Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff-Parkinson-White Syndrome

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15–56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0–25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 ± 16% to 1 ± 2% (mean ± standard deviation, p < 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blockcing the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QHS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.     

Electrophysiologic Demonstration of an Atriofascicular Accessory Pathway

Evidence of an atriofascicular accessory pathway has not been reported previously. In the patient presented in this case report, an electrophysiology study demonstrated a constant left bundle branch block QRS configuration despite varying degrees of ventricular preexcitation, in association with a constant artrioventricular interval during incremental atrial pacing and programmed atrial stimulation. The presence of an atrioventricular, nodoventricular, nodofascicular, and atrial-His accessory pathway was ruled out. The findings are best explained by the presence of an underlying left bundle branch block and an atriofascicular accessory pathway connecting the atrium and right bundle. The atriofascicular accessory pathway was a passive bystander during an atrial tachycardia and was not directly involved in the generation of the tachycardia. To our knowledge, this is the first report of an atriofascicular accessory pathway.     

An Analysis of Post-Pacing R-R Intervals During Atrial Fibrillation

Bursts of ventricular pacing at cycle lengths of 350-260 ms were introduced during atrial fibrillation in nine patients, and the post-pacing R-R intervals were compared to the R-R intervals of spontaneous QRS complexes. In eight of nine patients, the mean post-pacing R-R interval was 126-199 ms longer than the mean spontaneous R-R interval (p less than 0.005). Spontaneous runs of aberrantly conducted supraventricular complexes were recorded during atrial fibrillation in one patient. The mean R-R interval following the runs of aberrantly conducted supraventricular complexes was significantly longer than the mean R-R interval of spontaneous narrow QRS complexes (p less than 0.001), but not significantly different than the mean post-pacing R-R interval. The findings of this study suggest that the R-R interval that follows a wide-complex tachycardia during atrial fibrillation is unlikely to be of value in differentiating ventricular tachycardia from aberrantly conducted supraventricular complexes. Analysis of R-R intervals that follow bursts of ventricular pacing suggests that there is likely to be considerable overlap between the R-R intervals that follow runs of ventricular tachycardia and the spontaneous R-R intervals during atrial fibrillation. Furthermore, even when the post-tachycardia R-R interval clearly exceeds the longest spontaneous R-R interval during atrial fibrillation, this is still of little diagnostic value, because a long pause may occur after either a run of ventricular tachycardia or a run of aberrantly conducted QRS complexes of supraventricular origin.     

Effect of Antiarrhythmic Drug Therapy on the Incidence of Shocks in Patients who Receive an Implantable Cardioverter Defibrillator after a Single Episode of Sustained Ventricular Tachycardia/Fibrillation

Seventy-four patients (16 women, 58 men, age 58 ± 21 years, mean ± standard deviation) who received an implantable Cardioverter de/ibrillator (ICD) after experiencing a single episode of ventricular tachycardia or ventricular fibrillation were followed to determine if antiarrhythmic drug therapy affects the incidence of ICD discharges. Thirty-three patients (group A) were treated with an antiarrhythmic drug that was either untested or previously demonstrated during electropharmacological testing to be ineffective in suppressing the induction of ventricular tachycardia. Forty-one patients (group B) were not treated with an antiarrhythmic drug. There were no significant differences between the two groups in regards to age, sex, incidence of coronary artery disease, left ventricular function or the type of ICD pulse generator used. During a mean follow-up of 14 months for the entire cohort, 15 patients (46%) in group A and 18 patients (44%) in group B experienced at least one ICD shock. The time to the first appropriate shock (5 ± 5 months in both groups) and the frequency of ICD shocks (0.3 ± 0.2/month in group A vs 0.4 ± 0.5/month in group B) were similar in both groups. The incidence of syncope at the time of ICD discharge was higher in group A than group B patients (31% vs 5%, P < 0.05). In conclusion, antiarrhythmic drugs that are untested or have failed electropharmacological testing do not appear to reduce the probability of ICD discharge over a short-term (mean 14 months) follow-up in patients who have had only one clinical episode of VT/VF and may increase the risk of syncope during ICD discharge. Studies with a larger sample size and longer follow-up period will be needed to confirm these findings.     

Supraventricular Tachycardia Induced by Swallowing: A Case Report and Review of the Literature

A 64-year-old man who complained of palpitations brought on by swallowing was found to have short runs of paroxysmal supraventricular tachycardia (SVT) induced by swallowing. Electrophysiology studies suggested that the SVT was an automatic atrial tachycardia. An esophageal manometric study demonstrated that the tachycardia was coincident with relaxation of the upper esophageal spincter and preceded peristaltic activity in the esophageal body. Atropine and bethanechol did not affect the swallow-induced tachycardia. The patient's symptoms were controlled by verapamil and quinidine. After five months, these medications were discontinued, with no recurrence of symptoms. Based on analysis of ten prior cases and the present case, it appears that swallow-induced SVT generally occurs in men between the ages of 45–75 years who have no evidence of structural heart disease or an esophageal disorder. The SVT is usually either a nonsustained automatic atrial tachycardia or atrial fibrillation. The mechanism is conjectural, but the most likely possibility is a vagally-mediated neural reflex, probably involving a neu-rotransmitter other than acetylcholine.