Role of intravenous isoproterenol in the electrophysiologic induction of atrioventricular node reentrant tachycardia in patients with dual atrioventricular node pathways.

To assess the role of intravenous isoproterenol for the facilitation of electrophysiologic induction of atrioventricular (AV) node reentrant tachycardia, 20 patients with dual AV node pathways who lacked inducible AV node reentrant tachycardia at control study had a constant isoproterenol infusion administered and underwent repeat study. Six (30%) of 20 patients (group I) had inducible AV node reentrant tachycardia during isoproterenol infusion whereas the other 14 (70%) patients (group II) did not. Paroxysmal supraventricular tachycardia was clinically documented in all 6 group I patients compared to 3 (21%) of 14 group II patients (p = 0.002). The sensitivity and specificity of isoproterenol-facilitated induction of AV node reentrant tachycardia were 67 and 100%, respectively. The isoproterenol-facilitated induction of sustained AV node reentry was mediated by resolution of the weak link in anterograde slow pathway in 2 (33%) patients, in retrograde fast pathway in 3 (50%) and in both anterograde slow and retrograde fast pathways in 1 (17%) patient. Four group I patients were given intravenous propranolol, 0.2 mg/kg body weight, and had complete suppression of isoproterenol-facilitated induction of AV node reentry. Thus, intravenous isoproterenol is a rather sensitive and highly specific adjunct to electrophysiologic induction of AV node reentrant tachycardia in patients with dual AV node pathways but without inducible sustained AV node reentry.

Intravenous diltiazem for termination of reentrant supraventricular tachycardia: a placebo-controlled, randomized, double-blind, multicenter study.

To assess the efficacy and safety of intravenous diltiazem, 54 patients with inducible sustained supraventricular tachycardia received diltiazem, 0.25 mg/kg or 0.25 mg/kg, followed by 0.35 mg/kg body weight, or placebo in a double-blind, randomized study. Twenty patients had atrioventricular (AV) node reentrant tachycardia, whereas 34 had orthodromic AV reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Supraventricular tachycardia was terminated in 24 (86%) of 28 patients given intravenous diltiazem compared with 5 (19%) of 26 given placebo (p = 0.0000014). Nineteen (95%) of 20 patients initially given placebo had termination of supraventricular tachycardia after receiving diltiazem. Overall, 43 (90%) of 48 patients receiving intravenous diltiazem had conversion of supraventricular tachycardia to sinus rhythm; the median time to tachycardia termination was 2 min after initiation of a 2 min diltiazem infusion. All 20 patients (100%) with AV node reentrant tachycardia treated with diltiazem had conversion of tachycardia to sinus rhythm as did 26 (81%) of 30 patients with AV reciprocating tachycardia treated with diltiazem. Diltiazem prolonged refractoriness and slowed conduction of the AV node and thereby provided antiarrhythmic action to cause tachycardia termination. Diltiazem had no effect on the electrophysiologic properties of accessory AV connections. Adverse effects were seen in 3 (6%) of the 48 patients given diltiazem. For paroxysmal supraventricular tachycardia initiated in the electrophysiology laboratory, it is concluded that intravenous diltiazem is safe and very effective for acute tachycardia termination when the AV node is part of the reentrant circuit.

Electrophysiologic manifestations of the excitable gap of orthodromic atrioventricular reciprocating tachycardia demonstrated by single extrastimulation.

