Comparison of the ventricular response during atrial fibrillation in patients with enhanced atrioventricular node conduction and Wolff-Parkinson-White syndrome

Although ventricular fibrillation is a well known sequel to atrial fibrillation in the Wolff-Parkinson-White syndrome, ventricular fibrillation is not generally associated with supraventricular tachycardia in the presence of enhanced atrioventricular (AV) node conduction without pre-excitation. It was hypothesized that the ventricular response during atrial fibrillation may be less in patients with enhanced AV node conduction than in their counterparts with Wolff-Parkinson-White syndrome matched for anterograde effective refractory period. Slower ventricular rates during atrial fibrillation would suggest an increased propensity for concealed conduction in the enhanced AV node conduction group than in the group with an accessory pathway. Three groups of patients aged 16 to 65 years underwent electrophysiologic testing for supraventricular tachycardia or after surgical correction of Wolff-Parkinson-White syndrome. Sixteen patients had enhanced AV node conduction, 16 had Wolff-Parkinson-White syndrome and 16 had normal AV node conduction. Patients with enhanced AV node conduction and Wolff-Parkinson-White syndrome were well matched for anterograde effective refractory period (245 +/- 22 versus 258 +/- 25 ms) and minimal cycle length, maintaining 1:1 anterograde conduction (261 +/- 21 versus 260 +/- 40). There was no difference in intervals during atrial fibrillation (average RR interval = 372 +/- 37 versus 346 +/- 66) or shortest RR interval (266 +/- 27 versus 243 +/- 51). Thus, patients with Wolff-Parkinson-White syndrome and those with enhanced AV node conduction matched for anterograde refractory period exhibit similar ventricular rates during atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effect of sotalol in supraventricular tachycardias

The electrophysiological effects of sotalol, a beta-blocking drug with class III antiarrhythmic properties were assessed in 20 patients (mean age 33 +/- 14.3 years) with supraventricular tachycardias. Sixteen patients had Wolff-Parkinson-White syndrome (overt n = 9, concealed n = 7), three patients AV-nodal reentrant tachycardias and another patient atrial tachycardias. Sotalol was administered intravenously (n = 16) in a dose of 1.5 mg/kg over 15 min. The effects of 320 to 480 mg/day oral sotalol were assessed in 7 patients. By intravenous and oral application of sotalol a significant increase in the AH interval, the refractory periods of the atrium and ventricle as well as a decrease of the antegrade and retrograde conduction capacity of the AV node or the accessory pathway were observed. The mean R-R interval during induced atrial fibrillation increased significantly in patients with Wolff-Parkinson-White syndrome from 224 +/- 52 ms to 277 +/- 59 ms (p less than 0.05). In 10 patients, sotalol was administered during supraventricular reentrant tachycardia. The cycle length of supraventricular tachycardia increased from 276 +/- 90 ms to 358 +/- 25 ms (p less than 0.01). The tachycardia terminated in 7 patients: in 5 patients block was observed in the AV node, while in another 2 patients tachycardia terminated retrogradely. After intravenous application supraventricular arrhythmias were no longer inducible in 5 of 12 patients. In a further 4 patients only non-sustained supraventricular tachycardias (4-20 QRS complexes) were inducible. In 2 patients the supraventricular tachycardia terminated distal to the His bundle.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regular Wide QRS Complex Tachycardia During Atrial Fibrillation in a Patient with Preexcitation Syndrome: A Case Report

AV Conduction in WPW. We report an unusual case of a relatively regular wide QRS complex tachycardia alternating with periods of an irregular narrow QRS complex tachycardia during atrial fibrillation in a patient with Wolff-Parkinson-White syndrome. Both tachycardias resulted from atrial fibrillation, the wide QRS complex tachycardia being due to 2:1 AV conduction of a type I atrial fibrillation across a posteroseptal accessory AV connection.     

Effects of intravenous adenosine on antegrade refractoriness of accessory atrioventricular connections

BACKGROUND. Several groups have suggested the use of intravenous adenosine or adenosine triphosphate in the diagnosis of regular broad complex tachycardias. However, the short half-life of these agents has precluded assessment of their effects on refractoriness of accessory connections, and their safety in preexcited arrhythmias has not been demonstrated. METHODS AND RESULTS. We examined the effects of intravenous adenosine on accessory atrioventricular (AV) connections in 30 patients with the Wolff-Parkinson-White syndrome. Intravenous adenosine (12 mg, rapid bolus) was administered to 14 patients (group 1) during continuous atrial pacing at a cycle length 20 msec below that required to cause 2:1 conduction block in the accessory connection (mean pacing cycle length 261 +/- 41 msec). After adenosine, transient 1:1 conduction occurred via the accessory connection in 12 of 14 patients, indicating a shortening of antegrade refractoriness. In three of seven patients, this effect was abolished after intravenous propranolol (0.2 mg/kg). Nineteen patients (group 2) received adenosine (0.17 +/- 0.04 mg/kg) during induced, preexcited atrial arrhythmias. The minimum RR interval during preexcited atrial fibrillation transiently decreased (252 +/- 44 msec to 224 +/- 35 msec, p less than 0.01) after adenosine, but no change in average RR interval was observed (360 +/- 59 msec to 357 +/- 60 msec, NS). The preexcited ventricular response to atrial flutter was transiently accelerated in five of eight patients (415 +/- 21 msec to 360 +/- 49 msec, p less than 0.05) due to shortening of flutter cycle length (207 +/- 10 msec to 180 +/- 24 msec, p less than 0.05). However, 2:1 accessory connection conduction was maintained in all eight patients. All effects were short lived, with the decrease in RR interval during atrial fibrillation occurring for a maximum of two RR intervals only. No patient suffered ventricular arrhythmias or hemodynamic deterioration. CONCLUSIONS. Adenosine shortens antegrade refractoriness of accessory AV connections, and in some patients this action is mediated by beta-adrenergic stimulation. Adenosine may cause acceleration of preexcited atrial arrhythmias, but these effects are transient and should not discourage the use of adenosine as a diagnostic agent in broad complex, regular tachycardias of uncertain origin.     

AV nodal reentrant tachycardia with a bystander Mahaim fiber

A 13 year old boy had a wide QRS complex tachycardia. A discontinuity in the AV nodal functional curve was observed in the electrophysiologic study. The AV internal was prolonged in association with progressive ventricular preexcitation. At maximal preexcitation, the HV interval was -20 msec and the QRS complex was identical to that seen during clinical tachycardia. No VA conduction was found and atrial premature beats did not affect the tachycardia. The His deflection was found at variable timing when tachycardia was induced. These findings confirmed that tachycardia originated within the AV node and was conducted to the ventricle over the Mahaim fiber. The short effective period of the Mahaim fiber had clinical significance since when atrial fibrillation developed, a rapid ventricular response was observed.     

Ventricular tachycardia masquerading as supraventricular tachycardia: A wolf in sheep''s clothing

It is generally assumed that if a wide QRS complex tachycardia has the same morphology on the 12-lead electrocardiogram as during sinus rhythm, the tachycardia is supraventricular. The author presents unique electrocardiographic data on four patients with QRS complex morphologies that are nearly identical during ventricular tachycardia and during sinus rhythm. The QRS complex duration during sinus rhythm was 140-180 msec and was the same as that of the tachycardia. The QRS complex morphology on the electrocardiogram was a right bundle branch block, left axis in three patients and right bundle branch block, normal axis in one patient. The mean ventricular tachycardia cycle length was 345 msec. The diagnosis of ventricular tachycardia was established by electrophysiologic testing in two patients and by atrial electrograms demonstrating AV dissociation in two patients. Thus, if the 12-lead electrocardiogram morphology of a wide QRS complex tachycardia is similar to that during sinus rhythm, it does not necessarily imply that the tachycardia is supraventricular. Ventricular tachycardia can occur with the same QRS complex morphology as occurs during sinus rhythm.     

Patients with supraventricular tachycardia presenting with aborted sudden death: incidence, mechanism and long-term follow-up

A total of 13 (4.5%) of 290 patients with aborted sudden death had either documented (7; 54%) or strong presumptive evidence of supraventricular tachycardia that deteriorated into ventricular fibrillation. Six (46%) of the 13 had an accessory conduction pathway and either atrial fibrillation (5 patients) or paroxysmal atrioventricular (AV) reentrant tachycardia (1 patient) that deteriorated into ventricular fibrillation. Three patients with AV node reentrant tachycardia and four with atrial fibrillation and enhanced AV node conduction presented with supraventricular arrhythmias that deteriorated into ventricular fibrillation. Patients were treated with medical, surgical or catheter ablative procedures designed to prevent recurrences of supraventricular arrhythmias. Four patients received an implanted automatic defibrillator, but none had an appropriate device discharge. Over a follow-up period of 41.6 +/- 33.6 months, 12 patients are alive without symptomatic arrhythmias. One patient died because of severe chronic lung disease and heart failure. Supraventricular tachycardia was the cause of aborted sudden death in approximately 5% of patients referred for evaluation of sudden cardiac death. Treatment directed at prevention of supraventricular tachycardia was associated with an excellent prognosis. Current treatment techniques appear to obviate the need for automatic defibrillator therapy in these patients.     

Incessant supraventricular tachycardia due to upper atrioventricular nodal reentry

Three patients with recurrent supraventricular tachycardia were presented. Atrial cycle length unchanged during the tachycardia with antegrade Wenckebach AH block was observed. When AH block occurred during tachycardia, the first AH interval was shorter than the subsequent one. The tachycardia was initiated and terminated by atrial extrastimulation beyond the atrial relative refractory period and the atrial activation sequence during the tachycardia was low to high. The induction of tachycardia was dependent on a critical AH interval. Ventriculoatrial conduction was not observed in patient 1 and 2. In patient 3 who had ventriculoatrial conduction, the tachycardia was initiated by the premature ventricular stimulation followed by double atrial response, and the tachycardia was terminated by the ventricular stimulation without atrial capture. In patient 1, verapamil (5 mg) prolonged the atrial cycle length during tachycardia and rapid intravenous injection of adenosine triphosphate (10 mg) terminated the tachycardia. Oral diltiazem (180 mg/day) suppressed the tachycardia in patients 2 and 3. These findings suggest that the mechanism of the tachycardia may be fast-slow type of AV nodal reentry in the upper portion of the AV node and this type of arrhythmia has a tendency to be incessant.     

Effect of atrioventricular interval during pacing or reciprocating tachycardia on atrial size, pressure, and refractory period. Contraction-excitation feedback in human atrium

To determine whether a contraction-excitation feedback mechanism exists in human atrium, we investigated the effects of varying the atrioventricular (AV) interval from 0 to 360 msec during AV pacing at a cycle length of 400 msec on atrial pressure, size, and refractoriness in 10 patients (group 1, without supraventricular tachycardia). The same parameters were determined in another 10 patients (group 2, with different spontaneous AV relations) during AV reciprocating tachycardia or AV nodal reciprocating tachycardia and during high right atrial (RA) pacing at the tachycardia cycle length. In group 1 patients, peak and mean RA pressure, RA effective refractory period (RA-ERP), and left atrial (LA) size all decreased to minimal values at an AV interval of 120 msec and remained low as the AV interval was increased and approached 400 msec. The increase in each of the variables from its lowest to greatest value was as follows: Mean systemic blood pressure, 20.9 +/- 3.1 mm Hg; LA size, 0.55 +/- 0.05 cm; RA peak pressure, 10.4 +/- 1.8 mm Hg; RA mean pressure, 3.5 +/- 0.6 mm Hg; and RA-ERP, 22.5 +/- 3.0 msec, p less than 0.001 for each. The weighted mean correlation coefficient with RA-ERP was significant for RA peak pressure and LA size (p less than 0.001 for each). These same relations were investigated in five patients with the Wolff-Parkinson-White syndrome and AV reciprocating tachycardia and five patients with AV nodal reciprocating tachycardia (group 2).(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effects of intravenous diltiazem in patients with recurrent supraventricular tachycardias

The electrophysiologic effects of intravenous diltiazem were evaluated in 10 patients with recurrent supraventricular tachycardias. The tachycardia incorporated an accessory pathway in 7 patients and was due to AV nodal reentry in 3 patients. Diltiazem 0.25 mg/kg was administered intravenously over 5 minutes during sustained supraventricular tachycardia. Programmed electrical stimulation was used to restore sinus rhythm if diltiazem failed to terminate the arrhythmia within 10 minutes. Conduction intervals, refractory periods and tachycardia characteristics were evaluated before and immediately after drug administration. Diltiazem did not significantly modify sinus cycle length, AH and HV intervals. Atrial and ventricular effective refractory periods were similar before and after diltiazem. The effective refractory period of the AV node was prolonged by 42 msec after diltiazem (p less than 0.05). Diltiazem increased the tachycardia cycle length from 320 +/- 41 to 353 +/- 36 msec (p less than 0.01) but terminated the arrhythmia in only 2 patients. After diltiazem, supraventricular tachycardia could not be reinitiated in only 2 patients and the tachycardia initiating window was not significantly reduced (56 +/- 26 to 41 +/- 33 msec). The infusion of diltiazem was accomplished without side effects. Thus, 0.25 mg/kg of intravenous diltiazem produces a modest depression of AV nodal function and is not very effective in terminating supraventricular tachycardia or preventing its initiation in this study population. Further studies using higher doses of intravenous diltiazem would be useful to determine its maximal therapeutic benefit in patients with recurrent supraventricular tachycardias.     

Efficacy of propafenone in Wolff-Parkinson-White syndrome: electrophysiologic findings and long-term follow-up

The efficacy and safety of intravenous propafenone was studied in 10 patients with Wolff-Parkinson-White syndrome and in 2 patients with a concealed accessory pathway. During electrophysiologic study, the effect of propafenone on the effective refractory period of the accessory pathway was determined, as well as its effect during orthodromic atrioventricular (AV) reentrant tachycardia and atrial fibrillation. Propafenone caused significant increases in the accessory pathway refractory period, both in the anterograde direction (290 +/- 19 versus 474 +/- 50 ms, p less than 0.05) and in the retrograde direction (238 +/- 15 versus 408 +/- 44 ms, p less than 0.05). Complete anterograde accessory pathway conduction block occurred in four patients. Sustained AV reentrant tachycardia was inducible in 11 patients before administration of propafenone. Drug infusion during AV reentrant tachycardia promptly terminated arrhythmia in 10 of these 11 patients and caused slowing of AV reentrant tachycardia in the remaining patient. Before propafenone, sustained atrial fibrillation was inducible in six patients and nonsustained atrial fibrillation in four patients. After propafenone, no patient had inducible sustained atrial fibrillation. Furthermore, propafenone caused a marked decrease in peak ventricular rate during atrial fibrillation. Eight patients have been treated with oral propafenone and followed up for 12 +/- 2 months. All have remained virtually free of recurrent arrhythmia and none has developed significant side effects. Propafenone is a very promising agent for emergency intravenous therapy as well as long-term oral therapy in patients with Wolff-Parkinson-White syndrome.     

Ultrarapid subthreshold stimulation for termination of atrioventricular node reentrant tachycardia.

OBJECTIVES. We investigated the efficacy and safety of ultrarapid subthreshold electrical stimuli in terminating sustained atrioventricular (AV) node reentrant tachycardia. BACKGROUND. Subthreshold stimuli, singly and in trains, have been reported to prolong the effective refractory period, inhibit the response to subsequent suprathreshold extrastimuli and to terminate ventricular tachycardia and reciprocating tachycardia. METHODS. Seventeen consecutive patients with inducible sustained slow-fast AV node reentrant tachycardia (mean tachycardia cycle length 358 +/- 61 ms) were studied. Trains of subthreshold stimuli were tested at various right atrial sites. RESULTS. Trains of subthreshold stimuli reproducibly terminated AV node reentrant tachycardia in 15 patients without administration of adjunctive pharmacologic agents. Effective subthreshold current strength ranged from 0.5 to 1.5 mA (mean 0.9 +/- 0.3). The cycle length of effective subthreshold stimuli trains ranged from 30 to 80 ms (mean 57 +/- 17), and the number of stimuli in the train ranged from 4 to 16 (mean 8 +/- 4). The site of successful termination was the proximal coronary sinus in 6 patients and the right low atrial septum in 12. During successful subthreshold termination, no atrial capture could be detected. Neither atrial fibrillation nor flutter nor tachycardia acceleration occurred. CONCLUSIONS. Low current, high frequency trains of stimuli, when applied at a site presumed to be close to the reentrant circuit, provided a safe and effective method of terminating the common type of AV node reentrant tachycardia. This technique could be used to identify critical parts of the reentrant circuit suitable for ablation and further investigations with this method are warranted.     

Subthreshold atrial pacing in patients with a left-sided accessory pathway: an effective new method for terminating reciprocating tachycardia

This study investigated the possibility of terminating reciprocating atrioventricular (AV) tachycardia using subthreshold atrial pacing. Ten patients with a left-sided accessory pathway and sustained AV tachycardia underwent subthreshold atrial pacing from the coronary sinus site closest to insertion of the accessory pathway. In seven of these patients, the tachycardia could be reliably terminated with subthreshold atrial overdrive pacing. When pacing at a cycle length of 80 +/- 23% of the tachycardia cycle length, the minimal subthreshold current that was effective in tachycardia termination was 64 +/- 14% of threshold current and the maximal ineffective current was 49 +/- 17% of threshold (p less than 0.05). In all cases, the tachycardia was terminated by one or two instances of atrial capture that resulted in a premature atrial impulse (20 +/- 4% advancement of the atrial cycle) that blocked the AV node limb of the tachycardia. Anterograde conduction over the accessory pathway never occurred, either during the tachycardia or during subthreshold pacing after a return to normal sinus rhythm. No instances of atrial fibrillation were provoked by subthreshold pacing. Possible explanations for the intermittent atrial capture with critically placed subthreshold impulses include supernormal atrial conduction or summation of impulses at the atrial insertion site of the accessory pathway. It is concluded that subthreshold pacing is effective in selected patients with AV tachycardia due to an accessory pathway. Furthermore, because neither atrial fibrillation nor anterograde conduction over the accessory pathway is seen with subthreshold pacing, this modality may hold significant promise for permanent antitachycardia pacing in these patients.     

Antidromic tachycardia utilizing decremental,latent accessory atrioventricular fibers: Differentiation from adenosine-sensitive ventricular tachycardia

Objectives. We studied two patients with latent, decremental atrioventricular (AV) fibers in whom pre-excitation could be demonstrated only during wide complex tachycardia.Background. The presence of decremental AV fibers participating in antidromic AV reentrant tachycardia is usually suspected by the presence of pre-excitation either in sinus rhythm or during atrial pacing.Methods. Two patients were referred for evaluation and treatment of wide complex tachycardia whose configuration suggested ventricular tachycardia that could be terminated with adenosine infusion. They underwent standard electrophysiologic studies.Results. Baseline AH and HV intervals were normal. No pre-excitation was noted with atrial overdrive at multiple sites or during atrial extrastimulation. Retrograde conduction was present with a sequence compatible with AV node conduction. Sustained wide complex tachycardia was induced with ventricular overdrive pacing. Late atrial premature depolarizations during tachycardia pre-excited the subsequent ventricular activation. Earlier atrial premature depolarizations delayed the subsequent ventricular activation. In one patient, early atrial premature depolarizations terminated the tachycardia without activating the ventricle. In the other patient, spontaneous tachycardia termination was accompanied by ventriculoatrial block. The earliest ventricular activation was at the annulus in the posteroseptal region in one patient and at the left posterior region in the other. Atrioventricular node reentry and atrial tachycardia with by-stander AV fibers were also excluded. These findings establish the diagnosis of antidromic AV reentrant tachycardia utilizing a slow, decrementally conducting AV pathway.Conclusions. This is the first report describing the presence of latent, decremental accessory AV pathways in which conduction was manifest only during antidromic AV reentrant tachycardia. To differentiate these wide complex tachycardias from adenosine-sensitive ventricular tachycardia, we recommend that atrial premature depolarizations be applied during tachycardia to rule out the presence of a latent, decremental AV fiber even in patients who do not otherwise have pre-excitation with atrial pacing techniques.     

Slowing of the Ventricular Rate During Atrial Fibrillation by Ablation of the Slow Pathway of AV Nodal Reentrant Tachycardia

Influence of Slow Pathway Ablation on Atrial Fibrillation. Introduction : The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well-defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.
Methods and Results : In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P < 0.01), 673 ± 161 (P < 0.01), and 535 ± 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P < 0.05) immediately and to 400 ± 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P < 0.05), respectively.
Conclusion : This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node.     

Determinants of QRS alternans during narrow QRS tachycardia

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.     

The Response of Paroxysmal Supraventricular Tachycardia to Overdrive Atrial and Ventricular Pacing:

Pacing During Supraventricular Tachycardia. Introduction: Standard electrophysiologic techniques generally allow discrimination among mechanisms of paroxysmal Supraventricular tachycardia. The purpose of this study was to determine whether the response of paroxysmal Supraventricular tachycardia to atrial and ventricular overdrive pacing can help determine the tachycardia mechanism. Methods and Results: Fifty-three patients with paroxysmal Supraventricular tachycardia were studied. Twenty-two patients had the typical form of atrioventricular (AV) junctional (nodal) reentry, 18 patients had orthodromic AV reentrant tachycardia, 10 patients had atrial tachycardia, and 3 patients had the atypical form of AV nodal reentrant tachycardia. After paroxysmal Supraventricular tachycardia was induced, 15-beat trains were introduced in the high right atrium and right ventricular apex sequentially with cycle lengths beginning 10 msec shorter than the spontaneous tachycardia cycle length. The pacing cycle length was shortened in successive trains until a cycle of 200 msec was reached or until tachycardia was terminated. Several responses of paroxysmal Supraventricular tachycardia to overdrive pacing were useful in distinguishing atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia. During decremental atrial overdrive pacing, the curve relating the pacing cycle length to the VA interval on the first beat following the cessation of atrial pacing was flat or upsloping in patients with AV junctional reentry or AV reentrant tachycardia, but variable in patients with atrial tachycardia. AV reentry and AV junctional reentry could always be terminated by overdrive ventricular pacing whereas atrial tachycardia was terminated in only one of ten patients (P < 0.001). The curve relting the ventricular pacing cycle length to the VA interval on the first postpacing beat was flat or upsloping in patients with AV junctional reentry and AV reentry, but variable in patients with atrial tachycardia. The typical form of AV junctional reentry could occasionally be distinguished from other forms of paroxysmal Supraventricular tachycardia by the shortening of the AH interval following tachycardia termination during constant rate atrial pacing. Conclusions: Atrial and ventricular overdrive pacing can rapidly and reliably distinguish atrial tachycardia from other mechanisms of paroxysmal Supraventricular tachycardia and occasionally assist in the diagnosis of other tachycardia mechanisms. In particular, the ability to exclude atrial tachycardia as a potential mechanism for paroxysmal Supraventricular tachycardia has important implications for the use of catheter ablation techniques to cure paroxysmal Supraventricular tachycardia.     

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QT_c interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.     

Effects of resting vagal tone on accessory atrioventricular connections

The purpose of this study was to determine the effects of resting vagal tone on accessory atrioventricular (AV) connections. Atropine (0.04 mg/kg) was administered to 13 patients with the Wolff-Parkinson-White syndrome and was found to have the following effects on the accessory AV connection: the anterograde block cycle length shortened from 305 +/- 51 to 279 +/- 54 msec (mean +/- SD; p less than 0.001); the retrograde block cycle length shortened from 288 +/- 57 to 251 +/- 50 msec (p less than 0.001); and the effective refractory period measured at a basic drive cycle length of 400 msec shortened from 295 +/- 45 to 265 +/- 47 msec in the anterograde direction (p less than 0.001) and from 283 +/- 18 to 261 +/- 12 msec in the retrograde direction (p less than 0.01). During atrial fibrillation, the mean ventricular cycle length decreased from 434 +/- 88 to 352 +/- 56 msec (p less than 0.001), and the shortest preexcited RR interval decreased from 302 +/- 56 to 256 +/- 43 msec (p less than 0.01). In another seven patients, propranolol (0.2 mg/kg) was administered before atropine, and atropine lengthened the anterograde block cycle length and the effective refractory period of the accessory AV connection; the magnitude of these effects was similar to that in the patients who did not receive propranolol. In conclusion, these data demonstrate that resting vagal tone exerts a direct depressant effect on accessory AV connections that does not require background sympathetic activity to be manifest.     

New observations on atrial fibrillation before and after surgical treatment in patients with the Wolff-Parkinson-White syndrome.

The records of 342 patients who received surgical treatment for the Wolff-Parkinson-White syndrome between 1968 and 1986 were reviewed to evaluate the characteristics of atrial fibrillation. The patients were classified into two groups according to the presence (n = 166) or absence (n = 176) of documented episodes of atrial fibrillation preoperatively. The mean follow-up duration was 6 years (range 2 to 20). As compared with reports based on smaller patient groups and shorter follow-up, the study revealed several new findings. 1) During follow-up, nine patients in the atrial fibrillation group developed recurrent atrial fibrillation after a successful operation; five of these nine patients did not have associated heart disease. 2) All three patients with a history of atrial fibrillation and an accessory pathway conducting in the anterograde direction only had a successful surgical procedure and no postoperative atrial fibrillation. 3) The cycle length of atrioventricular (AV) reciprocating tachycardia was significantly shorter in the atrial fibrillation group (304 +/- 42 ms, mean +/- SD) than in the no-atrial fibrillation group (321 +/- 54 ms, p less than 0.005), and the cycle length of AV reciprocating tachycardia that degenerated into atrial fibrillation (289 +/- 26 ms) was shorter than that for the AV reciprocating tachycardia without subsequent atrial fibrillation (316 +/- 51 ms, p less than 0.005). 4) Sustained atrial fibrillation was induced in 30% of patients without a history of atrial fibrillation. 5) Atrial fibrillation occurred in four patients with an accessory pathway that conducted only in the retrograde direction.(ABSTRACT TRUNCATED AT 250 WORDS)