Sustained intraatrial reentrant tachycardia: clinical, electrocardiographic and electrophysiologic characteristics and long-term follow-up

Although intraatrial reentry has been traditionally listed as a mechanism for supraventricular tachycardia, few reports describing the clinical features of this arrhythmia exist. Nineteen patients with a clinical history of sustained supraventricular tachycardia were diagnosed as having intraatrial reentrant tachycardia. Seventeen (89%) patients of the 19 had underlying structural heart disease and 17 had echocardiographic evidence of atrial enlargement; the mean left ventricular ejection fraction was 51 +/- 16%. A history of concomitant atrial fibrillation or flutter was present in 13 patients (68%). The mean atrial cycle length during tachycardia was 326 +/- 57 ms (range 260 to 460). Fourteen patients had 1:1 atrioventricular (AV) conduction during tachycardia, of whom 50% had an RP'/RR' ratio greater than 0.5. Intravenous adenosine (dose range 37.5 to 150 micrograms/kg) and verapamil (dose range 5 to 10 mg) had no effect on atrial tachycardia cycle length in 13 of 14 and 9 of 9 patients, respectively, despite induction of second degree AV block. Type 1a antiarrhythmic drugs achieved long-term suppression of intraatrial reentrant tachycardia in only 6 patients, whereas amiodarone (326 +/- 145 mg/day) was successful in 11 patients during a 32 +/- 20 month follow-up period. The remaining two patients and one patient who later developed amiodarone toxicity either progressed to (n = 1) or had (n = 2) catheter-induced high grade AV block and were treated with long-term ventricular pacing. It is concluded that intraatrial reentrant tachycardia is often associated with structural heart disease, particularly of types that cause atrial abnormalities, but left ventricular dysfunction is not a requisite finding. Other arrhythmias are frequently observed in these patients. This arrhythmia responds poorly to type 1a antiarrhythmic drugs, but is effectively treated with amiodarone. Catheter ablation of the AV junction offers a therapeutic option for patients who are refractory to medical therapy.     

Vagal tone, significance of electrophysiologic findings and clinical course in symptomatic sinus node dysfunction

The relation of hypersensitive carotid sinus syndrome (HCSR) to sick sinus syndrome (SSS) is not clear; vagal role, relevance of electrophysiological testing, and the natural course of both syndromes are ill defined. In 186 symptomatic patients, resting heart rate (HR), carotid sinus pressure results (CSP), and corrected sinus node recovery time (CSRT) were determined before and after atropine (A). According to test results 102 patients had HCSR (group I), 33 had HCSR + SSS (group II), 30 patients had isolated SSS (group III) and 20 served as control (group IV). HR below 60 b.p.m. in groups I to III and lower than controls (p < 0.01) rose after A by approximately 31 per cent in groups I to IV. This indicates predominant vagal tone, and establishes that rate response to A is unreliable as a diagnostic test for groups I and III. CSP normalized after A but CSRT remained unchanged (p > 0.05), which implies increased vagal tone in HCSR but destructive affection of the SA node in SSS. Bradycardia, S-A block, supraventricular tachyarrhythmias and the combination of dizziness and syncope served as diagnostic clues for HCSR or SSS in a limited number of patients. CSP and CSRT separated HCSR from SSS but failed to predict syncope in groups I to III (p > 0.05) and thereby cannot aid the indication for pacer application. SSS test results remained unchanged over 16 months showing an unfavorable prognosis. We conclude that HCSR and SSS, although frequently occurring together, are entities made separate by specific testing, which, however, fails to aid in therapeutic decision-making. Vagal tone plays but one role in HCSR and SSS and electrophysiologic pathology of SSS does not improve in its course.     

The effects of adenosine on sinus node reentrant tachycardia

The effects of adenosine given during sinus node reentrant tachycardia were investigated in two patients. Both patients received intravenous bolus doses of 0.1 mg/kg and 0.15 mg/kg. Adenosine slowed the atrial rate in both patients and terminated the tachycardia in one. These effects of adenosine on sinus node reentrant tachycardia suggest that sinus nodal tissue (as opposed to perinodal atrial tissue) is involved in the tachycardia circuit and that these effects should be considered when adenosine is used as a diagnostic agent in narrow-complex tachycardia.     

