Acetylcholine chloride (ACh) induces nonstationary meandering reentrant wave fronts in the atrium. We hypothesized that an anatomic obstacle of a suitable size prevents meandering by causing attachment of the reentrant wave front tip to the obstacle. Eight isolated canine right atrial tissues (area, 3.8 x 3.2 cm) were mounted in a tissue bath and superfused with Tyrode's solution containing 10 to 15 mumol/L ACh. Holes with 2- to 10-mm diameters were sequentially created in the center of the tissue with biopsy punches. Reentry was induced by a premature stimulus after eight regular stimuli at 400-ms cycle length. The endocardial activation maps and the motion of the induced reentry were visualized dynamically before and after each test lesion using 509 bipolar electrodes. In the absence of a lesion (n = 8), the induced single reentrant wave front, in the form of a spiral wave, meandered irregularly from one site to another before terminating at the tissue border. Holes with 2- to 4-mm diameters (n = 6) had no effect on meandering. However, when the hole diameters were increased to 6 mm (n = 8), 8 mm (n = 8), and 10 mm (n = 6), the tip of the spiral wave attached to the holes, and reentry became stationary. Transition from meandering to an attached state converted the irregular and polymorphic electrogram to a periodic and monomorphic activity with longer cycle lengths (101 +/- 11 versus 131 +/- 9 ms for no hole versus 10-mm hole, respectively; P < .001). Regression analysis showed a significant positive linear correlation between the cycle length of the reentry and the hole diameter (r = .89, P < .01) and between the cycle length of the reentry and the excitable gap (r = .89, P < .05). We conclude that a critically sized anatomic obstacle converts a nonstationary meandering reentrant wave front to a stationary one. This transition converts an irregular "fibrillation-like" activity into regular monomorphic activity.

Functional reentry in the atrium is compatible with a spiral wave of excitation with an excitable but nonexcited core and a large excitable gap. Reentry may be terminated either by direct excitation of the core that displaces the wave front to the tissue border or by collision with an outside new wave front.

This study was designed to test the hypothesis that the effects of a strong electrical stimulus on reentrant wavefronts in ventricular fibrillation (VF) are dependent on the timing of the stimulus. We studied six open-chest dogs by computerized mapping techniques. A plaque electrode array with up to 509 bipolar electrodes was placed on the right ventricular epicardium. The interelectrode distance was 1.6 mm, and the interpolar distance was 0.5 mm. After eight baseline pacing stimuli (S1) with cycle lengths of 300 ms, a strong premature stimulus (S2) (73 +/- 10 mA) was given to induce VF. In subsequent episodes, a second strong premature stimulus (S3) was given at progressively longer S2-S3 intervals in 20-ms increments. The results showed that, at baseline, the S2 consistently induced figure-eight reentry and VF. The VF cycle length immediately after the S2 averaged 108 +/- 17 ms. The S3 resulted in one of the following responses: (1) termination of reentry and VF; (2) induction of different reentrant wavefronts or a focal pattern of repetitive activation; or (3) persistence of the same figure-eight reentry. The intervals between the S3 and the immediately preceding activation at the site of the S3 (the recovery intervals) were 39 +/- 12 ms (range, 20 to 60 ms) and 61 +/- 20 ms (range, 30 to 90 ms) for response patterns 1 and 2, respectively. The recovery intervals associated with response pattern 3 were either < or = 30 ms (22 +/- 8 ms) or > or = 80 ms (94 +/- 15 ms). The differences among these four intervals were significant (P < .001). We conclude that the effects of strong electrical stimulation on the reentrant wavefronts in VF are dependent on the recovery interval since the previous local activation. A protective zone occurred between 20 and 60 ms, during which time a strong electrical stimulus could terminate reentry and abort VF. This zone was followed by a vulnerable period during which new activation wavefronts could be induced. If a strong electrical stimulus was given shortly after or sufficiently long after the previous local activation, the same figure-eight reentrant pattern continued.

Background-There is increasing evidence that both functional reentrant wave fronts and multiple wavelets are present during ventricular fibrillation (VF). However, the effects of procainamide on the characteristics of activation waves during VF are poorly understood. Methods and Results-Seven dogs were studied; six underwent subendocardial chemical ablation procedures. A plaque with 317 to 480 bipolar electrodes was sutured to the right ventricular free wall, and the patterns of activation were registered with a computerized mapping system. VF was electrically induced, and the patterns of activation were registered at baseline and during procainamide infusion (serum concentration, 9.3Ϯ1.9 g/mL). Among the six dogs that had their subendocardium ablated, reentrant wave fronts were present in 6 of the 108 runs of VF at baseline and in 6 of the 100 runs of VF during procainamide infusion. By analyzing the wave fronts, we found that the cycle length, refractory period, conduction velocity, and wavelength at baseline were 101Ϯ9 ms, 54Ϯ5 ms, 0.93Ϯ0.21 mm/ms, and 51Ϯ16 mm, respectively, and during procainamide infusion, values became 125Ϯ11 ms (PϽ.001), 119Ϯ7 ms (PϽ.001), 0.42Ϯ0.02 mm/ms (PϽ.001), and 50Ϯ4 mm (Pϭ.8), respectively. The vast majority of the activation waves do not form organized reentry. These activation waves broke up more frequently at baseline than during procainamide administration.