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The electrophysiologic effects of encainide were studied in 10 patients with Wolff–Parkinson– White syndrome after intravenous (1 mg kg in 60 minutes) and oral administration of two dose regimens (75 and 150 mg daily). Under control conditions atrial fibrillation (AF) with a rapid ventricular response was induced in all patients andatrioventricular reciprocating tachycardia (A VRT) in 9 patients. After intravenous encainide AF was no longer induced in 3/9 patients; in 3 of the remaining the accessory pathway (AP) was totally blocked and in the others the shortest RR interval increased from 213 ±6 to 297 ±91 ms and the mean RR interval from 293 ± 39 to 362 ± 79 ms. The lower dose of oral encainide prolonged the shortest RR interval from 206 ± 24 to 273 ± 64 ms and the mean RR interval from 280 ± 48 to 368 ±52 ms in 6 patients; in 2 cases no preexcitedbeats were recorded and in 1 AF was not inducible. After the higher dose of oral encainide A F was still inducible in 7/8 cases; in 3 the A P was blocked and in the others the shortest and mean RR intervals increased from 202 ±30 to 280 ± 24 ms and from 276 ±59 to 436 ± 80 ms, respectively. After intravenous encainide antegrade conduction over the A P was blocked in 4/9 patients and the antegrade effective refractory period (ERP) was prolonged in another 4. Oral encainide blocked A P conduction in 4 cases and prolonged ERP considerably in the others. Induction of A V RT was prevented in 1/8 patients after intravenous and in 5/9 patients after oral encainide; in the 4 patients in whom AVRTremained inducible cycle length increasedfrom 306±31 to 3 54 ±49 ms after intravenous encainide and to 392 ±46 ms after oral administration. All patients were discharged on encainide (mean maintenance dose, 127 mg daily) and followed for 21 ±7 months; no recurrence of AF was observed; two patients complained of transient mild side effects. These data show that in patients with Wolff-Parkinson- White syndrome encainide prolongs refractoriness and slows conduction over the AP; it prevents induction of AVRT and markedly slows ventricular response during AF, thus protecting patients against life-threatening arrhythmias [ABSTRACT FROM PUBLISHER]

In order to evaluate the effects of increases of sympathetic tone in ventricular response during atrial fibrillation and in the relationship between the accessory pathway effective refractory period (ERP) and ventricular rate during atrial fibrillation, 20 male subjects, aged 19 +/- 6 years, were studied electrophysiologically in basal conditions, after isoproterenol infusion (2-4 micrograms/min) and during submaximal bicycle exercise test, at a constant workload equal to that which increases the sinus rate to the same extent (140 beats/min) induced by isoproterenol infusion. Accessory pathway ERP was evaluated at the same driven rate (150 beats/min) in both instances. In the control study as during both tests atrial fibrillation paroxysms were induced by burst stimulation. In control conditions the rate increase from 100 to 150 beats/min induced a reduction of accessory pathway ERP from 266 +/- 27 msec to 244 +/- 22 msec (P less than 0.005). At the same driven rate of 150 beats/min, isoproterenol infusion and exercise test induced a more marked shortening of accessory pathway ERP to 211 +/- 28 msec (P less than 0.005) and to 214 +/- 29 msec (P less than 0.005), respectively. Atrial fibrillation paroxysms lasting more than 10 seconds were induced in 20/20 cases in the control study, in 15/20 during isoproterenol infusion and in 13/19 cases during exercise test. The shortest cycle length during atrial fibrillation was reduced from a basal value of 253 +/- 72 msec to 204 +/- 27 msec (P less than 0.05) during isoproterenol infusion and to 236 +/- 32 msec (NS) during exercise test.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic ectopic atrial tachycardia in an uncommon form of arrhythmia which is rarely complicated by congestive cardiomyopathy, ictus, sudden death. This possibility has led many authors to ascertain the need of an aggressive diagnostic and therapeutic approach. In need of an aggressive diagnostic and therapeutic approach. In this study the Authors describe the case of one patient who, at the age of 10 years, presented this form of arrhythmia. Due to its benign aspects (relatively low rate, few symptoms, no signs of anatomic-functional heart deterioration), the authors chose a non-aggressive approach. The arrhythmia, which was persistent during the following 3 years, at puberty became intermittent. Now, 4 years later, the subject is asymptomatic and the arrhythmia is beginning to regress spontaneously.

