Induction Of Paroxysmal Supraventricular Tachycardia Research Articles

Clinical and Electrophysiologic Effects of Dofetilide in Patients with Supraventricular Tachyarrhythmias

The clinical and electrophysiologic effect of intravenous dofetilide was evaluated in patients with paroxysmal atrial fibrillation (AF) of recent onset (< 7 days) and paroxysmal supraventricular tachycardia (PSVT). From 2.5 to 5.0 micrograms/kg of dofetilide was administered intravenously for the termination of arrhythmias. For the electrophysiologic study (EPS), 3.0 micrograms for loading and subsequently 2 micrograms/kg was injected for 45 min as a maintenance dose. The EPSs were performed before the loading and during the maintenance dose. AF was successfully converted to sinus rhythm in seven (54%) of 13 patients. The duration of AF from its onset was significantly shorter in responders than that of nonresponders (p < 0.05). Dofetilide also terminated PSVT in four of six patients. In the EPS, dofetilide proportionately lengthened the effective refractory period of the atrium, ventricle, and the accessory pathways without slowing of the intracardiac conduction. Dofetilide completely suppressed the induction of PSVT in seven of 13 patients, restricted the induction zone in five, and inhibited perpetuation of the arrhythmia in the remaining one. The cycle length of PSVT remained unchanged after dofetilide. These results imply that the suppression of the development and maintenance of reentrant arrhythmias may result from the lengthening effect of dofetilide on the refractoriness and the consequent elimination of the excitable gap at the critical part of the reentrant loop.

Heart rate during spontaneous and induced paroxysmal supraventricular tachycardia.

It is generally assumed that paroxysmal supraventricular tachycardia (PSVT) induced during invasive electrophysiological study reproduces the patient's spontaneous, clinical arrhythmia. Even in the absence of antiarrhythmic drugs, however, there may be significant differences in characteristics of the induced and spontaneous arrhythmias. We compared the heart rate of PSVT in 38 patients who had undergone electrophysiological study with induction of PSVT who also had a spontaneous episode of PSVT documented by transtelephonic ECG monitoring during a period when all antiarrhythmic drugs were withheld. The heart rate during spontaneous PSVT was faster than the heart rate of PSVT induced during electrophysiological study; the mean difference was 16 beats/min (P < 0.001). We conclude that heart rate of PSVT induced during electrophysiological study generally underestimates the heart rate of spontaneous PSVT in the antiarrhythmic drug-free state. This may be due to differences in the autonomic and hemodynamic states during spontaneous and induced arrhythmias.

Observations on Induction and Termination of Paroxysmal Supraventricular Tachycardia by External Pacing

Paroxysmal supraventricular tachycardia (PSVT) can be reproducibly induced and terminated by critically timed atrial or ventricular depolarizations. In this study, noninvasive transcutaneous (external) cardiac pacing (NTCP) was compared to endocardial ventricular pacing for the termination and induction of PSVT. In 24 patients, either atrioventricular (AV) nodal reentrant tachycardia or AV reciprocating tachycardia was reproducibly terminated with either critically timed ventricular depolarizations or overdrive ventricular pacing from an endocardial right ventricular site. There were 32 trials of NTCP attempts to interrupt PSVT in the 24 patients. External pacing was successful at terminating PSVT in 23 patients and in 30 of 32 (94%) trials. In 20 patients, there were 26 trials of external pacing attempts to induce PSVT. External pacing initiated PSVT in 21 of 26 trials (81%). The pacing sequences used to induce and terminate PSVT with external pacing were copied from the endocardial sequences. The external pacing threshold averaged 77 +/- 22 mA but the current needed to terminate PSVT was about 1.5 greater than threshold at 117 +/- 27 mA. Serial external pacing studies were performed in seven patients. The thresholds for external pacing were similar from trial to trial as were the mode of termination and induction between the endocardial and external methods. External pacing can terminate most AV reciprocating tachycardias and many AV nodal reentrant tachycardias. It appears promising as a means of inducing PSVT. However, the high stimulation amplitudes needed will prohibit wide acceptance of external pacing for induction and termination of PSVT.

