Reyes Santiago, Terzic Andre, Mahoney Douglas W, Redfield Margaret M, Rodeheffer Richard J, Olson Timothy M
Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN, USA.
Hum Genet. 2008 Jul;123(6):665-7. doi: 10.1007/s00439-008-0519-3. Epub 2008 May 27.
ATP-sensitive K+ (K(ATP)) 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 K(ATP) channels within the population.
在患有扩张型心肌病和明显心力衰竭的个体中已发现ATP敏感性钾离子（K(ATP)）通道突变。在此，在一个基于社区的横断面队列（n = 2031）中研究了Kir6.2通道孔中常见的E23K功能多态性与心脏表型的关系。在因高血压导致应激负荷增加的受试者中，KK基因型与更大的左心室大小相关。这些发现表明Kir6.2 K23是亚临床心肌不良重塑的一个危险因素，并强调了心脏K(ATP)通道在人群中的重要性。
