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The rationale for repurposing funny current inhibition for management of ventricular arrhythmia

  • Praloy Chakraborty
    Affiliations
    The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada

    University Health Network, Toronto, Ontario, Canada
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  • Robert A. Rose
    Affiliations
    Libin Cardiovascular Institute of Alberta, An entity of the University of Calgary and Alberta Health Services, Calgary, Alberta, Canada
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  • Krishnakumar Nair
    Affiliations
    The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada

    University Health Network, Toronto, Ontario, Canada
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  • Eugene Downar
    Affiliations
    The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada

    University Health Network, Toronto, Ontario, Canada
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  • Kumaraswamy Nanthakumar
    Correspondence
    Address reprint requests and correspondence: Dr Kumaraswamy Nanthakumar, Division of Cardiology, University Health Network, Toronto General Hospital, 150 Gerrard St West, GW3-526, Toronto, Ontario, Canada M5G 2C4.
    Affiliations
    The Hull Family Cardiac Fibrillation Management Laboratory, Toronto General Hospital, University Health Network, Toronto, Ontario, Canada

    University Health Network, Toronto, Ontario, Canada
    Search for articles by this author
      Management of ventricular arrhythmia in structural heart disease is complicated by the toxicity of the limited antiarrhythmic options available. In others, proarrhythmia and deleterious hemodynamic and noncardiac effects prevent practical use. This necessitates new thinking in therapeutic agents for ventricular arrhythmia in structural heart disease. Ivabradine, a funny current (If) inhibitor, has proven safety in heart failure, angina, and inappropriate sinus tachycardia. Although it is commonly known that funny channels are primarily expressed in the sinoatrial node, atrioventricular node, and conducting system of the ventricle, ivabradine is known to exert effects on metabolism, ion homeostasis, and membrane electrophysiology of remodeled ventricular myocardium. This review considers novel concepts and evidence from clinical and experimental studies regarding this paradigm, with a potential role of ivabradine in ventricular arrhythmia.

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