(Circulation. 2001;103:2447.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
From the National Heart, Lung, and Blood Institute (P.M.S., R.B.), Bethesda, Md; Brigham and Womens Hospital (C.A.), Boston, Mass; Boston University (E.J.B.), Boston, Mass; Case Western Reserve University (R.C.E.), Cleveland, Ohio; Vanderbilt University (A.L.G.), Nashville, Tenn; Hospital Boucicaut, Paris, France (X.J.); University of Pittsburgh (L.H.K.), Pittsburgh, Pa; Southwest Foundation for Biomedical Research (J.W.M.), San Antonio, Tex; Johns Hopkins Medical School (E.M.), Baltimore, Md; Harvard Medical School (J.E.M.), Boston, Mass; University of Pavia (P.J.S.), Pavia, Italy; University of Washington (D.S.S.), Seattle, Wash; University of Vermont (R.P.T.), Colchester, Vt; University of Rochester (W.Z.), Rochester, NY; and Indiana University (D.P.Z.), Indianapolis, Ind.
Correspondence to Peter M. Spooner, PhD, Director, Arrhythmias, Ischemia, and Sudden Cardiac Death, Division of Heart and Vascular Diseases, National Heart, Lung, and Blood Institute, Two Rockledge Center, Suite 9192, 6701 Rockledge Dr, MSC 7940, Bethesda, MD 20892-7940. E-mail PS48J{at}nih.gov
AbstractThis is Part II of a 2-part article dealing with malignant ventricular arrhythmias, which are the leading mechanism of death in common cardiac diseases. Genetic population studies directed at discovering common proximal sources of inherited molecular risk most directly linked to arrhythmia initiation and propagation would appear to have considerable potential in helping reduce cardiovascular mortality.
Key Words: genetics death, sudden arrhythmia tachyarrhythmias epidemiology mortality ion channels
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