Ramanna H, Hauer R N, Wittkampf F H, de Bakker J M, Wever E F, Elvan A, Robles De Medina E O
Heart-Lung Institute, University Medical Center Utrecht, Utrecht, the Netherlands.
Circulation. 2000 Mar 7;101(9):995-1001. doi: 10.1161/01.cir.101.9.995.
Experimental studies have shown that atrial fibrillation (AF) causes remodeling, which facilitates AF perpetuation. AF may also, however, occur in patients without remodeling and underlying structural cardiac disease. The substrate for enhanced vulnerability in these patients is unknown.
We studied 43 patients without structural heart disease: 18 patients with documented sporadic paroxysmal AF and 25 control patients without AF. In each patient, a decapolar catheter was positioned against the right atrial free wall, and a quadripolar catheter was positioned in the right atrial appendage. Unipolar electrograms were recorded. Atrial vulnerability was assessed according to an increasingly aggressive stimulation protocol. Mean local fibrillatory interval (FI) was used as an index of local refractoriness. Spatial dispersion of refractoriness was assessed through the calculation of the coefficient of dispersion (CD), which was defined as the SD of mean local FI expressed as a percentage of the mean FI. In the AF group, AF was induced with a single extrastimulus in 16 of 18 patients; the CD was 5.4+/-2.6, and the mean FI was 164+/-29 ms. In the control group, AF could be induced only with more aggressive pacing in 23 of the 25 patients; the CD was 1.4+/-0.7 (P<0.0001), and the mean FI was 175+/-26 ms (NS).
Patients with idiopathic AF showed increased dispersion of refractoriness, which may be the substrate for the observed enhanced inducibility and spontaneous occurrence of AF.
