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In order to compare the long-term safety of flecainide and propafenone, an open label, randomized, parallel group study was performed in 335 patients with paroxysmal atrial fibrillation (n = 200) or paroxysmal supraventricular tachycardia (n = 135), and no history of heart disease. Patients were treated with an initial daily dose of flecainide 100 mg (n = 72) or propafenone 450 mg (n = 63) for paroxysmal supraventricular tachycardia and flecainide 200 mg (n = 97) or propafenone 450 mg (n = 103) for paroxysmal atrial fibrillation. Dose escalations were permitted after > or = 2 attacks, up to a maximum of flecainide 300 mg or propafenone 900 mg.day-1.Follow-up duration was 12 months, or when patients stopped the treatment as a result of inadequate efficacy or adverse experiences. Twelve patients on flecainide reported 16 cardiac adverse experiences, of whom six discontinued the treatment. Seven propafenone patients had eight cardiac adverse experiences, of whom five discontinued the treatment. Serious proarrhythmic events were infrequent: one case of ventricular tachycardia on propafenone: two cases of atrial fibrillation with rapid ventricular response on flecainide, associated in one patient with pulmonary oedema. An intention-to-treat analysis showed that the probability of 12 months' safe and effective treatment of paroxysmal supraventricular tachycardia was 93% for flecainide and 86% for propafenone (P = 0.24), whereas in paroxysmal atrial fibrillation it was 77% for flecainide and 75% for propafenone (P = 0.72). In conclusion, flecainide and propafenone were safe in the long-term treatment of patients with paroxysmal supraventricular tachyarrhythmias and without evidence of clinically significant heart disease.

A case of a patient with variant angina associated with severe ventricular tachyarrhythmias studied by continuous electrocardiographic and haemodynamic monitoring is reported. Severe ventricular arrhythmias developed both during maximal ST-segment elevation, in association with haemodynamic signs of acute ischaemic cardiac dysfunction and after nitroglycerin-induced reversion of ischaemia and return of the haemodynamic variables to the basal state. Thus, in this patient, ventricular arrhythmias during acute ischaemia could be related not only to acute vasospastic coronary occlusion but probably also to reperfusion after relief of coronary spasm.

37 consecutive patients with frequent episodes of palpitation and/or dizziness underwent electrophysiological study. They had no signs of ventricular preexcitation during either sinus rhythm or atrial pacing. In 17 (46%), the supraventricular tachycardia was sustained by a reentry mechanism involving an anomalous AV pathway with unidirectional antegrade block (AV tachycardia). Some findings were accepted to demonstrate the existence of the anomalous pathway (AP) and others, its participation in the reentry circuit. The possible location of the AP was established in 15 cases at the following sites: left lateral in 5 cases, left posterior in 5 cases, left posteromedial in 1 case, right posterior in 1 case, right anterior in 1 case, posterior septal in 1 case, and anterior septal in 1 case. The rate of the AV tachycardia can be influenced not only by the ventriculoatrial interval but also by the other pathways included in the reentry circuit. It may change conspicuously in cases with dual AV pathway and anomalous AV pathway in relation to the modality of antegrade conduction by the AV node.

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.

Two cases of paroxysmal supraventricular tachycardia sustained by an atrioventricular junctional reentry mechanism are presented. During the electrophysiological study it was possible to induce paroxysms of tachycardia showing 3:2 Lucianai-Wenckebach type and 2:1 atrioventricular block. The site of the block, its functional nature and the possible involvement of an anterogradely blocked atrio-nodal or atrio-His accessory pathway in the reentry circuit are discussed.

Some clinical and electrocardiographic characteristics are reviewed in two groups of patients with paroxysmal junctional reciprocating tachycardia (JRT) (21 cases) and atrioventricular reciprocating tachycardia involving an atrioventricular bypass tract with unidirectional anterograde block (AVRT) (26 cases). Mechanisms of tachycardia were established in all cases by intracavitary electrophysiologic study. Mean age (+/- S.D.) was 46 +/- 18 yrs (range: 14-75) in the JRT group and 32 +/- 16 yrs (6-67) in the AVRT group (p < 0.02). Male/female ratio was 11/10 in the former and 15/11 in the latter. Mean tachycardia rate of the JRT was 178 +/- 24 b/min (130-215) vs. 205 +/- 21 b/min (160-240) of the AVRT (p < 0.001). Only in 4 cases of JRT a second degree A-V block was observed during tachycardia. P wave was recorded just after the end of QRS complex in all cases of AVRT; on the contrary it was completely hidden in the QRS complex in 11 cases (52%), partially superimposed on the end of QRS in 6 cases (29%) and on the beginning of QRS in 4 cases (19%) of the JRT group. A functional bundle branch block during tachycardia was observed only in 3 cases of JRT (14%) vs. 15 cases (58%) of AVRT. The block never induced any change in the tachycardia rate either in the JRT group or in those cases of AVRT with the anomalous pathway heterolateral to the bundle branch block. On the contrary, the block ipsilateral to the anomalous bypass tract constantly induced variations in cycle length during tachycardia. In conclusion, analysis of some clinical and electrocardiographic features may give useful information for the differential diagnosis of JRT and AVRT and so be helpful for a better therapeutic approach.