To assess the electrophysiologic characteristics of the excitable gap, 12 patients with orthodromic atrioventricular (AV) reciprocating tachycardia were studied. During tachycardia, 8 patients used a left-sided and 4 patients a right-sided anomalous bypass tract for retrograde conduction. QRS complex-synchronized single extrastimuli were delivered from high right atrium, right ventricular apex and coronary sinus, respectively, scanning the whole cycle length of tachycardia. An excitable gap was determined to be present if tachycardia resetting or tachycardia termination occurred. The duration of the excitable gap varied among different pacing sites and occupied 0 to 48% (mean 17 +/- 16) of basic tachycardia cycle length (240 to 480 ms, mean 327 +/- 70). Three patterns of tachycardia resetting were observed: the sum of coupling interval and return cycle being (1) less than a fully compensatory pause in 12 of 12 patients, (2) more than a fully compensatory pause in 5 of 12 patients and (3) equal to a fully compensatory pause in 2 of 12 patients, depending on extent of AV nodal conduction delay exhibited in return cycle. Tachycardia termination was possible when extrastimuli were delivered from right ventricular apex and coronary sinus but not from high right atrium, and only when basic tachycardia cycle length was greater than or equal to 290 ms in 7 of 12 patients. Tachycardia termination was accounted for by development of orthodromic conduction block in AV node in 7 of 7 patients and in bypass tract in 2 of 7 patients. Therefore, site of extra-stimulation and basic tachycardia cycle length affect electrophysiologic manifestations of excitable gap. Further, functional properties of the AV node influence patterns of tachycardia resetting and are primarily responsible for tachycardia termination during programmed single extrastimulation.

Effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability in patients with paroxysmal supraventricular tachycardia.

To assess the effects of beta-adrenergic stimulation on atrial latency and atrial vulnerability, the electrophysiologic properties of the atrium were studied before and during intravenous infusion of isoproterenol at 2 to 5 micrograms/min in 11 patients with paroxysmal supraventricular tachycardia exhibiting atrial latency during programmed atrial extrastimulation. In all patients, the isoproterenol infusion reduced the extent of maximum atrial latency (from 86 +/- 19 to 62 +/- 16 ms, p less than 0.001). This was accompanied by a significant shortening of both effective and functional refractory periods of the atrium (from 213 +/- 31 to 174 +/- 40 ms, p less than 0.005 and from 259 +/- 31 to 215 +/- 29 ms, p less than 0.001, respectively). The intra-atrial and interatrial conduction times were also significantly reduced (from 24 +/- 15 and 63 +/- 17 to 15 +/- 10 and 48 +/- 15 ms, p less than 0.005, respectively). In 3 patients with demonstrable atrial vulnerability, the isoproterenol infusion abolished the inducibility of repetitive atrial responses or atrial flutter, or both. Although the clinical significance of the suppressive action of beta-adrenergic stimulation on atrial vulnerability remains to be determined, the present study has demonstrated that beta-adrenergic stimulation significantly reduces atrial latency.

Supraventricular tachyarrhythmias. Mechanisms, types, and management.

Advances in the area of clinical electrophysiology have allowed definition of the mechanisms of most forms of supraventricular tachyarrhythmias. Reentry, automaticity, and triggered activity are the three basic mechanisms. Treatment of the arrhythmias is based on frequency and hemodynamic severity. After accurate diagnosis, empirical therapy with currently available medications usually controls symptomatic supraventricular tachyarrhythmias. Nonpharmacologic therapy with permanent antitachycardia pacemakers, percutaneous catheter ablation, or surgery is indicated for selected patients with medically recalcitrant supraventricular tachyarrhythmia.

Effects of beta-adrenergic blockade on verapamil-responsive and verapamil-irresponsive sustained ventricular tachycardias.

To assess effects of beta-adrenergic blockade on ventricular tachycardia (VT) of various mechanisms, electrophysiology studies were performed before and after intravenous infusion of propranolol (0.2 mg/kg) in 33 patients with chronic recurrent VT, who had previously been tested with intravenous verapamil (0.15 mg/kg followed by 0.005 mg/kg/min infusion). In the verapamil-irresponsive group, 10 patients (group IA) had VT that could be initiated by programmed ventricular extrastimulation and terminated by overdrive ventricular pacing, and 11 patients (group IB) had VT that could be provoked by isoproterenol infusion (3-8 micrograms/min) but not by programmed electrical stimulation, and that could not be converted to a sustained sinus rhythm by overdrive ventricular pacing. Notably, in the group IA patients, all 10 patients had structural heart disease (coronary arteriosclerosis or idiopathic cardiomyopathy); beta-adrenergic blockade accelerated the VT rate in one patient but exerted no effects on the VT rate in the remaining 9 patients, and VT remained inducible in all 10 patients. By contrast, in the group IB patients, 7 of the 11 patients had no apparent structural heart disease; beta-adrenergic blockade completely suppressed the VT inducibility during isoproterenol infusion in all 11 patients. There were 12 patients with verapamil-responsive VT (group II). 11 of the 12 patients had no apparent structural heart disease. In these patients, the initiation of VT was related to attaining a critical range of cycle lengths during sinus, atrial-paced or ventricular-paced rhythm; beta-adrenergic blockade could only slow the VT rate without suppressing its inducibility. Of note, 14 of the total 33 patients had exercise provocable VT: two in group IA, five in group IB, and seven in group II. Thus, mechanisms of VT vary among patients, and so do their pharmacologic responses. Although reentry, catecholamine-sensitive automaticity, and triggered activity related to delayed afterdepolarizations are merely speculative, results of this study indicate that beta-adrenergic blockade is only specifically effective in a subset group (group IB) of patients with VT suggestive of catecholamine-sensitive automaticity.

