CARDIOVASCULAR GENOMIC MEDICINE
Genomics and Cardiac Arrhythmias
Robert Roberts, MD, FACC*
University of Ottawa Heart Institute, Ottawa, Ontario, Canada
Manuscript received July 20, 2005;
revised manuscript received August 4, 2005,
accepted August 17, 2005.
* Reprint requests and correspondence: Dr. Robert Roberts, University of Ottawa Heart Institute, 40 Ruskin Street, Ottawa, Ontario, K1Y 4W7 Canada. (Email: rroberts{at}ottawaheart.ca).
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.
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Abbreviations and Acronyms
| | AMPK = adenosine monophosphate-activated protein kinase | | AP = action potential | | HCM = hypertrophic cardiomyopathy | | ICD = implantable cardioverter-defibrillator | | LQTS = long QT syndrome | | SCD = sudden cardiac death | | SNP = single nucleotide polymorphism | | SQTS = short QT syndrome | | WPW = Wolff-Parkinson-White syndrome |
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