Acute and chronic effects of verapamil in patients with paroxysmal supraventricular tachycardia

Efficacy of acute intravenous verapamil, 10 mg, and chronic oral verapamil, 320 mg, daily were studied electrophysiologically in 15 patients with paroxysmal supraventricular tachycardia (PSVT). Plasma verapamil concentrations were measured concurrently. Both intravenous and oral verapamil significantly increased the AV node conduction time, the cycle length producing a Wenckebach period, and the refractory period of the AV node. These changes were reflected in changes in plasma verapamil concentration. The echo zone and the supraventricular tachycardia (SVT) zone markedly narrowed after administration of both intravenous and chronic oral verapamil. Verapamil's efficacy was found to be related to the type of SVT. For instance, verapamil was more effective in SVT due to AV nodal re-entry than in SVT due to concealed accessory pathway. Fourteen patients were followed from 3 to 31 months and all except one were well controlled. In conclusion, verapamil was effective in prophylaxis of paroxysmal SVT.     

Effect of intravenous propranolol or verapamil on infant orthodromic reciprocating tachycardia

The effects of intravenous verapamil (0.15 mg/kg) and propranolol (0.2 mg/kg) with regard to atrioventricular (AV) conduction and tachycardia termination during paroxysmal atrial tachycardia were compared in 2 groups of infants (verapamil n = 14, propranolol n = 18, mean age 80 +/- 21 days, range 1 to 364). Using transesophageal recording techniques, tachycardia cycle length, AV intervals and ventriculoatrial intervals were measured before and after drug administration. Both intravenous propranolol and verapamil significantly prolonged tachycardia cycle length and AV interval (cycle length--propranolol 230 +/- 30 to 262 +/- 33 ms, p less than 0.05, verapamil 223 +/- 38 to 245 +/- 32 ms, p less than 0.05; AV interval--propranolol 98 +/- 26 to 126 +/- 38 ms, p less than 0.05, verapamil 96 +/- 19 to 109 +/- 24 ms, p less than 0.05). Neither drug prolonged the ventriculoatrial interval. Tachycardia terminated after intravenous verapamil in 11 of 14 infants (79% efficacy rate). Tachycardia terminated in 0 of 18 after intravenous propranolol (0% efficacy rate). In 8 infants an atrial deflection was recorded on the esophageal electrocardiogram at the time of tachycardia termination after intravenous verapamil, which suggested that tachycardia terminated by block occurring in the AV node. In 2 infants a ventricular deflection was recorded at the time of tachycardia termination after verapamil, which suggested that block occurred in the accessory connection. Both drugs prolonged tachycardia cycle length by prolonging AV conduction to a similar degree.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparative effects of adenosine triphosphate on accessory pathway and atrioventricular nodal conduction

Adenosine triphosphate (ATP) has potent negative dromotropic effects on the atrioventricular (AV) node, but variable effects on accessory pathway conduction have been described. The effects of an intravenous bolus injection of 8 mg ATP on accessory pathway and AV nodal conduction were determined during electrophysiologic testing with controlled atrial and ventricular rates. AV conduction was monitored during atrial or ventricular pacing at a constant cycle length, 30 msec longer than the cycle length at which block occurred. During atrial pacing antegrade block after administration of ATP occurred in 1 of 30 (3.2%) patients with accessory pathway conduction and 12 of 13 (92%) patients with AV nodal conduction (p less than 0.001). During ventricular pacing only 5 of 26 (16%) patients had accessory pathways blocked, whereas 25 of 35 (71%) patients with AV nodal conduction had block (p less than 0.001). Thus, failure of ATP to produce ventriculoatrial block identified the presence of an accessory pathway with a sensitivity of 84%, specificity of 71%, and predictive value of 72%. There was no correlation between accessory pathway properties and the effects of ATP. The effects of ATP on the AV node were concordant with the effects of a combination of verapamil and propranolol in 21 of 23 patients, suggesting that this dose ATP is an equipotent AV nodal blocker with a short duration of action. Thus, although the effects of ATP on accessory pathways and the AV node differ, block in ventriculoatrial conduction after administration of ATP cannot be used as the sole criterion to distinguish the mechanism of conduction.     

