The automatic implantable cardioverter-defibrillator: effect of patch polarity on defibrillation threshold.

An automatic implantable cardioverter-defibrillator (AICD) was implanted in 40 patients with sudden cardiac arrest (n = 29), sustained monomorphic ventricular tachycardia (n = 10) or recurrent syncope (n = 1) who were unsuitable for direct ablative surgery or had had unsuccessful medical therapy. The effect of patch electrode polarity on the defibrillation threshold was prospectively evaluated. Two large epicardial patches were used. Initial polarity was selected at random. Ventricular fibrillation was induced by direct current and a preestablished defibrillation protocol employed to assess the minimal energy that would reproducibly defibrillate the heart. Nineteen patients had a lower defibrillation threshold with the inferior left ventricular patch as an anode and nine patients had a lower defibrillation threshold with this patch as a cathode. In general, the defibrillation threshold was lower when this patch was used as an anode than when it was used as a cathode (18 +/- 10 versus 22.6 +/- 12.2 J; p less than 0.01). No preoperative variable predicted optimal polarity. Therefore, the effect of patch polarity on defibrillation threshold should be assessed in each patient at the time of AICD implantation so that the safety margin for satisfactory device function can be maximized.

Termination of acute atrial fibrillation in the Wolff-Parkinson-White syndrome by procainamide and propafenone: importance of atrial fibrillatory cycle length.

The effects of intravenous procainamide (n = 30) or propafenone (n = 25) were evaluated in 55 patients with acute atrial fibrillation and the Wolff-Parkinson-White syndrome. All patients received either procainamide (12 to 15 mg/kg body weight) or propafenone (1 to 2 mg/kg) during sustained (greater than 10 min) atrial fibrillation or after termination of nonsustained atrial fibrillation. Termination of atrial fibrillation was attributed to a drug if it occurred less than or equal to 15 min after infusion. Measurements included mean cycle length of fibrillatory electrograms (mean AA interval) as measured at the high right atrium and shortest RR interval between pre-excited cycles during atrial fibrillation. Atrial fibrillation terminated more frequently after procainamide administration (65%) than after propafenone (46%), although this difference was not significant. Procainamide prolonged the shortest pre-excited RR interval (228 +/- 41 to 339 +/- 23 ms, p = 0.0001) as did propafenone (215 +/- 40 to 415 +/- 198 ms, p = 0.0001) and the magnitude of increase was greater for propafenone (p = 0.048). Patients with sustained atrial fibrillation had shorter mean AA intervals than did their counterparts with nonsustained atrial fibrillation (123 +/- 25 versus 186 +/- 35 ms, p = 0.0001). Termination of sustained atrial fibrillation by either drug was accompanied by prolongation of the mean AA interval but not necessarily by the shortest pre-excited RR interval. Termination of atrial fibrillation was heralded by a 68% increase in the mean AA interval after procainamide administration compared with a 30% increase when the arrhythmia persisted. For propafenone the increases were 90% and 68%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Value of a revised procainamide test in the Wolff-Parkinson-White syndrome.

A shortest preexcited RR interval less than 250 ms during atrial fibrillation identifies the patient with Wolff-Parkinson-White syndrome potentially at risk for ventricular fibrillation. Loss of preexcitation after infusion of up to 10 mg/kg of procainamide during sinus rhythm has been reported to correlate with a slow ventricular response during atrial fibrillation and has been proposed as a noninvasive test to establish risk of sudden death in these patients. Others have failed to establish this relation and have questioned the usefulness of the procainamide test. Such conflicting results were hypothesized to be a result of differing dosages and methodology. Consequently, this study tested the effect of incremental doses of procainamide (to a cumulative dose of 1 g) on the anterograde effective refractory period of the accessory pathway and related the reliability of the procainamide test to the dose at which preexcitation was lost. The effect of procainamide on the anterograde effective refractory period of the accessory pathway was dose dependent; patients who lost preexcitation had a steeper dose-response curve. Loss of preexcitation by a cumulative dose of 550 mg provided the best balance for sensitivity (60%) and specificity (89%) in identifying patients with preexcited shortest RR greater than 250 ms. Specificity fell steeply after this dosage and higher doses were not useful. The diagnostic accuracy of the procainamide test is critically related to dosage and method of infusion.

The diagnostic sensitivity of electrophysiologic testing in patients with syncope caused by transient bradycardia.

Although electrophysiologic testing accurately delineates abnormalities in patients with fixed cardiac-conduction defects, its sensitivity in identifying transient rhythm disturbances is unknown. We prospectively studied 21 patients who had electrocardiographically documented intermittent atrioventricular block (n = 13) or sinus pauses (n = 8) causing syncope, but whose cardiac rhythm had reverted to normal by the time of referral. There were 14 men and 7 women, with a mean age (+/- SD) of 63 +/- 13 years. Fourteen patients had organic heart disease, and 8 were taking cardioactive medications. Electrophysiologic testing was performed before the implantation of a permanent pacemaker. Only three of the eight patients with documented sinus pauses had abnormalities during their tests that suggested the correct diagnosis (sensitivity, 37.5 percent), including a prolonged sinus-node recovery time in one and carotid-sinus hypersensitivity in two. Three of the eight patients had abnormalities detected that were unrelated to syncope, including atrial flutter, dual atrioventricular nodal pathways, and sustained monomorphic ventricular tachycardia. Of the 13 patients with documented atrioventricular block, only 2 had abnormalities suggesting the correct diagnosis (sensitivity, 15.4 percent). Additional observations unrelated to syncope among these 13 patients included abnormal sinus-node function, atrial flutter, and atrial fibrillation causing hypotension. These preliminary observations suggest that a negative electrophysiologic test in a patient with a normal cardiac rhythm who has experienced syncope does not exclude a transient bradyarrhythmia as a cause of the syncope. Furthermore, electrophysiologic testing may sometimes reveal unrelated rhythm disturbances that may mistakenly be designated as the cause of the syncope.