Susceptibility genes & modifiers for cardiac arrhythmias.
Cardiac arrhythmias in the absence of structural heart diseases can be subdivided in those cases which are acquired and those which are linked to genetic defects on cardiac ion channels and regulatory subunits. Although acquired arrhythmias do not contain any obviously genetic component the observation of frequently occurring single nucleotide polymorphism (SNPs) identified in cardiac ion channel genes lead to the question if these natural variants can influence the development of acquired forms of cardiac arrhythmias and thus serve as genetic susceptibility markers. This review summarizes the results of genetic association and linkage studies in drug induced long-QT syndrome and atrial and ventricular fibrillation and discusses advantages and future directions of this topic in cardiac research.
Schulze-Bahr
Eric
E
Leibniz Institute for Arteriosclerosis Research (LIFA), Molecular Cardiology, University of Münster, Germany. eric.schulze-bahr@ukmuenster.de <eric.schulze-bahr@ukmuenster.de>
D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000235:genetics*; D001281:Atrial Fibrillation / Q000209:etiology / Q000235:genetics; D008040:Genetic Linkage; D020022:Genetic Predisposition to Disease; D006801:Humans; D008133:Long QT Syndrome / Q000139:chemically induced / Q000235:genetics; D009124:Muscle Proteins / Q000235:genetics; D062554:NAV1.5 Voltage-Gated Sodium Channel; D020641:Polymorphism, Single Nucleotide; D015222:Sodium Channels / Q000235:genetics; D014693:Ventricular Fibrillation / Q000209:etiology / Q000235:genetics
D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels