,"@type":110,"acceptedAnswer":120},"What do the more recent randomized-controlled data suggest about ivabradine?",{"text":121,"@type":113},"The letter states that the most recent controlled evidence does not show consistent benefit in preventing anthracycline-induced left ventricular dysfunction or biomarker elevation at conventional dosing, and utility remains uncertain across patient contexts.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},435632,1790812364,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":24,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":14,"language":139,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":140,"faqs":141,"seo_title":142,"seo_description":67,"update_tm":143,"read_time":24,"preview_page_count":4},5909893218464,"https://ap-avatar.wpscdn.com/davatar_085a072bc5b1113ac321206ff7593b45","Letter to the Editor  \nIvabradine foranthracycline-inducedcardiotoxicity: emerging promise and currentevidence  \nSaad Arsalan Wasti, MBBSa , Areesha Wasti, MBBSb , Marzhan Berkinbayeva, MBBSc ,Muhammad Usman Iqbal, MBBSa , Naseeb Danaf, MDd ,*  \nDear Editor,  \nAnthracycline-based chemotherapy (including doxorubicin,epirubicin) remains foundational in the management of manytypes of cancers, including breast cancers, lymphomas, sarcomas,and other malignancies. However, its cumulative dose-dependentcardiotoxicity, manifesting from subclinical left-ventricular dys -function to overt heart failure, limits optimal therapy. Emergingstrategies are focussing on early detection and prevention ofcardiotoxicity instead of waiting for symptomatic heart failure.  \nThe pharmacologic rationale for ivabradine as a prophylacticapproach in this regard is plausible. Ivabradine selectively inhibitsthe If (“funny”) current in the sino-atrial node, reducing heart ratewithout adverse effects on myocardial contractility or systemicblood pressure. Lower heart rate reduces myocardial oxygenconsumption, extends diastolic perfusion time and may enhancemyocardial reserve under stress. Preclinical work in rat models ofdoxorubicin (DXR) cardiotoxicity showed that ivabradine atte -nuated cardiac troponin-I release and reduced malondialdehyde(MDA) levels compared to control, suggesting that ivabradinecould be effective in mitigating DXR-induced cardiotoxicity[1] .  \nEarly clinical trials also suggested possible benefits. A 2023 open -label randomized trial in breast cancer patients reported that ivab -radine reduced the incidence of troponin elevation (four-fold lower)compared to controls during anthracycline therapy[2] . Another ran -domized trial discussed the feasibility of ivabradine inpatients withbreast cancer undergoing anthracycline chemotherapy[3] . It foundsignificant differences in the left ventricular global longitudinalstrain in the earlier months of observation (P \u003C 0.05), but after  \naDepartment of Medicine, King Edward Medical University, Lahore, Pakistan,bDepartment of Medicine, Continental Medical College, Lahore, Pakistan,cDepartment of Medicine, Asfendiyarov Kazakh National Medical University, Almaty,Kazakhstan and dDepartment of Medicine, Faculty ofMedical Sciences, LebaneseUniversity, Beirut, Lebanon  \nSponsorships or competing interests that maybe relevant to content are disclosedatthe end of this article.  \n*Corresponding author. Address: Faculty ofMedical Sciences, Lebanese University,Beirut 1100, Lebanon. Tel.: +96171164810. E-mail: naseeb.danaf@st.ul.edu.lb(N. Danaf).  \nCopyright © 2025 The Author(s). Published by Wolters Kluwer Health, Inc. This is anopen access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where itis permissible todownload and share the work provided itis properly cited. The work cannot bechanged in any way or used commercially without permission from the journal.  \nAnnals of Medicine & Surgery (2026) 88:941–942Received 22 October 2025; Accepted 24 October 2025Published online 11 November 2025http://dx.doi.org/10.1097/MS9.0000000000004258  \n12 months the groups were comparable in longitudinal strainvalues.  \nHowever, the evidence is not yet definitive. A recent triple -blind, placebo-controlled trial (IPAC) assessing ivabradine,given 5 mg twice daily, in patients receiving anthracyclinesfound no major differences in global longitudinal strain declineor biomarker release[4] . Importantly, this trial excluded breastcancer patients, leaving ivabradine’s utility in cancer patientsuncertain. Furthermore, a network meta-analysis of 128 trialsin 10 431 cancer patients found that while agents such as beta -blockers and dexrazoxane showed benefit, ivabradine was notamong the high-ranked agents for preventing cardiotoxicity[5] .  \nIvabradine represents an innovative concept in cardio-oncol -ogy prophylaxis, offering selective heart rate reducti","cbCaiqPFHzNkQ29D","https://ap.wps.com/l/cbCaiqPFHzNkQ29D","pdf",183818,"English","# Letter to the Editor\n## Rationale and pharmacologic mechanism\n## Preclinical and early clinical evidence\n## Emerging trials, limitations, and overall assessment\n## Need for larger studies and future directions\n## Ethics approval and consent\n## Consent for publication\n## Funding\n## Author contributions","[{\"question\":\"Why is anthracycline cardiotoxicity clinically challenging?\",\"answer\":\"It is cumulative and dose-dependent, progressing from subclinical left-ventricular dysfunction to overt heart failure, which limits optimal therapy.\"},{\"question\":\"What is the proposed mechanism of ivabradine for cardioprotection?\",\"answer\":\"Ivabradine selectively inhibits the If (“funny”) current in the sino-atrial node to reduce heart rate, potentially improving diastolic perfusion and myocardial oxygen balance without harming contractility or systemic blood pressure.\"},{\"question\":\"What do the more recent randomized-controlled data suggest about ivabradine?\",\"answer\":\"The letter states that the most recent controlled evidence does not show consistent benefit in preventing anthracycline-induced left ventricular dysfunction or biomarker elevation at conventional dosing, and utility remains uncertain across patient contexts.\"}]","Ivabradine for anthracycline-induced cardiotoxicity - emerging promise and current evidence | PDF",1790674442]