Effect of digitalis in patients with paroxysmal atrioventricular nodal tachycardia.

Atrioventricular (A-V) conduction, ventriculo-atrial conduction and mechanism of tachycardia were studied by programmed electrical stimulation before and after the administration of ouabain in 15 patients suffering from paroxysmal supraventricular re-entrant tachycardia. In 13 patients the tachycardia circuit was confined to the A-V node. In two patients the stimulation study showed that an accessory pathway was used in a ventriculo-atrial direction during tachycardia. Ouabain lengthened the effective and functional refractory period of the A-V node and A-V nodal transmission time in all patients in whom this could be studied. Only six patients showed lengthening in ventriculo-atrial conduction time or refractory period of the ventriculo-atrial conduction system. In seven patients no tachycardia could be initiated after ouabain. The width of the zone of atrial premature beats able to initiate tachycardia (the tachycardia zone) narrowed in five patients, showed no change in two patients, and increased in one patient. In these eight patients the tachycardia zone shifted to longer premature beat intervals. Ouabain resulted in slowing of cardiac rate during tachycardia. Both patients who used an accessory pathway during tachycardia showed no change in width of their tachycardia zone following ouabain administration. Seven patients were restudied two weeks after chronic oral administration of digoxin. The results were similar to those obtained following ouabain administration. This indicates that in patients suffering from paroxysmal A-V nodal tachycardia the effect of chronic oral digoxin administration can be predicted from the study of the effect of ouabain during programmed stimulation of the heart.     

Verapamil effects in AV node reentry tachycardia with intermittent supra-Hisian AV block

The electrophysiologic details of two patients with atrioventricular (AV) node reentry tachycardia with intermittent 2:1 supra-Hisian block are presented. Both patients had clear evidence for atrial arrhythmias as well, emphasizing the need for a careful diagnostic analysis. Evidence supporting a diagnosis of AV node reentry tachycardia included: (1) short ventriculoatrial (VA) coupling intervals, (2) normal retrograde sequence of atrial activation, (3) dependence on critical AV node conduction times for initiation of tachycardia by atrial pacing, (4) ability to pace and capture the atria or ventricles without interrupting the tachycardia, and (5) fixed VA coupling intervals despite changes in tachycardia cycle length. Ten milligrams of verapamil was administered during sustained supraventricular tachycardia with 1:1 AV conduction, but despite prompt termination of tachycardia in both cases, 2:1 AV block was not induced. Atrial echoes could still be induced after verapamil, and diagnostic features (3) and (5) were particularly evident after the drug. Further analysis confirmed that verapamil did not have any observable effects on the likely site for supra-Hisian block—that is, the “final common pathway” of the AV node. This would support a contention that verapamil may have a selective effect on tissues within the confines of the AV node.     

Atrioventricular node reentry: Intravenous verapamil as a method of defining multiple electrophysiologic types

Fourteen patients with recurrent supraventricular tachycardia (SVT) underwent electrophysiological evaluation. Each patient was shown to have reentry confined to the region of the atrioventricular (AV) node. Verapamil, 0.075 to 0.15 mg/kg was administered intravenously to each patient during a stable episode of SVT, resulting in termination in each instance. There was more than one mechanism for termination of SVT. Nine patients showed termination by anterograde AV node block preceded by an increase in conduction time in the anterograde limb of the tachycardia circuit (Ae-H intervals) with no change in the conduction time in the retrograde limb (H-Ae intervals). Three patients showed termination by block in the retrograde limb of the circuit preceded by increases in both Ae-H and H-Ae intervals. An additional example of termination by spontaneous ventricular premature complexes and usurpation by sinus rhythm were also seen. Common features were that verapamil had significant effects on anterograde and retrograde conduction and refractoriness in the AV node. It prolonged the refractory periods of both fast and slow pathways in patients with dual anterograde AV node pathways, and observable effects on retrograde conduction and refractoriness were seen even in patients with constant ventriculoatrial conduction times during incremental ventricular pacing in a control study. However, three distinct groups of patients were identified on the basis of their response to ventricular pacing in a control study and upon verapamil effects recorded during their SVT. An explanation for these latter findings may be that there is a normal variation in the retrograde response of parts of the AV node to ventricular pacing, and a variability in some of the patients' responses to verapamil.     

