Cardiac arrhythmia and thyroid dysfunction: A novel genetic link |
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| Authors: | Kerry Purtell Torsten K Roepke Geoffrey W Abbott |
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| Institution: | 1. Department of Pharmacology, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY, USA;2. Department of Medicine, Weill Medical College of Cornell University, 1300 York Avenue, New York, NY, USA;3. Clinic for Cardiology and Angiology, Charité University-Medicine, Berlin, Campus Mitte and Experimental and Clinical Research Center, Max Delbrueck Center for Molecular Medicine, Berlin, Germany;2. Mercy Heart & Vascular Institute, Sacramento, California;3. Helmsely Cardiac Arrhythmia Service, Mount Sinai School of Medicine, New York, New York;2. Biomedical Engineering Laboratory D.E.I., University of Bologna, Cesena, Italy;2. Washington Adventist Hospital, Takoma Park, Maryland;2. Cardiovascular Center, Yokosuka Kyosai Hospital, Kanagawa, Japan;3. Hôpital Cardiologique du Haut-Lévêque and the Université Victor Segalen Bordeaux II, Bordeaux, France;4. Heart Rhythm Center, Tokyo Medical and Dental University, Tokyo, Japan |
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| Abstract: | Inherited Long QT Syndrome (LQTS), a cardiac arrhythmia that predisposes to the often lethal ventricular fibrillation, is commonly linked to mutations in KCNQ1. The KCNQ1 voltage-gated K+ channel α subunit passes ventricular myocyte K+ current that helps bring a timely end to each heart-beat. KCNQ1, like many K+ channel α subunits, is regulated by KCNE β subunits, inherited mutations in which also associate with LQTS. KCNQ1 and KCNE mutations are also associated with atrial fibrillation. It has long been known that thyroid status strongly influences cardiac function, and that thyroid dysfunction causes abnormal cardiac structure and rhythm. We recently discovered that KCNQ1 and KCNE2 form a thyroid-stimulating hormone-stimulated K+ channel in the thyroid that is required for normal thyroid hormone biosynthesis. Here, we review this novel genetic link between cardiac and thyroid physiology and pathology, and its potential influence upon future therapeutic strategies in cardiac and thyroid disease. |
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