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KATP channel polymorphism is associated with left ventricular size in hypertensive individuals: a large-scale community-based study

Santiago Reyes1, 2, Andre Terzic1, 2, 3, Douglas W. Mahoney4, Margaret M. Redfield1, Richard J. Rodeheffer1 and Timothy M. Olson1, 2, 3, 5 Contact Information

(1)  Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN, USA
(2)  Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Rochester, MN, USA
(3)  Department of Medical Genetics, Mayo Clinic, Rochester, MN, USA
(4)  Division of Biostatistics, Department of Health Sciences Research, Mayo Clinic, Rochester, MN, USA
(5)  Division of Pediatric Cardiology, Department of Pediatric and Adolescent Medicine, Mayo Clinic, Stabile 5, 200 First Street SW, Rochester, MN 55905, USA

Received: 14 April 2008  Accepted: 19 May 2008  Published online: 27 May 2008

Abstract  ATP-sensitive K+ (KATP) channel mutations have been identified in individuals with dilated cardiomyopathy and overt heart failure. Here, a common E23K functional polymorphism in the Kir6.2 channel pore versus cardiac phenotype was studied in a cross-sectional community-based cohort (n = 2,031). The KK genotype was associated with greater left ventricular size among subjects with increased stress load due to hypertension. These findings implicate Kir6.2 K23 as a risk factor for adverse subclinical myocardial remodeling, and underscore the significance of cardiac KATP channels within the population.

Contact Information Timothy M. Olson
Email: olson.timothy@mayo.edu
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Referenced by
5 newer articles

  1. Olson, Timothy M. (2009) Human KATP channelopathies: diseases of metabolic homeostasis. Pflügers Archiv - European Journal of Physiology
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  2. Reyes, Santiago (2009) Targeted Disruption of KATP Channels Aggravates Cardiac Toxicity in Cocaine Abuse. Clinical and Translational Science
    [CrossRef]
  3. Reyes, Santiago (2009) KATP channel Kir6.2 E23K variant overrepresented in human heart failure is associated with impaired exercise stress response. Human Genetics
    [CrossRef]
  4. Yamada, Satsuki (2008) Embryonic Stem Cell Therapy of Heart Failure in Genetic Cardiomyopathy. Stem Cells 26(10)
    [CrossRef]
  5. Zlatkovic, Jelena (2009) Proteomic profiling of KATP channel-deficient hypertensive heart maps risk for maladaptive cardiomyopathic outcome. PROTEOMICS 9(5)
    [CrossRef]
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