Double-blind study of intravenous propafenone for paroxysmal supraventricular reentrant tachycardia

Propafenone was administered during electrophysiologic testing to determine its efficacy and safety for terminating and preventing reinduction of paroxysmal supraventricular reentrant tachycardia. Four men and 10 women (mean age 50 years, range 28 to 69) were studied. Five patients had Wolff-Parkinson-White syndrome with orthodromic atrioventricular (AV) reentrant tachycardia, three had a concealed accessory pathway with AV reentrant tachycardia and six had tachycardia due to reentry within the AV node. In the five patients with Wolff-Parkinson-White syndrome, propafenone terminated reentrant tachycardia in three (the tachycardia was reinducible in one) and had no effect in two. In the three patients with a concealed accessory pathway, propafenone terminated reentrant tachycardia in all three and prevented reinduction of the tachycardia in two. In the six patients with tachycardia due to reentry within the AV node, propafenone terminated and prevented reinduction of reentrant tachycardia. Propafenone had no effect on blood pressure, heart rate, PA interval, AV node refractoriness or rate of reentrant tachycardia. Propafenone significantly (p less than 0.05) prolonged the AH, HV, QRS and ventriculoatrial intervals and decreased the AV node Wenckebach rate. Of the nine patients receiving long-term oral propafenone therapy, eight had a reduction of at least 90% in reentrant tachycardia during a mean follow-up period of 14.5 months (range 11 to 22); all eight patients had had noninducible reentrant tachycardia after intravenous propafenone. One patient had increased frequency of reentrant tachycardia; this patient had had inducible reentrant tachycardia after intravenous propafenone. In conclusion, intravenously administered propafenone terminated reentrant tachycardia in 85% of patients and prevented reinduction in 71%, with no adverse hemodynamic effects.     

Electrophysiologic and antiarrhythmic actions of bepridil : Comparison with verapamil and ajmaline for atrioventricular reentrant tachycardia

Bepridil (2 mg/kg intravenously) was given to 20 patients with atrioventricular (AV) reentrant tachycardia and its effects were compared with those of verapamil (0.15 mg/kg intravenously) in 8 patients and ajmaline (0.75 mg/kg intravenously) in 12. After baseline electrophysiologic measurements, the drugs were given during sustained AV reentrant tachycardia (8 patients had dual AV nodal pathways and 12 had an accessory AV pathway). Verapamil terminated AV reentrant tachycardia in 7 patients and bepridil terminated it in 6. In 8 of the patients who received ajmaline, AV reentrant tachycardia was terminated and in 6 of this group bepridil did so. Bepridil was more successful in terminating AV reentrant tachycardia in those with dual AV nodal pathways than in those with an accessory AV pathway. Bepridil slowed sinus rate by 10% (p <0.0001), whereas verapamil did not change it significantly. Both verapamil and bepridil administration prolonged AV nodal conduction (39% and 44%, respectively), lengthened AV nodal effective refractory period (18% and 17% respectively) and increased the Wenckebach cycle length of the AV node (24% and 25%, respectively) to a significant degree (p <0.05). Bepridil also lengthened atrial and ventricular effective refractory periods (p <0.01) and QT interval (p <0.0001) in the group as a whole; in those receiving ajmaline and bepridil only atrial refractoriness was significantly altered (p <0.05). After treatment for 3 to 5 days with oral bepridil, 19 patients underwent repeat study. There was further slowing in sinus rate and prolongation in both atrial effective refractory period and QT interval; the AV Wenckebach cycle length had returned toward the control level, but was still significantly increased (p <0.01). In the 17 cases in whom reinducibility of AV reentry tachycardla was tested, 7 had no inducible arrhythmia, 6 had non-sustained AV reentrant tachycardia and 4 had sustained but slower tachycardia. Thus, bepridil has both AV nodal and myocardial electrophysiologic actions which suggest a useful role in the treatment and prophylaxis of supraventricular arrhythmias.     

Electrophysiological effects of L 9394 (benzoyl-indolizine) in man.

The electrophysiological effects of L 9394 (benzoyl-indolizine), a substance chemically related to amiodarone, but devoid of iodine atoms, were investigated by programmed electrical stimulation of the heart in 12 patients with various forms of tachycardia. Four subjects had electrocardiographic evidence of the WPW syndrome and episodes of circus movement tachycardia. Paroxysmal supraventricular tachycardia, confined to the atrioventricular (AV) node, was found in 3 patients. In 2 cases, where a short PR interval was present, the main complaint was the occurrence of paroxysmal atrial fibrillation. In the remaining 3 instances, the arrhythmia consisted of slow ventricular tachycardia (1 case), supraventricular tachycardia of the focal type (1 case), and episodes of primary ventricular fibrillation, not related to acute myocardial ischaemia (1 case). L 9394 injected intravenously was seen to lengthen the transnodal conduction time as well as the effective and functional refractory periods of the node. Similar effects were found on the retrograde VA pathway. The drug had no action on the infra-Hisian conduction system, on the refractory periods of ventricular muscle, or on the refractory periods of accessory bypasses. The drug was injected during an episode of tachycardia in 6 cases with reproducible supraventricular re-entrant tachycardia. Three had a tachycardia circuit confined to the node. In those instances, the drug had beneficial effects (slowing and interruption of tachycardia, decrease or abolition of echo zone; loss of ability to induce tachycardia). In the other 3 cases, an accessory pathway was incorporated in the circuit. L 9394 interrupted the tachycardia in 2 instances (by anterograde AV block), but failed to protect all 3 patients against reinitiation of tachycardia by premature stimuli. It is concluded that L9394 does not share all the pharmacological properties of amiodarone and will not replace it in all its indications.     

Electrophysiological effects of L 9394 (benzoyl-indolizine) in man.

The electrophysiological effects of L 9394 (benzoyl-indolizine), a substance chemically related to amiodarone, but devoid of iodine atoms, were investigated by programmed electrical stimulation of the heart in 12 patients with various forms of tachycardia. Four subjects had electrocardiographic evidence of the WPW syndrome and episodes of circus movement tachycardia. Paroxysmal supraventricular tachycardia, confined to the atrioventricular (AV) node, was found in 3 patients. In 2 cases, where a short PR interval was present, the main complaint was the occurrence of paroxysmal atrial fibrillation. In the remaining 3 instances, the arrhythmia consisted of slow ventricular tachycardia (1 case), supraventricular tachycardia of the focal type (1 case), and episodes of primary ventricular fibrillation, not related to acute myocardial ischaemia (1 case). L 9394 injected intravenously was seen to lengthen the transnodal conduction time as well as the effective and functional refractory periods of the node. Similar effects were found on the retrograde VA pathway. The drug had no action on the infra-Hisian conduction system, on the refractory periods of ventricular muscle, or on the refractory periods of accessory bypasses. The drug was injected during an episode of tachycardia in 6 cases with reproducible supraventricular re-entrant tachycardia. Three had a tachycardia circuit confined to the node. In those instances, the drug had beneficial effects (slowing and interruption of tachycardia, decrease or abolition of echo zone; loss of ability to induce tachycardia). In the other 3 cases, an accessory pathway was incorporated in the circuit. L 9394 interrupted the tachycardia in 2 instances (by anterograde AV block), but failed to protect all 3 patients against reinitiation of tachycardia by premature stimuli. It is concluded that L9394 does not share all the pharmacological properties of amiodarone and will not replace it in all its indications.     