The significance of electrophysiologic findings and clinical course in symptomatic sinus node dysfunction (author's transl)

Under investigation in this study were the relationship between hypersensitive carotid sinus reflex (HCSR) and sick sinus snydrome (SSS), the significance of clinical symptomatology versus electrophysiologic test results and the natural course of both syndromes. In 186 symptomatic patients (pts) resting heart rate, maximal corrected sinus node recovery time (CSRTmax) and maximal carotid sinus pressure results (CSPmax) were determined. According to test results, 103 pts had HCSR (I), 33 had HCSR + SSS (II), 30 pts had SSS (III), and 20 pts with normal test results served as controls (IV). Mean age was the same in groups I--IV (p greater than 0.05). Groups I--III had a heart rate less than or equal to 60 bpm. There was no correlation between patients test data and the occurrence of syncopes in each of groups I--III (p greater than 0.05). In 16 pts with SSS, test results remained unchanged 16 months later (p greater than 0.05). More pts (31%) in group II died in a shorter period of time after pacer application (1.4 +/- 1 year) than pts with AV III degrees block (25%, 1.8 +/- 1.6 years) after pacer application. We conclude that the combination HCSR + SSS seems rather frequent. Specific testing separated HCSR from SSS, but failed to predict syncopes and thereby cannot aid in the indication for pacer application. The 16 months prognosis of SSS proved unfavorable. Mortality after pacer application in HCSR + SSS seems less favorable than in AV III degrees block (p less than 0.05), but depends largely on the severity of associated diseases.     

Atrioventricular nodal reentrant tachycardia associated with idiopathic ventricular tachycardia: clinical and electrophysiologic characteristics

Background

Case reports have described the coexistence of ventricular tachycardia (VT) and supraventricular tachycardia in the same patient. This study examines the frequency of dual atrioventricular nodal (AVN) physiology, AVN echo beats, and atrioventricular nodal reentrant tachycardia (AVNRT) in patients with VT.

Methods

Programmed atrial and ventricular stimulation was performed in 132 consecutive patients referred for electrophysiologic study of symptomatic VT. Of the 132, 99 patients had structural heart disease, and 33 patients had idiopathic ventricular tachycardia (IVT).

Results

Among the 33 patients with IVT, 23 had dual AVN physiology. Compared with patients with structural heart disease undergoing VT ablation, dual AVN pathways (70% vs 27%, P < .0001), dual AVN pathways with echo beats (24% vs 8%, P = 0.03), and AVNRT (21% vs 1%, P = .0002) were more common in patients with IVT.

Conclusion

Dual AVN physiology and AVNRT appear to be associated with IVT. This finding suggests that patients with IVT should undergo a complete electrophysiologic evaluation, and the diagnosis of coexistent AVNRT should be considered in this population.     

Effects of the pacing site in sinus node reentrant tachycardia.

His bundle recordings and premature atrial stimulation from coronary sinus, mid-right atrium and high-right atrium were performed in a patient with repetitive supraventricular tachycardias. Regardless of the paced site, there was a range of coupling intervals during which testing stimuli elicited short runs of premature beats. The corresponding P waves were positive in leads I, II and III and had a high-to-low right atrial activation sequence. Their morphology was similar to that of sinus beats. However, sustained tachycardia occurred only when pacing was performed from the coronary sinus. Therefore, it is postulated that the site of stimulation might be important in the genesis and (perhaps) perpetuation of this arrhythmia by changing the site and (or) mode of entry into the area where this type of tachycardia occurs. Though sinus node reentry was the most likely mechanism, it could not be determined whether the circuit involved the sinus node per se or the so called perinodal fibers.     

