Electrophysiological Remodeling in Chronic Mitral Regurgitation: Underlying Substrates for Atrial Fibrillation

Atrial fibrillation is commonly associated with mitral regurgitation (MR). Using a canine model of MR, we studied the electrophysiological substrates driving the inducibility of atrial tachyarrhythmias (ATAs).

Study animals (n = 12) underwent endovascular avulsion of chordae tendineae under echocardiographic guidance until the ratio of regurgitant jet area to left atrial area (RJA/LAA) was >70%. Noninvasive electrocardiographic imaging (ECGI), delayed enhancement MRI (DE-MRI), and echocardiography were completed before avulsion and repeated up to the terminal surgery. At terminal surgery, rapid atrial pacing was performed to test the inducibility of ATAs, followed by ex vivo optical mapping of left atrial posterior wall (LAPW) preparations.

Twelve MR animals were survived for 8.8±1.3 months while maintaining severe MR. Left atrial (LA) volume increased by 121% (24.9±6.2 vs 55.0±26.5; P < .01) and left ventricular end diastolic area increased by 63% (11.2±1.2 vs 18.3±4.6; P < .01), indicating anatomical remodeling. In 6/12 (50%) MR animals ATAs were induced lasting >30 s. In 4 of these 6 (67%), ATAs lasted >300 s. ECGI showed a 29%±23% increase in biatrial activation times (P < .01). During optical mapping, 3/12 (25%) LAPW preparations exhibited sustained ATAs, compared to none of the control animals. On DE-MRI, total LA enhancement of MR dogs increased from 2.2±1.8% to 4.3±1.8% (P < .01), and LAPW enhancement was higher in inducible vs non-inducible animals (5.5±1.1% vs 3.1±1.6%; P = .03).

After prolonged MR, canines developed ATA vulnerability, dramatic enlargement of the LA, and increased total atrial activation time. LAPW enhancement was increased in inducible animals.