Genomics and cardiac arrhythmias

Abstract

Genomics and Cardiac Arrhythmias Robert Roberts Sudden cardiac death in patients younger than 35 years of age is primarily due to genetic causes. Familial hypertrophic cardiomyopathy accounting for 30% to 40% is associated with structural heart disease while the Brugada syndrome and the long QT syndrome (LQTS) are associated with normal cardiac function. This is a review of the genetics of supraventricular and ventricular arrhythmias. Atrial fibrillation is mapped to nine chromosomal loci and four genes are identified. AMP-activated protein kinase is one gene responsible for Wolff-Parkinson-White syndrome. The LQTS and the Brugada syndromes are due to defects primarily in cardiac sodium and potassium ion channels. The role of single nucleotide polymorphisms in predisposing to arrhythmias in acquired disorders such as hypertrophy is discussed. Sudden cardiac death in patients younger than 35 years of age is primarily due to genetic causes. Familial hypertrophic cardiomyopathy accounting for 30% to 40% is associated with structural heart disease while the Brugada syndrome and the long QT syndrome (LQTS) are associated with normal cardiac function. This is a review of the genetics of supraventricular and ventricular arrhythmias. Atrial fibrillation is mapped to nine chromosomal loci and four genes are identified. Adenosine monophosphate-activated protein kinase is one gene responsible for Wolff-Parkinson-White syndrome. The LQTS and the Brugada syndromes are due to defects primarily in cardiac sodium and potassium ion channels. The role of single nucleotide polymorphisms in predisposing to arrhythmias in acquired disorders such as hypertrophy is discussed. © 2006 by the American College of Cardiology Foundation.