Patterns of atrioventricular conduction during postexercise recovery in patients with atrial fibrillation and Wolff-Parkinson-White syndrome.

The effects of the postexercise recovery phase on the functional anterograde conduction properties of the accessory pathway (AP) were evaluated. Twenty-nine patients with Wolff-Parkinson-White (WPW) syndrome were submitted to supine maximal bicycle exercise testing. In seven patients (group I), in whom sustained atrial fibrillation (AF) could be induced by transesophageal pacing (TP), mean ventricular rate (MVR), the shortest R-R interval (SRR) between preexcited beats, and the observed percentage of preexcited beats were evaluated at rest, after each step of exercise and 2 minutes after the end of exercise. In 22 patients (group II), in whom sustained AF could not be induced, decremental TP was performed to evaluate the shortest atrial cycle length (SCL) with 1:1 conduction over AP at rest, after each step of exercise, and 2 minutes after the end of exercise. In four patients in group I, the protocol was repealed with atropine injected during the last minute of exercise. In 12 patients (three from group I and nine from group II), catecholamine plasma levels were measured at rest, at peak exercise, and during recovery. MVR was 144 ± 20 beats/min at rest, 186 ± 21 beats/min at peak exercise (P < 0.001 vs rest), and 179 ± 21 beats/min during recovery (P < 0,001 vs rest; P < 0.05 vs peak exercise). SRR was 289 ± 73 msec at rest, 223 ± 25 msec at peak exercise (P < 0.05 vs rest), and 227 ± 29 msec during recovery. Preexcited beat percentage was 95.4 ± 12 at rest, 35.2 ± 24.2 at peak exercise (P < 0.001 vs rest), and 85.1 ± 22.5 during recovery fP < 0.01 vs peak exercise and n.s. vs rest). In patients in whom atropine was injected MVR was 139 ± 17 beafs/min at rest, 184 ± 19 beats/min at peak exercise (P < 0.05 vs rest), and 172 ± 16 beats/min during recovery (P < 0.05 vs peak exercise, P < 0.05 vs rest); SRR was 320 ± 71 msec at rest, 225 ± 25 msec at peak exercise, and 232 ± 3 inset; during recovery; preexcited beat percentage was 99 ± 1 at rest, 26 ± 18 at peak exercise (P < 0.01 vs rest), and 28 ± 20 during recovery (NS vs peak exercise, P < 0.01 vsrest). In group II. mean sinus rate was 84 ± 12 beats/min at rest, 151 ± 15 beats/min at peak exercise, and 117 ± 21 beats/min 2 minutes after the end of exercise; mean SCL was 328 ± 75 msec at rest, 273 ± 76 msec at peak exercise (P < 0.0001 vs rest), and 280 ± 79 msec during recovery (P < 0.0001 vs rest and NS vs peak exercise). Mean epinephrineand norepinephrine plasma levels (12 patients from groups I and II) were; 4 7.9 ± 76.6 and 355.5 ± 185.1 pg/mL at rest; 193.0 ± 88.0 and 823.9 ± 390.3 pg/mL at peak exercise (P < 0.0001 vsrest); 148.5 ± 94.5 and 672.7 ± 272.3 during recovery (P < 0.001 vs rest; P < 0.01 vs peak exercise). Thus, during early recovery versus peak exercise: SCL and SRR are still lower and confirm the persistence of increased AP conductivity; in patients with atrial fibrillation preexcited beat percentage is markedly enhanced while the duration of preexcited complexes is increased and MVR is still high. The poslexercise recovery phase in patients with WPWand atrial fibrillation determines a higher ventricular response rate with major preexcitation than does rest and peak exercise. The fact that atropine prevents increases in preexcited beats percentage demonstrates that the underlying electrophysiological basis is a discordance of autonomic effects on the conduction properties of the two afrioventricular pathways.