Abstract
Paired-like homeodomain 2: a novel therapeutic target for atrial fibrillation?
Highlights
Atrial fibrillation (AF), as a sustained arrhythmia, is featured by uncoordinated atrial activation with the consequent deterioration of mechanical function in the atrium (Mestroni, 2003; Fye, 2006; Fatkin et al, 2007; Otway et al, 2007)
Three classical models have been proposed for the genesis of AF, including focal activity, single-circuit reentry, and multiple-circuit reentry model (Fatkin et al, 2007)
The multiple-circuit reentry hypothesis assumes that several reentry circuits exist and randomly propagating wave fronts persist in receptive tissue while the single-circuit reentry hypothesis focuses on the interaction of a rotor with irregular waves in the atrium and “fibrillatory conduction,” the spatially variable refractory properties of atrial tissue (Nattel, 2002; Xiao et al, 2011)
Summary
Atrial fibrillation (AF), as a sustained arrhythmia, is featured by uncoordinated atrial activation with the consequent deterioration of mechanical function in the atrium (Mestroni, 2003; Fye, 2006; Fatkin et al, 2007; Otway et al, 2007). The common variants in AF in the general population have been paid special attention with the recently published results from several large genome-wide association studies (GWAS) (Darbar et al, 2003; Fox et al, 2004; Christophersen et al, 2009; Sinner et al, 2011; Mahida, 2014).
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