The electrophysiologic effects of encainide (E) after acute i.v. (1 mg/kg in 60') and oral administration (75 to 150 mg/die for 48-72 h) were evaluated in 10 pts with PSVT (5 men and 5 women, mean age 48 +/- 15 years). The mechanism of PSVT was related to a reentry through an accessory A-V pathway in 6 cases while in the other 4 the reentry was confined in the A-V node. PA, AH and HV intervals lengthened from 42.8 +/- 5.1, 77.8 +/- 19.7 and 38.3 +/- 6.6 msec to 50 +/- 13.5, 91.7 +/- 22.9 and 49.4 +/- 12.9 and to 48.3 +/- 7.1, 94.4 +/- 33.9 and 44.4 +/- 9.2 msec, after i.v. and oral E respectively. Atrial and ventricular refractory periods showed slight not significant variations. Wenckebach point lengthened from 316 +/- 28 msec to 354 +/- 32 and to 359 +/- 45 msec, after i.v. and oral E respectively. Tachycardia cycle length was 358 +/- 32 msec in basal conditions. After i.v. E tachycardia was inducible only in 6 cases, with a mean cycle length of 403 +/- 48 msec. After oral E tachycardia was reproduced only in 3 patients with a mean cycle length of 433 +/- 85 msec. Nine patients were treated chronically with E, at a mean dose of 89 +/- 36 mg/day. After a follow-up of 18 +/- 8 months, tachycardia recurred but with a marked reduction of the attacks, in 3 patients; only 3 patients complained of side effects (blurred vision). Thus E is highly effective in the prevention of PSVT; the drug seems well tolerated thanks to the low dosage required for the control of PSVT.

The electrophysiologic effects of oral encainide (75 to 150 mg daily) were evaluated in 14 patients (6 male and 8 female, aged 49 +/- 9 years) with atrioventricular (AV) node reentrant tachycardia of the slow-fast type. The patients were studied in control conditions and after 2 to 12 days of treatment. Encainide increased the AH interval from 67 +/- 10 to 82 +/- 23 ms (p less than 0.02). Anterograde Wenckebach cycle length was increased in three patients, reduced in four, unchanged in one; it was not measurable in the remaining patients because tachycardia was induced. Retrograde Wenckebach periodicity increased from 307 +/- 71 to 401 +/- 92 ms (p less than 0.005) in all nine patients in whom it was measurable; complete retrograde block was observed in one patient. At the control study, tachycardia was induced in all patients, with a mean cycle length of 341 +/- 50 ms; after encainide, tachycardia was inducible in only 1 patient, with an increase in cycle length from 270 to 320 ms; in the other patients, tachycardia was not inducible because of a lack of retrograde (11 patients) or anterograde (2 patients) conduction. The mean plasma concentrations of encainide and its metabolites O-demethyl-encainide and 3-methoxy-O-demethyl-encainide measured in 13 patients during the repeat study were 161 +/- 304, 128 +/- 100 and 95 +/- 85 ng/ml, respectively; three poor metabolizers who presented a high concentration of the parent compound were observed in this series. All patients were discharged on encainide at a mean daily dose of 112 +/- 39 mg.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular tachycardia has become a relatively common complication of myocardial infarction and often is an important therapeutic problem, as it is recurrent and life-threatening. Here we report a group of 36 patients with ventricular tachycardia occurring 13 days to 30 years after a myocardial infarction. All patients were resistant to medical treatment and 34 of the 36 patients had had at least one cardiac arrest. All were candidates for surgery for their arrhythmia. The study protocol included prolonged ECG monitoring, a preoperative electrophysiological study with catheter mapping and intraoperative epicardial and endocardial mapping. A total of 52 different tachycardias were mapped in 36 patients. The procedure was facilitated by an automatic mapping device, that allowed the acquisition of 35 simultaneous signals, so that even pleomorphic ventricular tachycardias could be mapped. The information obtained from both preoperative and intraoperative maps guided surgery and restricted the extent of the surgical damage.

Ergonovine testing was carried out in a selected group of 25 patients with Prinzmetal's variant angina treated with calcium-antagonists in order to: define its usefulness in the evaluation of the short-term effectiveness of calcium-antagonist treatment; compare the results of the test with those of Holter monitoring; verify if the results of the test during the acute phase are correlated with the long-term response to treatment. In all patients a control period lasting 2-6 days was carried out, after which a treatment period with calcium-antagonists (nifedipine, diltiazem, verapamil), lasting 2-8 days, was instituted. In 20 patients only 1 calcium-antagonist was evaluated, in 1 patient 2 calcium-antagonists and in 4 all of them. Scalar ergonovine test was carried out in control conditions and repeated during each calcium-antagonist treatment period. During both control and treatment periods all patients underwent Holter monitoring for evaluation of frequency of the spontaneous attacks. After the acute phase 21 of the 25 patients were discharged on calcium-antagonist treatment and followed-up for a mean period of 11 +/- 7 months. In control conditions ergonovine test was positive in 24 patients at a mean dose of 0.11 +/- 0.09 mg.(ABSTRACT TRUNCATED AT 250 WORDS)