Advertisement
Canadian Journal of Cardiology

Correlation of Serum Alanine Transaminase With Amiodarone Parent and Metabolite Concentrations Persists for 16 Years of Follow-up

  • Syed Qutb Shah
    Affiliations
    Department of Medicine, Cummings School of Medicine, University of Calgary, Calgary, Alberta, Canada

    Libin Cardiovascular Institute, Cummings School of Medicine, University of Calgary, Calgary, Alberta, Canada
    Search for articles by this author
  • Satish R. Raj
    Affiliations
    Department of Cardiac Sciences, Cummings School of Medicine, Calgary, Alberta, Canada

    Libin Cardiovascular Institute, Cummings School of Medicine, University of Calgary, Calgary, Alberta, Canada
    Search for articles by this author
  • P. Timothy Pollak
    Correspondence
    Corresponding author: Dr P. Timothy Pollak, University of Calgary, 3330 Hospital Drive NW-1410 HSC, Calgary, Alberta T2N 4N1, Canada. Tel.: +1-403-210-8743; fax: +1-403-283-6151.
    Affiliations
    Department of Medicine, Cummings School of Medicine, University of Calgary, Calgary, Alberta, Canada

    Department of Cardiac Sciences, Cummings School of Medicine, Calgary, Alberta, Canada

    Libin Cardiovascular Institute, Cummings School of Medicine, University of Calgary, Calgary, Alberta, Canada
    Search for articles by this author
Published:April 13, 2022DOI:https://doi.org/10.1016/j.cjca.2022.04.008
      Amiodarone (AMIO) is an antiarrhythmic agent with superior efficacy for atrial fibrillation (AF) and ventricular arrhythmias but also carrying a reputation for hepatotoxicity. Although its unique pharmacokinetic properties promote efficacy, they also pose challenges for optimizing dosing. Concentration measurements of serum AMIO and its active metabolite, desethylamiodarone (DEA), can provide objective information to guide dose adjustment and help avoid potential adverse effects. We observed a consistent temporal relationship between serum alanine transaminase (ALT) and serum AMIO-DEA concentrations persisting over 16 years in a patient who intermittently self-adjusted her dosing in response to anxiety over palpitations.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'

      Subscribe:

      Subscribe to Canadian Journal of Cardiology
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect

      References

        • Pollak P.T.
        • Bouillon T.
        • Shafer S.L.
        Population pharmacokinetics of long-term oral amiodarone therapy.
        Clin Pharmacol Ther. 2000; 67: 642-652
        • Babatin M.
        • Lee S.S.
        • Pollak P.T.
        Amiodarone hepatotoxicity.
        Curr Vasc Pharmacol. 2008; 6: 228-236
        • Pollak P.T.
        • Shafer S.L.
        Use of population modeling to define rational monitoring of amiodarone hepatic effects.
        Clin Pharmacol Ther. 2004; 75: 342-351
        • Rotmensch H.H.
        • Belhassen B.
        • Swanson B.N.
        • et al.
        Steady-state serum amiodarone concentrations: relationships with antiarrhythmic efficacy and toxicity.
        Ann Intern Med. 1984; 101: 462-469
        • Ruzieh M.
        • Moroi M.K.
        • Aboujamous N.M.
        • et al.
        Meta-analysis comparing the relative risk of adverse events for amiodarone versus placebo.
        Am J Cardiol. 2019; 124: 1889-1893