Radiofrequency catheter ablation for sinoatrial node reentrant tachycardia: electrophysiologic features of ablation sites

The aim of this study was to investigate catheter ablation of sino-atrial reentrant tachycardia (SART) and the electrophysiologic characteristics of the ablation sites. From January 1990 to October 1997, 651 patients with supraventricular tachycardia were referred and 11 patients were found to have SART. Ablation was successful in all cases with a mean number of 3.3 radiofrequency (RF) current pulses. SART terminated during 22 of 36 RF pulses. In spite of prompt termination, tachycardia could be re-induced in 3 of 11 patients with its earliest activation site shifted. At effective ablation sites, the electrograms during tachycardia were characterized as fractionated (75+/-17 ms), and 38+/-16 ms prior to surface P wave, and 42+/-18 ms prior to the high right atrium. Unipolar electrograms revealed a sharp negative unipolar deflection, so called QS pattern, in 15 of 20 sites during SART and 15 of 15 sites during sinus rhythm. During effective applications, atrial premature beats (APB) with activation sequences identical to sinus rhythm appeared in 14 of 22 cases. Effective ablation sites of SART showed fractionated electrograms during tachycardia and sinus rhythm. Unipolar electrogram with a QS pattern and APB during energy application could be an indicator of the optimal ablation sites.     

Efficacy and electrophysiologic effects of encainide for atrioventricular nodal reentrant tachycardia

To prospectively determine the clinical efficacy and electro-physiologic effects of encainide in atrioventricular nodal reentrant tachycardia (AVNRT), 49 patients refractory to 2.7 ± 1.5 previous antiarrhythmic drug trials underwent electrophysiologic study before and 47 did so after administration of oral encainide (75 to 240 mg/day). Encainide prolonged the minimum atrial pacing cycle length maintaining 1:1 atrioventricular (AV) nodal conduction from 334 ± 55 to 391 ± 55 ms (p = 0.0001). Encainide induced ventriculoatrial (VA) block in 12 patients (25%) and slowed the minimum ventricular pacing cycle length maintaining 1:1 VA conduction from 315 ± 46 to 485 ± 89 ms (p = 0.0001) in the remaining 35 patients. After encainide, AVNRT was not inducible in 32 of 47 patients (68%) primarily because of the effects on retrograde AV nodal conduction. In the remaining 15 (32%) patients, AVNRT remained inducible; however, the tachycardia cycle length slowed from 397 ± 86 to 492 ± 90 ms (p = 0.0001). There was no significant difference in the baseline minimum ventricular pacing cycle length maintaining 1:1 VA conduction in patients whose inducible tachycardia was or was not suppressed.

Forty-seven patients were treated for 18.9 ± 12.9 months (range 1 to 50) with oral encainide. Encainide was completely effective in eliminating recurrences of supraventricular tachycardia in 26 of 47 patients (55%) and partially effective in an additional 42%. Recurrences of arrhythmia occurred in 15 of 32 patients (47%) whose inducible tachycardia was suppressed by encainide and 7 of 15 patients (47%) whose inducible tachycardia was not suppressed by encainide (p = not significant).

It is concluded that encainide is effective in the treatment of patients with AVNRT. Encainide's primary antiarrhythmic effect is depression of conduction in the retrograde limb of the reentrant circuit. Results of serial electrophysiologic testing with encainide in AVNRT are not predictive of long-term clinical response.     

Electrophysiologic and clinical effects of oral encainide in paroxysmal atrioventricular node reentrant tachycardia

The electrophysiologic effects of oral encainide (75 to 150 mg daily) were evaluated in 14 patients (6 male and 8 female, aged 49 +/- 9 years) with atrioventricular (AV) node reentrant tachycardia of the slow-fast type. The patients were studied in control conditions and after 2 to 12 days of treatment. Encainide increased the AH interval from 67 +/- 10 to 82 +/- 23 ms (p less than 0.02). Anterograde Wenckebach cycle length was increased in three patients, reduced in four, unchanged in one; it was not measurable in the remaining patients because tachycardia was induced. Retrograde Wenckebach periodicity increased from 307 +/- 71 to 401 +/- 92 ms (p less than 0.005) in all nine patients in whom it was measurable; complete retrograde block was observed in one patient. At the control study, tachycardia was induced in all patients, with a mean cycle length of 341 +/- 50 ms; after encainide, tachycardia was inducible in only 1 patient, with an increase in cycle length from 270 to 320 ms; in the other patients, tachycardia was not inducible because of a lack of retrograde (11 patients) or anterograde (2 patients) conduction. The mean plasma concentrations of encainide and its metabolites O-demethyl-encainide and 3-methoxy-O-demethyl-encainide measured in 13 patients during the repeat study were 161 +/- 304, 128 +/- 100 and 95 +/- 85 ng/ml, respectively; three poor metabolizers who presented a high concentration of the parent compound were observed in this series. All patients were discharged on encainide at a mean daily dose of 112 +/- 39 mg.(ABSTRACT TRUNCATED AT 250 WORDS)     

莫雷西嗪对功能低下窦房结的电生理作用

单剂静注莫雷西嗪５０ｍｇ或２５ｍｇ对功能低下窦房结有抑制作用（Ｐ〈０．０５），呈非量效关系。本实验提示：单剂静注莫雷西嗪５０ｍｇ或２５ｍｇ治疗具有窦房结功能低下病人的心律失常时，可能导致严重的窦性心动过缓或窦性停搏。     

Successful ablation of sinus node reentrant tachycardia using remote magnetic navigation system

Ablation of sinus node reentrant tachycardia (SNRT) may be difficult with risk of sinus node injury by using conventional catheters. We report successful ablation of SNRT by using remote magnetic navigation system (Stereotaxis).     

Flecainide: electrophysiologic and antiarrhythmic properties in refractory ventricular tachycardia

Twenty-two patients with coronary artery disease and spontaneous ventricular tachycardia (VT) or ventricular fibrillation (VF) underwent intracardiac electrophysiologic evaluation and, when possible, ambulatory monitoring before and after therapy with flecainide (mean dose 418 +/- 87 mg [mean +/- standard deviation]). An average of 4 antiarrhythmic agents were used and were unsuccessful before therapy with flecainide was begun. During 64 +/- 16 hours of control Holter monitoring in 16 patients, all had 1 or more salvos of VT, as well as ventricular premature complexes (VPCs). Programmed stimulation during the control period induced VT in 17 of 22 patients. After flecainide therapy, Holter monitoring showed elimination of all forms of VT in all but 1 patient, as well as significant reduction of paired VPCs by 95% (p less than 0.03) and single VPCs by 70% (p less than 0.005). Electrophysiologic study during flecainide therapy showed significant increases in AH, HV, PR, QRS and QTc intervals, and the ventricular effective refractory period. Programmed stimulation in 17 patients taking flecainide, with a mean plasma level of 1,075 +/- 521 ng/ml, showed ablation of inducible VT in only 2 patients, a worsening in 5 and continued VT inducibility in 10. Adverse effects that required drug withdrawal were infrequent and encountered in patients who received higher drug levels: 1 patient with congestive heart failure and 1 with severe sinus bradycardia. Thus, although flecainide suppresses complex ventricular arrhythmias on Holter recordings, it rarely alters the response to programmed stimulation. Caution is recommended in its use for recurrent sustained VT or VF and in the interpretation of electrophysiologic studies until the predictive value of programmed stimulation with flecainide therapy is established.     

Comparative quantitative electrophysiologic effects of adenosine triphosphate on the sinus node and atrioventricular node

A pharmacologic approach was used to characterize the sinus node (SN) and atrioventricular (AV) node responses to intravenous adenosine triphosphate (ATP) in 21 patients during electrophysiologic testing. ATP produced dose-dependent prolongation of spontaneous sinus cycle length. The mean maximal increase in sinus cycle length was 294 +/- 60 ms (n = 10). The mean dose of ATP required to produce this maximal sinus cycle length prolongation was 3.5 +/- 1.0 mg. The dose-response curve for sinus cycle length prolongation was sigmoid in shape with an EC50 of 0.39 mg derived from a median effect plot. There was a negative correlation between the control sinus cycle length and the dose of ATP required to produce the maximal prolongation of cycle length (p less than 0.05). In contrast, the mean dose of ATP producing AV block was 4.4 +/- 0.97 mg and the EC50 was 2.98 mg. There was a positive correlation between the AV nodal functional refractory period and the prolongation of the AH interval with a 2 mg dose (p less than 0.05). Consistent with the AV nodal dose-response curves, 8 mg ATP terminated paroxysmal reentrant supraventricular tachycardia at the AV node in 8 of 9 patients. Thus, SN and AV node responses to ATP have differences in their electrophysiologic correlates and EC50. These findings suggest that ATP has potentially different mechanisms of action on SN automaticity and AV nodal conduction that requires further investigation.     

