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Genes related to pathogenesis of AF identified
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Researchers from the National Taiwan University in Taipei have mapped several genetic variants and polymorphisms related to the pathogenesis of atrial fibrillation.
The researchers presented a review of genetic studies of familial and nonfamilial AF.
The gene loci 11p15.5, 21q22, 17q, 7q35-36, 5p13, 6q14-16 and 10q22 were mapped for familial (monogenetic) AF. Gene loci responsible for the coding of potassium channels also were identified in some genes (KCNQ1, KCNE2, KCNJ2 and KCNH2). Many other gene loci remained unidentified by the researchers. Mutations in the genes encoding for units or subunits of potassium channels were associated with a gain in function, shortening atrial action potential duration and a shortening of the atrial refractory period.
“These observations demonstrate that potassium channels play a very important role in the pathogenesis of AF in patients without underlying heart disease and provide specific targets of novel drug therapy to treat AF,” the researchers wrote.
For more information:
- J Am Coll Cardiol. 2008;52:241-250.
There is little question that genes play an important role in the development of many arrhythmias, including monogenic disorders like the long QT and Brugada syndromes and, as this article highlights, monogenic atrial fibrillation. Importantly, however, the researchers note that, although the gain of function of repolarization in potassium currents fits nicely with shortening of action potential duration and reentry, other genes related to ionic channels, calcium handling protein, fibrosis, conduction and inflammation play important roles in the pathogenesis of common AF. Thus, many challenges remain in understanding the genetic basis of AF, its use in diagnosis, and ultimately, its therapy.
– Douglas P. Zipes, MD
Cardiology Today Section Editor