Effects of verapamil on supraventricular tachycardia in patients with overt and concealed Wolff-Parkinson-White syndrome

Verapamil (0.15 mg/kg) intravenously, was administered to 19 patients with recurrent supraventricular tachycardia (SVT) undergoing electrophysiological evaluation. Twelve patients had overt Wolff-Parkinson-White (WPW) syndrome and seven patients had concealed accessory pathways conducting in the retrograde direction only. Verapamil had a significant effect in delaying conduction and prolonging refractoriness in the atrioventricular (AV) node, but no significant actions on any of the other cardiac tissues that formed the tachycardia circuit in these patients. In particular, it had no significant effects on anterograde or retrograde bypass conduction or refractoriness. Sustained SVT was initiated in 15 patients, and was terminated within 60 to 105 seconds of a 30-second injection of verapamil in 13 patients. Cycle length alternation during SVT was seen in six patients prior to reversion, and spontaneous ventricular complexes (VPCs) were observed following verapamil administration in five patients. Two patients with apparently normal sinus node function showed prolongation of their sinus node recovery times immediately following reversion of SVT by verapamil. Echo zones were assessed before and after verapamil, and sustained or self-terminating SVT could still be induced after the drug in 13 of the 15 patients who had sustained SVT beforehand. It was concluded that intravenous verapamil was effective in terminating sustained SVT in the majority of patients with overt or concealed WPW and that, despite a potential for sinus node depression and the initiation of VPCs, it had no clinically significant side effects. The ability to reinitiate SVT following its administration suggests the need for immediate follow-up with maintenance drug therapy.     

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.     

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.     

导管消融具有双向传导特性的Mahaim结室纤维

目的介绍具有双向传导特性Mahaim结室纤维的电生理机制及导管消融方法。方法患者女性,34岁,反复发作性心动过速病史7年。外院心电图示“阵发性室上性心动过速”。心动过速可被维拉帕米及普罗帕酮终止。入院各项检查排除器质性心脏病后行电生理检查及导管消融术。结果电牛理检查示窦性心律时AH=73ms、HV=42ms,QRS时限100ms。心动过速时QRS波形态与窦性心律时相似,伴有轻度电交替。心动过速在多数情况下室房呈分离状态,HV问期为42ms,与窦性节律时相同,有时室房呈1：1传导,最早心房激动位于希氏束记录处。右心室心尖部以400ms周长刺激时室房呈分离状态。心房增频刺激时QRS波逐渐增宽,直至充分预激。在QRS波增宽过程中,HV逐渐缩短直至H波融合于QRS波之中,刺激信号至QRS波的间期逐渐延长,反映了递减传导的过程。继续缩短心房刺激周长后突然旁路传导受阻,经房室结下传并出现传导跳跃现象,继传导跳跃后心动过速被诱发。心动过速可被三磷酸腺苷（ATP）终止,终止后房室经旁路前传,其QRS波形态与充分预激时相似。在心房刺激保持充分预激的前提下,沿三尖瓣环标测,于左前斜位45。三尖瓣环4点钟处标测到最早V波,此处较体表心电图QRS波提前25ms,单极记录呈Qs型,HA波与V波之间未见高频电位。于该点消融放电（60W×60℃）,2S后旁路传导消失。放电过程中未出现交界性心律。消融结束后心房程序电刺激仍有房室传导跳跃现象。随访18个月,未再有心动过速发作。结论本病例心动过速系Mahaim结室纤维所介导,该纤维具有双向传导功能,其上插入端位于房室结慢径区域,下插入端位于邻近房室沟的局部心室肌。心动过速时房室结-希氏-浦肯野系统为前传支,结室纤维作为逆传支。     

Treatment of paroxysmal reentrant supraventricular tachycardia with flecainide acetate

The electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were studied in 15 patients with spontaneous and inducible sustained paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous flecainide (2 mg/kg body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral flecainide administration (200 to 400 mg/day). After intravenous or oral flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after flecainide therapy, the cycle length of tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of flecainide on the mechanism of the SVT. Twelve patients continued oral flecainide treatment for a mean of 16 months (range 5 to 28). Tachycardia recurred in 3 of 4 patients whose arrhythmia remained inducible after flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

Usefulness of combined propranolol and verapamil for evaluation of surgical ablation of accessory atrioventricular connections in patients without structural heart disease