Accessory pathway and atrioventricular node reentrant tachycardia in elderly patients: Clinical features,electrophysiologic characteristics and results of radiofrequency ablation

Objectives. This study was designed to evaluate the clinical features, electrophysiologic characteristics and results of radio-frequency ablation in elderly patients with accessory atrioventricular (AV) pathways or AV node reentrant tachycardia. Background. Radiofrequency ablation in elderly patients with paroxysmal supraventricular tachycardia has not been well described, and comparative study between elderly and younger patients is limited.Methods. Electrophysiologic studies and radiofrequency ablation were performed in 92 elderly patients (45 with an accessory pathway, 47 with AV node reentrant tachycardia).Results. The elderly patients had poorer electrophysiologic properties in accessory pathways and dual AV node pathways than those of younger patients. The success rate of radiofrequency ablation was similar in elderly and younger patients. However, elderly patients had more complications (14%) in left-sided accessory pathways.Conclusions. Radiofrequency ablation in elderly patients with supraventricular tachycardia was effective. However, it must be performed cautiously in those patients with left-sided accessory pathways.     

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.     

Sustained ventricular tachycardia in patients with idiopathic dilated cardiomyopathy: electrophysiologic testing and lack of response to antiarrhythmic drug therapy

Eleven consecutive patients with idiopathic dilated cardiomyopathy and spontaneous, sustained ventricular tachycardia (VT) of uniform morphology underwent programmed ventricular stimulation and serial antiarrhythmic drug testing. The mean ejection fraction was 30 +/- 6.4%. Sustained VT was induced by programmed electrical stimulation in all 11 patients. A mean of 3.7 +/- 2.4 antiarrhythmic drugs were evaluated by programmed stimulation, including at least one experimental agent in eight patients. In nine of 11 patients VT remained inducible on all drug therapy. During a mean follow-up period of 21 +/- 14 months there were four sudden deaths and two patients with recurrences of VT. In all six patients with sudden death or recurrence of VT, the arrhythmia remained inducible on drug therapy. Three patients who died suddenly had a hemodynamically stable, induced tachycardia on antiarrhythmic therapy. Of eight patients treated with amiodarone, only two were successfully treated. We conclude that in patients with sustained VT and idiopathic dilated cardiomyopathy, VT can be induced by programmed electrical stimulation. VT will usually remain inducible on antiarrhythmic therapy, and sudden death can occur despite slowing and improved tolerance of the induced arrhythmia. Amiodarone may have limited efficacy, and more aggressive therapy, such as surgery or implantation of an automatic internal defibrillator, should be considered in this patient population.     

New aspects of the electrophysiologic effect of antiarrhythmic agents

BASIC ACTIONS: According to Vaughan Williams antiarrhythmic agents are divided into four classes of action (Table 1). A given agent may display actions of several classes. In general, except for class II drugs there is no causal relationship between the class of action and the mechanism precipitating the arrhythmia. MECHANISM OF ACTION OF CLASS I DRUGS: The effect of class I antiarrhythmic drugs is primarily based on prolongation of the refractory period. It is assumed that the sodium channel can be in one of at least three functional conditions (Figure 1), resting, activated or inactivated. Conductance is achieved only in the state of activation, during the initial phase of the action potential which is caused by rapid sodium influx. The transition from inactivation to resting condition, which is prerequisite for renewed activation, takes place during repolarization and is responsible for the refractory period of the action potential (Figure 1). Class I antiarrhythmic drugs block the sodium channels such that they remain in a nonconductive state. As a function of the number of inoperative sodium channels, sodium influx is reduced and the rate of rise of the action potential is diminished. In order to enable sufficient sodium channels to make the transition from inactivated to resting condition, repolarization of the action potential has to continue and, concomitantly, the absolute refractory period is increased. Since the attenuation of the rapid sodium influx also causes a decrease in the conduction velocity in myocardium and in the intraventricular conduction system, reentry arrhythmias can be precipitated. DIFFERENCES IN THE ACTION OF CLASS I DRUGS: Due to different rate-dependency of the various class I drugs and the effect on the duration of the action potential as well as on specified ECG parameters, subclasses a, b and c were designated (Table 2). Access of the drug to the sodium channel receptor is facilitated during activation and inactivation but not in the resting condition. Accordingly, the effect increases in proportion to the frequency with which the sodium channel is opened. With the beginning of the cardiac cycle, there is an exponential increase in the number of blocked sodium channels and, with transition to the resting condition, an exponential decrease (Figure 2). The velocity of the increase or decrease is dependent on the properties of the given agent. Substance with rapid binding kinetics, that is time constants of 0.2 to 2.0 s are assigned to group Ib, those with time constants of 8 to 14 s to group Ic (Table 3). Group Ia is intermediate. A similar grouping is yielded on assignment according to the temporal course of deblocking. EXPLANATION FOR THE DIFFERENCES IN EFFECTS: With antiarrhythmic agents of class Ib, due to their rapid binding kinetics, at a rate of approximately 1 Hz (60/min) steady-state is achieved with no accumulation of block. Each incoming impulse with a normal interval can activate the unblocked membrane (Figure 2). Premature impulses occurring with shorter intervals are inhibited more the earlier their incidence. Consequently, class Ib antiarrhythmic drugs are particularly effective for premature beats and frequent tachycardias while, during normal sinus rhythm, in some instances, no effect such as PQ or QRS prolongation can be observed (Table 2).(ABSTRACT TRUNCATED AT 400 WORDS)     