Management of supraventricular tachyarrhythmias.

Supraventricular tachyarrhythmias are common and treatment is based on the frequency and hemodynamic severity caused by these arrhythmias. Empiric therapy with currently available medications often satisfactorily controls symptomatic arrhythmias. Nonpharmocologic therapy with permanent antitachycardia pacemakers, percutaneous catheter ablation or surgery can be effective for selected patients with medically refractory supraventricular tachyarrhythmias after thorough electrophysiologic evaluation. In selected patients with life-threatening supraventricular tachyarrhythmias due to the WPW syndrome, surgical ablation is the therapy of choice.

Efficacy and safety of oral nadolol for exercise-induced ventricular arrhythmias.

Sixty-four patients with reproducible exercise-induced ventricular arrhythmias were enrolled in an open-label, multicenter study to assess the efficacy and safety of oral nadolol therapy. There were 53 men and 11 women ranging in age from 19 to 75 years (mean 53.9). The severity of arrhythmias varied from frequent ventricular premature beats to nonsustained and sustained ventricular tachycardias. Using serial treadmill exercise tests, patients underwent dose titration for 1 month and were followed up for 3 to 6 months. Depending on drug tolerance and response to treadmill exercise testing, the single daily required dose of oral nadolol ranged from 20 to 240 mg (average 66). Twenty-three (36%) of the patients experienced a total of 30 adverse effects of nadolol therapy; however, only 9 (14%) patients had to be withdrawn from the study. The adverse effects observed were those commonly associated with beta-adrenergic blocking agents, and all were dose-dependent and reversible. At the last patient visit, the severity of exercise-induced ventricular arrhythmias was significantly decreased compared with pretreatment in 36 (75%) of 48 evaluable patients. Eighteen (38%) of the patients demonstrated total suppression of arrhythmias. This was accompanied by significant increases from pretreatment in both the mean duration of symptom-limited exercise (+1.02 +/- 0.41 minutes, p less than 0.05) and the mean time of exercise required for arrhythmia induction (+1.80 +/- 0.66 minutes, p less than 0.01), a significant decrease from pretreatment in the mean peak exercise double-product (-4,775, p less than 0.001) and a decrease in the incidence of exercise-induced ST-segment depression (-33%).(ABSTRACT TRUNCATED AT 250 WORDS)

Intravenous propafenone for termination of reentrant supraventricular tachycardia. A placebo-controlled, randomized, double-blind, crossover study.

To assess the antiarrhythmic efficacy of intravenous propafenone, 20 patients with inducible sustained supraventricular tachycardia received propafenone, 2 mg/kg body weight, or placebo in a double-blind, randomized, crossover study. Three patients had intra-atrial reentrant tachycardia, 3 had atrioventricular nodal reentrant tachycardia, and 14 had atrioventricular reciprocating tachycardia associated with the Wolff-Parkinson-White syndrome. Termination of supraventricular tachycardia occurred in 15 of the 20 patients receiving propafenone but 0 of the 11 patients receiving placebo (p less than 0.01). Propafenone prolonged refractoriness and slowed conduction of the atrium, the atrioventricular node, and accessory atrioventricular bypass tracts, and these effects provided antiarrhythmic action to halt tachycardia. No adverse effects were observed in any patient. We conclude that intravenous propafenone is safe and effective in the acute treatment of various forms of reentrant supraventricular tachycardia.