Successful surgical ablation of atrioventricular (AV) accessory connections may be confirmed during postoperative electrophysiologic testing by the absence of accessory connection conduction in both the anterograde and retrograde directions. Whereas the former may be readily apparent by examination of the surface electrocardiogram during sinus rhythm or atrial pacing, assessment of the latter may be complicated by the frequent presence of enhanced retrograde AV nodal conduction in the postoperative period. Consequently, availability of interventions that selectively affect AV nodal conduction and refractoriness without concomitant effects on accessory connections may be helpful for assessing the success of the surgical procedure. In this study the effects of combined propranolol and verapamil administration on electrophysiologic properties of the AV node and the accessory AV connection were assessed both pre- and postoperatively in 17 patients (12 men and 5 women, mean age 33 years) undergoing surgical ablation of accessory connections. Preoperatively, electrophysiologic characteristics of all but 1 of the accessory AV connections were unaffected by propranolol and verapamil administration. Postoperatively, on the other hand, propranolol and verapamil significantly prolonged both the retrograde AV node effective refractory period (baseline: 272 +/- 34 ms vs after drugs: 384 +/- 70 ms [p less than 0.0001]) and the shortest cycle length maintaining 1:1 ventriculoatrial conduction (baseline: 357 +/- 99 ms vs after drugs: 485 +/- 64 ms [p less than 0.0001]). Late postoperative electrophysiologic evaluation (7 +/- 3 weeks) revealed no evidence of residual accessory AV connection conduction, and all patients remain asymptomatic at 21 +/- 10 months follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H2A2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated in 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 +/- 27 vs 352 +/- 40 ms, p less than 0.01), but prolonged H2A2 interval in only 5 of 11 patients (37 +/- 6 vs 60 +/- 31 ms, p less than 0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H2A2 interval was prolonged. Correlation between the paced cycle length which induced VA block, the shortest V1H2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H2A2 or H-Ae interval, the shortest V1H2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block.(ABSTRACT TRUNCATED AT 250 WORDS)     

Combined verapamil and propranolol for supraventricular tachycardia

The electrophysiologic effects of intravenous verapamil and propranolol were compared alone and in combination in 14 patients (aged 21 to 69 years) with paroxysmal Supraventricular tachycardia (SVT). Ten patients had atrioventricular (AV) reentry utilizing a manifest (7 patients) or concealed (3 patients) accessory pathway. Four patients had AV nodal reentry. Electrophysiology studies were performed using standard techniques in the control state and after verapamil (0.15 mg/kg intravenous bolus and 0.005 mg/kg/min). The next day, studies were repeated after propranolol (0.1 mg/kg) and a combination of verapamil and propranolol. No adverse effects occurred with the drug combination. Each drug intervention prolonged anterograde functional refractory period of the AV node (control, 370 ± 50 ms; verapamil, 446 ± 90 ms; propranolol, 436 ± 92, p < 0.05), with the greatest increase occurring after the drug combination (502 ± 103 ms, p < 0.001). In 2 patients prolonged sinus node recovery time developed after the drug combination. Verapamil or propranolol prevented SVT induction in 7 patients (50%). However, only the drug combination prevented reinduction of sustained SVT in 6 patients. These 6 patients were treated chronically with verapamil and propranolol, with no recurrence of SVT in any patient after 2 to 26 months.     

Limitation of tachycardia zone resulting from longitudinal dissociation of the atrioventricular node in concealed pre-excitation.

Two cases with a concealed left-sided accessory atrioventricular bypass tract are described. In both, functional longitudinal dissociation of the atrioventricular node narrowed the range of atrial premature beat coupling intervals which could initiate re-entry using the accessory pathway. In case 1 early premature atrial beats were followed by an atrioventricular nodal re-entrant echo. The atrial echo pre-empted retrograde conduction over the Kent bundle and thus limited the development of paroxysmal supraventricular tachycardia. In case 2 atrioventricular nodal conduction showed typical features ascribed to dual atrioventricular nodal pathways. In addition there was a bradycardia-related retrograde block in the concealed accessory pathway. Early premature atrial beats, because of exclusive "slow pathway" anterograde conduction, arrived at the ventricles during the period of bradycardia-dependent retrograde block and failed to initiate a macro re-entrant tachycardia. This study shows that (1) longitudinal dissociation within the atrioventricular node may limit the ability to initiate tachycardia in patients with concealed pre-excitation; and (2) discontinuous atrioventricular nodal conduction curves occasionally help to reveal bradycardia-related retrograde block in a concealed accessory pathway.