Electropharmacology of nonsustained ventricular tachycardia: effects of class I antiarrhythmic agents, verapamil and propranolol

Forty-seven patients with spontaneous and inducible nonsustained ventricular tachycardia (VT) underwent serial electrophysiologic studies to evaluate the effects of antiarrhythmic agents on inducible arrhythmias, the role of electrophysiologic testing in the evaluation of pharmacologic therapy for these arrhythmias, and potential mechanisms underlying these arrhythmias. Type I antiarrhythmic agents prevented induction of VT by programmed stimulation in 18 of 37 patients and by isoproterenol in 9 of 11 patients. Verapamil and propranolol did not prevent or alter the mode of induction of VT by programmed stimulation, nor did they slow the induced tachycardias. Propranolol prevented induction of VT by isoproterenol in all 14 patients tested. Type I antiarrhythmic agents converted nonsustained into sustained VT in 2 of 37 patients. Inducible VT was prevented in 88% of patients without underlying heart disease, in contrast to only 38% of patients with associated cardiac disease (p less than 0.02). This study demonstrates that electrophysiologic studies may be used to identify antiarrhythmic agents with both beneficial and potentially harmful effects in patients with nonsustained VT. The responses of inducible tachycardias to antiarrhythmic agents in this group of patients with spontaneous nonsustained VT are similar to those previously observed in patients with sustained VT. Finally, the results suggest that VT induced by isoproterenol may frequently respond to type I antiarrhythmic agents in addition to beta blockers.     

Proarrhythmic effects of antiarrhythmic drugs assessed by electrophysiologic study in recurrent sustained ventricular tachycardia

Proarrhythmic responses were evaluated in repeated electrophysiologic studies (EPS) in 27 patients with inducible ventricular tachycardia (VT). Class Ia drugs were administered to 23, Ib to 6, Ic to 4, III to 5 and IV to 9 patients. The mean age was 53 years, and 18 patients had structural heart diseases. Pleomorphism was observed in 11 patients. In 4 patients (15%), the VT cycle length (CL) shortened by 50 ms or more in EPS during the administration of antiarrhythmic drugs. VT was inducible by a less aggressive induction mode than the control study in 9 patients (33%). In 4 patients (15%), the induced VT changed to the incessant form, and the other 2 patients (7%) required DC shocks due to hemodynamic deterioration. Patients with pleomorphic VT and/or structural heart diseases seemed to develop proarrhythmia more frequently. In total, some proarrhythmic response was observed in 13 (48%) of the 27 patients. Therefore, it should be kept in mind that proarrhythmic effects are frequently observed during antiarrhythmic therapy in patients with sustained VT. The action of the drugs on the slow conduction zone may vary, which may provide a basis for the development of proarrhythmia.     

Incidence and clinical significance of inducible atrial tachycardia in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. METHODS AND RESULTS: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351+/-95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7+/-5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. CONCLUSION: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia.