10
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Multifactorial QT Interval Prolongation and Takotsubo Cardiomyopathy

      case-report

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A 71-year-old woman collapsed while working as a grocery store cashier. CPR was performed and an AED revealed torsades de pointes (TdP). She was subsequently defibrillated resulting in restoration of sinus rhythm with a QTc interval of 544 msec. Further evaluation revealed a diagnosis of Takotsubo Cardiomyopathy (TCM) contributing to the development of a multifactorial acquired long QT syndrome (LQTS). The case highlights the role of TCM as a cause of LQTS in the setting of multiple risk factors including old age, female gender, hypokalemia, and treatment with QT prolonging medications. It also highlights the multifactorial nature of acquired LQTS and lends support to growing evidence of an association with TCM.

          Related collections

          Most cited references11

          • Record: found
          • Abstract: found
          • Article: not found

          Acquired long QT syndrome from stress cardiomyopathy is associated with ventricular arrhythmias and torsades de pointes.

          Stress cardiomyopathy (SCM) is a syndrome of transient ventricular dysfunction triggered by severe emotional or physical stress, likely resulting from catecholamine-mediated myocardial toxicity. Repolarization abnormalities associated with other hyperadrenergic states can cause QT prolongation and lethal arrhythmia including torsades de pointes (TdP). Despite the development of repolarization abnormalities and QT prolongation in SCM, little is known about the risk of ventricular fibrillation (VF) and TdP.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Clinical and genetic determinants of torsade de pointes risk.

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Novel therapeutics for treatment of long-QT syndrome and torsade de pointes.

              Long-QT syndrome is a clinically and genetically heterogeneous syndrome characterized by lengthening of the QT interval and increased dispersion of the ventricular repolarization on surface electrocardiogram and a propensity to malignant ventricular arrhythmias, torsade de pointes and ventricular fibrillation, which may lead to sudden cardiac death. Long-QT syndrome mostly affects adolescents and young adults with structurally and functionally normal hearts and is caused by aberrations in potassium and sodium ion channels. Standard therapies for long-QT syndrome include correction of the underlying cause, alleviation of the precipitating factors, magnesium sulfate, isoproterenol, antiadrenergic therapy (beta-adrenergic receptor blockers, left cervicothoracic sympathectomy), cardiac pacing, and implantable cardioverter defibrillator. The potential therapies include sodium channel blockers (mexiletine, flecainide, lidocaine, pentisomide, phenytoin), potassium, potassium channel activators (nicorandil, pinacidil, cromakalim), alpha-adrenergic receptor blockers, calcium channel blockers, atropine, and protein kinase inhibitors. The purpose of this review is to outline the established therapies and update the recent advances and potential future strategies in the treatment of long-QT syndrome and torsade de pointes.
                Bookmark

                Author and article information

                Journal
                Case Rep Cardiol
                Case Rep Cardiol
                CRIC
                Case Reports in Cardiology
                Hindawi Publishing Corporation
                2090-6404
                2090-6412
                2014
                14 April 2014
                : 2014
                : 213842
                Affiliations
                1Department of Medicine, Kingston General Hospital, Queen's University, Kingston, ON, Canada K7L 3N6
                2Department of Medicine, Yale University, Bridgeport Hospital, Bridgeport, CT 06610, USA
                3School of Physiology and Pharmacology, University of Bristol, Bristol BS8 1TD, UK
                4Cardiac Electrophysiology and Pacing, Kingston General Hospital, Queen's University, Kingston, ON, Canada K7L 2V7
                Author notes

                Academic Editor: Hajime Kataoka

                Author information
                http://orcid.org/0000-0002-9897-5038
                http://orcid.org/0000-0002-6534-685X
                http://orcid.org/0000-0001-5138-4620
                Article
                10.1155/2014/213842
                4009330
                24822130
                3de5cbca-6beb-45c4-ad3d-5881cc65b107
                Copyright © 2014 Michael Gysel et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 11 March 2014
                : 29 March 2014
                Categories
                Case Report

                Comments

                Comment on this article