Chronic effects of antiarrhythmic drugs which suppress electrical induction of paroxysmal supraventricular tachycardia

Chronic effects of antiarrhythmic drugs which suppress electrical induction of paroxysmal supraventricular tachycardia

Effects of standing on the induction of paroxysmal supraventricular tachycardia

To evaluate the effects of standing on induction of paroxysmal supraventricular tachycardia, electrophysiologic studies were performed in both the supine and standing positions in 22 patients with atrioventricular (AV) reciprocating tachycardia and in 11 with AV node reentrant tachycardia. AV reciprocating tachycardia was induced in 9 of the 22 patients with AV reciprocating tachycardia when they were in the supine position and in 17 when standing. The effective refractory period of the AV node markedly shortened, from 275 +/- 72 to 203 +/- 30 ms (n = 16, p less than 0.005) after standing. The effective refractory period of the accessory pathway shortened slightly, from 293 +/- 75 to 278 +/- 77 ms (n = 8, p less than 0.005), after standing. AV node reentrant tachycardia was induced in 3 of the 11 patients with AV node reentrant tachycardia when they were in the supine position and in 6 when standing. The effective refractory periods of the slow pathway and fast pathway shortened markedly, from 293 +/- 72 to 216 +/- 40 ms (n = 6, p less than 0.025) and from 416 +/- 85 to 277 +/- 50 ms (n = 10, p less than 0.005), respectively, after standing. Plasma norepinephrine levels increased during standing both in patients with AV reciprocating and in those with AV node reentrant tachycardia (n = 11, p less than 0.005, n = 8, p less than 0.005, respectively). In conclusion, standing, which is associated with increased sympathetic tone, changed the electrophysiologic properties of the reentrant circuits, facilitating induction of AV reciprocating tachycardia and AV node reentrant tachycardia.

Epinephrine-induced reversal of verapamil's electrophysiologic and therapeutic effects in patients with paroxysmal supraventricular tachycardia.

The purpose of our study was to determine whether an infusion of epinephrine reverses the electrophysiologic effects of verapamil and whether reversal of verapamil's effects on the induction of paroxysmal supraventricular tachycardia (PSVT) by epinephrine during electropharmacologic testing is predictive of stress-related recurrences of PSVT during long-term treatment with verapamil. The infusion rates of epinephrine used in this study were 25 and 50 ng/kg/min, which previously have been demonstrated to result in plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. The subjects of this study were 17 patients with recurrent PSVT who underwent an electrophysiologic study in the control state and after at least 2 days of treatment with 240-480 mg/day verapamil. After assessing the response to verapamil, epinephrine was infused and testing was repeated. Verapamil significantly slowed atrioventricular conduction and prolonged refractoriness in the atrium and atrioventricular node. The effects of the two infusion rates of epinephrine were generally similar in magnitude and, therefore, the results were pooled. Epinephrine partially or completely reversed all of verapamil's electrophysiologic effects. Verapamil suppressed the induction of sustained PSVT in 15 patients. Epinephrine facilitated the induction of PSVT in seven of these 15 patients. All 15 patients were treated on a long-term basis with verapamil. The eight patients in whom epinephrine did not facilitate the induction of PSVT had no recurrences of PSVT during 9-18 months of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of oral disopyramide phosphate on induction of paroxysmal supraventricular tachycardia.

The effects of oral disopyramide phosphate on laboratory induction of paroxysmal supraventricular tachycardia (PSVT) were studied in 16 patients with clinical PSVT. After control electrophysiologic study to determine the inducibility and mechanism of PSVT, patients were given 200-300 mg (275 +/- 45 mg, mean +/- SD) of disopyramide for three to five doses over 24 hours and were then restudied. All patients had inducible, sustained PSVT during the control study. After disopyramide, PSVT was noninducible in eight patients (50%), including six of nine with atrioventricular nodal reentrance and two of seven with atrioventricular reentrance; inducible but nonsustained in two (12.5%) (both with atrioventricular reentrance); and inducible and sustained in six (37.5%). The benefit of disopyramide seemed predominantly to reflect depression of conduction in the retrograde limb of the circus movements, although effects upon the antegrade limb were also observed. In the eight patients with inducible PSVT before and after disopyramide, tachycardia cycle length increased from 348 +/- 33 to 404 +/- 29 msec (mean +/- SEM) (p less than 0.001). These results suggest that disopyramide would be effective in preventing recurrence of clinical PSVT in selected patients.