New onset atrial flutter termination by overdrive transoesophageal pacing: effects of different protocols of stimulation.

AIM: We evaluated the effect of different stimulation protocols on atrial flutter interruption by transoesophageal pacing. METHODS AND RESULTS: Eighty patients with new onset atrial flutter were randomized into four groups. Pacing was attempted under the following conditions: with short bursts (5 s), without treatment (group A) and after oral administration of propafenone 600 mg (group B); with prolonged bursts (30 s), without treatment (group C) and after oral administration of propafenone 600 mg (group D). Pacing interrupted atrial flutter in 20% of patients in A, 55% in B, 50% in C and 85% in D. The use of longer bursts gave better results both in patients without treatment (P < 0.05: C vs A) and in patients with propafenone (P < 0.05: D vs B). Comparing groups with the same stimulation protocol, we observed a better response in patients treated with propafenone (P < 0.05: B vs A and D vs C). In the groups without treatment the use of shorter bursts was associated with a lower induction of stable atrial fibrillation (three vs nine episodes), in the groups on propafenone no differences were observed (one vs one episode). CONCLUSIONS: We conclude that the association of propafenone with long bursts gives the best result for interruption of new onset atrial flutter by transoesophageal pacing.

Type II atrial flutter interruption with transesophageal pacing: use of propafenone and possible change of the substrate.

Type II atrial flutter (AFII) is an arrhythmia which usually cannot be interrupted by atrial pacing: the underlying mechanism is considered to be a leading circle without an excitable gap. We investigated whether the administration of propafenone, an antiarrhythmic drug, which primarily decreases conduction velocity, has a beneficial effect on AFII interruption using transesophageal pacing. Twelve patients with an AFII were randomized into 2 groups in which pacing was performed without treatment (group A) or two hours after the administration of 600 mg of oral propafenone (group B). Sinus rhythm was attained in 0 of 6 patients in group A and in 4 of 6 patients in group B (P < 0.05). The baseline mean cycle length was the same in both groups (175 +/- 7 (A) vs 168 +/- 8 ms (B); it lengthened significantly after the administration of propafenone (219 +/- 33 vs 168 +/- 8 ms; P < 0.05). Propafenone did not significantly lengthen the cycle in the two patients in whom interruption of the arrhythmia was impossible. Our data show that propafenone has a facilitating effect on atrial pacing only when it significantly prolongs the cycle length of the arrhythmia, possible expression of a conversion of AFII into type I, with an anatomical substrate and an excitable gap allowing arrhythmia capture and interruption. In the two patients in whom sinus rhythm was not restored, the absence of a direct dependence of the cycle length on the change in conduction velocity induced by propafenone may be explained by the persistence of a functionally determined circuit, resistant to atrial pacing.

[Facilitating effect of propafenone pretreatment in the interruption of atrial flutter by transesophageal pacing]. / Effetto facilitante del pretrattamento con propafenone nell'interruzione del flutter atriale mediante stimolazione transesofagea.

Transesophageal atrial pacing is effective in the interruption of atrial flutter, and being simple and minimally invasive, is easily performed even on outpatients. The influence of antiarrhythmic drugs on this procedure is controversial. We investigated whether the administration of oral propafenone may facilitate the procedure. Thirty patients with type I atrial flutter were randomized into two groups in which transesophageal pacing was attempted, respectively, without treatment (Group A) and after oral administration of propafenone 600 mg (Group B). Transesophageal pacing was effective in interrupting atrial flutter in 53% (8/15) of patients in Group A and in 85% (13/15) of patients in Group B. A significant lengthening of the flutter cycle was observed in patients treated with propafenone (261 +/- 23 vs 217 +/- 25 ms, p < 0.01). Sinus rhythm resumed at a shorter paced cycle in patients of Group A (166 +/- 13 vs 187 +/- 14 ms, p < 0.01). The transesophageal threshold for stable atrial capture was significantly lower in Group A (20.5 +/- 0.2 vs 23.3 +/- 1.2 mA, p < 0.01). In no patient the threshold for atrial capture was higher than the pain threshold. We did not observe abrupt enhancement of atrioventricular conduction. We can conclude that propafenone is effective and safe when used with transesophageal pacing in the termination of atrial flutter. The depressing effect of the drug on intraatrial conduction and the possible stabilizing effect on the reentry circuit appear to be outweighed by the positive effect of propafenone on the excitable gap of the circuit, facilitating its capture and account for the beneficial effect of the drug on arrhythmia termination.

Atrial flutter termination by overdrive transesophageal pacing and the facilitating effect of oral propafenone.

Transesophageal overdrive atrial pacing is effective and safe for atrial flutter termination. The influence of antiarrhythmic drug therapy on this procedure is controversial. In this study, we investigated whether oral propafenone may facilitate this procedure. Thirty patients with type I atrial flutter were randomized into 2 groups in which transesophageal pacing was attempted: group A, without treatment; and group B, after oral administration of propafenone 600 mg. Transesophageal pacing was effective in interrupting atrial flutter in 53% of patients (8 of 15) in group A and in 87% of patients (13 of 15) in group B. A significant lengthening of the flutter cycle was observed with respect to the baseline in patients given propafenone (261 +/- 23 vs 217 +/- 25, p < 0.01). Sinus rhythm resumed at a shorter paced cycle in group A patients (166 +/- 13 vs 187 +/- 14 ms, p < 0.01). The transesophageal threshold for stable atrial capture was significantly lower in group A (20.5 +/- 0.2 vs 23.3 +/- 1.2, p < 0.01). In no patient was the threshold for atrial capture higher than the pain threshold. We did not observe abrupt enhancement of atrioventricular conduction. We conclude that propafenone is effective and safe when used with transesophageal pacing in the termination of atrial flutter. The slowing effect of the drug on intraatrial conduction and the possible stabilizing effect on the reentry circuit appear to be outweighed by the positive effect of propafenone on the excitable gap of the circuit, facilitating its capture and accounting for the beneficial effect of the drug on arrhythmia termination.

Comparative evaluation of three dosages of slow-release isosorbide dinitrate (60, 80, 100 mg) in chronic angina of the aged.

In a single-blind, placebo-controlled study the acute and chronic antianginal effects of three slow-release (SR) new formulations of isosorbide dinitrate (ISDN 60, 80, 100 mg) have been comparatively evaluated in a group of aged affected by chronic stable effort-induced angina. Compared to placebo, overall the active dose paritetically improved the effort tolerance up to 24 h after the first assumption. In the time course of the trial (2 and 4 weeks) the resting hemodynamic changes induced by the first dose were partially blunted without affecting the exercise related-parameters. Also if plasma levels of ISDN and of its metabolites did not correlate to the degree of physical improvement, the peak increase in effort tolerance was observed under 100 mg treatment. Mild to moderate transient headache was experienced by 50% of actively treated and by 20% of placebo treated patients and no other serious adverse effects have been noted. One may conclude that ISDN in slow-release formulations of 60-100 mg isan effective, safe and well tolerated medication in the management of angina in the aged.