[Sotalol in the Wolff-Parkinson-White syndrome: an electrophysiological and clinical study]

Distinctly different from the other beta-blocking agents, sotalol prolongs action potential duration in myocardial and Purkinje fibers, and increases atrial as well as ventricular effective refractory periods. Similarly, antegrade and retrograde accessory pathway refractory periods are increased by sotalol. The electrophysiologic and clinical effects of sotalol were studied in 40 patients (31 male and 9 female, mean age 32 +/- 14 years) with Wolff-Parkinson-White Syndrome (WPW). All patients had disabling episodes of supraventricular tachyarrhythmias (ST). Of the 40 patients, 15 (37%) had spontaneous recurrence of paroxysmal supraventricular reciprocating tachycardia (PSRT), 14 (35%) of atrial fibrillation (AF) and 11 (28%) of both PSRT and AF. All of the patients were non responders to serial transesophageal electropharmacological tests using I C class drugs. Sotalol 252 +/- 73 mg daily was administered, and, in steady-state, a new transesophageal study (TS) was performed to observe the re-induction of PSRT and/or AF. 34 patients (85%) were responders to TS (noninducibility of ST, or nonsustained ST or AF inducibility with an increase of 30% in the minimum R-R interval between pre-excitated beats during AF) and the results were confirmed during a follow-up of 17 +/- 9 months. In the non-responder group (5 patients), a I C class drug was associated with sotalol. One patient, who was a "non responder" to sotalol, sotalol + I C class drug, and to amiodarone, underwent surgical therapy. In the 26 patients (65%) who had episodes of PSRT (37%) or episodes of PSRT and AF (28%), it was impossible to reinduce PSRT in 85% of the cases. AF was induced at baseline in all of the studied patients, but after sotalol administration in 15 patients, it was impossible to reinduce AF. The rate of induced AF decreased from 208 +/- 39 beats/min to 156 +/- 36 beats/min (p < 0.001). The mean shortest R-R interval between pre-excitated beats increased from 214 +/- 35 (baseline) to 293 +/- 97 msec (sotalol steady state) (p < 0.001). No side effects were observed. A significant prolongation (p < 0.001) of the QTc interval was observed in all the patients after sotalol administration (from 0.39 +/- 0.2 to 0.42 +/- 0.02 sec.). On the basis of our results, we may conclude that sotalol has a potent effect on the antegrade refractoriness of the anomalous pathway and, in WPW syndrome at risk, is also effective in patients who don't respond to I C class drugs.