Orthodromic Atrioventricular Reentrant Tachycardia Research Articles

Nonreentrant atrioventricular nodal tachycardia due to triple nodal pathways manifested by radiofrequency ablation at coronary sinus ostium

We report a case of complex supraventricular tachycardia manifested by radiofrequency delivery. Initially, the patient presented with orthodromic atrioventricular reentrant tachycardia via a left-sided accessory pathway that was successfully eliminated. Atrial tachycardia originating from coronary sinus ostium was also induced. Radiofrequency delivery at the coronary sinus ostium induced a narrow QRS tachycardia with irregular R-R intervals. A detailed analysis explained that the tachycardia could be a nonreentrant mechanism due to triple atrioventricular nodal pathways: an atrial excitation evokes double ventricular response due to simultaneous activation of the fast and slow pathways, and the next one activates ventricle through the intermediate pathway.

Congenital and surgically acquired Wolff-Parkinson-White syndrome in patients with tricuspid atresia

There are reports associating an increased incidence of Wolff-Parkinson-White syndrome with tricuspid atresia. Here we report on electrophysiologic studies in patients with tricuspid atresia and Wolff-Parkinson-White syndrome after the Fontan operation. In these patients the atrial arrhythmia often seen in patients undergoing the Fontan operation triggered atrioventricular re-entrant tachycardia or caused life-threatening arrhythmias. Five patients with tricuspid atresia after palliation with a modified Fontan operation (atrioinfundibular connections) and Wolff-Parkinson-White syndrome are presented. Four of these patients had symptomatic paroxysmal orthodromic atrioventricular re-entrant tachycardia and a history of syncope; one of them additionally had atrial flutter with 2:1 conduction to the ventricle. A fifth patient presented with a life-threatening broad-complex tachycardia. In electrophysiologic studies an accessory pathway was localized in the right septal area in 3 patients. In 2 patients the accessory atrioventricular pathways were created by means of surgical intervention, connecting the right atrial appendage to the right ventricular outflow tract. All patients could be managed successfully by means of catheter ablation. In patients with tricuspid atresia, there are congenital and surgically acquired accessory pathways responsible for the increased rate of Wolff-Parkinson-White syndrome. Both types of accessory pathways can and should be treated by means of catheter ablation because atrial arrhythmia often seen in patients undergoing the Fontan operation can trigger atrioventricular re-entrant tachycardia or cause life-threatening tachycardia. Congenital accessory pathways should be excluded carefully before surgical intervention for total cavopulmonary anastomosis in patients with tricuspid atresia.

Electrophysiological evaluation of asymptomatic ventricular pre-excitation in children and adolescents

Background: Diagnostic assessment and treatment have been described in detail in symptomatic WPW syndrome, but little information exists about significance and prognosis of an incidentally found ventricular pre-excitation (VPE) in asymptomatic children. The aim of the study was to evaluate, retrospectively, the role of electrophysiological study (EPS) in the assessment of the arrhythmic risk in asymptomatic patients with VPE. Material and Methods: Sixty-two asymptomatic children and adolescents (38 M/24 F, aged 9.8±5.1 years) referred to our Division between 1996 and 2002 for an incidentally found VPE underwent an EPS for arrhythmic risk stratification. The following parameters were examined: anterograde effective refractory period of the accessory pathway (AP), the 1-to-1 conduction over the AP, the inducibility of atrio-ventricular re-entrant tachycardia (AVRT) and the inducibility of atrial fibrillation (AF) with measurement of minimal RR between two consecutive preexcitated QRS complexes, the average RR interval of all cycles, and the percentage of preexcitated QRS complexes. Result: During the EPS, 36 patients (58.1%) experienced sustained SVT. The tachycardia was initiated in the basal state in 22 patients and after isoproterenol in the other 14. Orthodromic AVRT (cycle length 305.9±48.5 ms) was recorded in 29 patients. In three patients, both orthodromic and antidromic AVRT were recorded, with different cycle length (CL). Antidromic AVRT alone (CL 239.5±13.7 ms) was recorded in four patients. AF was recorded in nine patients: in six patients, it was recorded after the induction of orthodromic or antidromic AVRT, in the other three cases AF was the first and only arrhythmic event. The minimal RR between two consecutive pre-excitated QRS ranged between 250–230 ms (mean 237.5±9.6 ms). In the 26 patients who presented no induced sustained tachycardia in the EPS, the 1:1 conduction over the AP ranged between 210 and 600 ms (mean 279.6±75.2 ms). Conclusions: Electrophysiological evaluation remains the gold standard for assessing risk of life-threatening arrhythmias in patients with VPE. However, a high proportion of healthy children and adolescents with VPE can experience sustained AVRT and/or AF during EPS. These results raise questions about the necessity of an aggressive treatment approach to prevent those “rare” cases of sudden death.

Transgenic mouse model of ventricular preexcitation and atrioventricular reentrant tachycardia induced by an AMP-activated protein kinase loss-of-function mutation responsible for Wolff-Parkinson-White syndrome.

We identified a gene (PRKAG2) that encodes the gamma-2 regulatory subunit of AMP-activated protein kinase (AMPK) with a mutation (Arg302Gln) responsible for familial Wolff-Parkinson-White (WPW) syndrome. The human phenotype consists of ventricular preexcitation, conduction abnormalities, and cardiac hypertrophy. To elucidate the molecular basis for the phenotype, transgenic mice were generated by cardiac-restricted expression of the wild-type (TG(WT)) and mutant(TG(R302Q)) PRKAG2 gene with the cardiac-specific promoter alpha-myosin heavy chain. ECG recordings and intracardiac electrophysiology studies demonstrated the TG(R302Q) mice to have ventricular preexcitation (PR interval 10+/-2 versus 33+/-5 ms in TG(WT), P<0.05) and a prolonged QRS (20+/-5 versus 10+/-1 ms in TG(WT), P<0.05). A distinct AV accessory pathway was confirmed by electrical and pharmacological stimulation and substantiated by induction of orthodromic AV reentrant tachycardia. Enzymatic activity of AMPK in the mutant heart was significantly reduced (0.009+/-0.003 versus 0.025+/-0.001 nmol x min(-1) x g(-1) in nontransgenic mice), presumably owing to the mutation disrupting the AMP binding site. Excessive cardiac glycogen was observed. Hypertrophy was confirmed by increases in heart weight (296 versus 140 mg in TG(WT)) and ventricular wall thickness. We have developed a genetic animal model of WPW that expresses a mutation responsible for a familial form of WPW syndrome with a phenotype identical to that of the human, including induction of supraventricular arrhythmia. The defect is due to loss of function of AMPK. Elucidation of the molecular basis should provide insight into development of the cardiac conduction system and accessory pathways.

Radiofrequency Catheter Ablation of an Accessory Pathway in a Patient with Wolff‐Parkinson‐White and Kartagener's Syndrome

We report a case of a manifest left free wall accessory pathway in a patient with Kartagener's syndrome and recurrent episodes of orthodromic atrioventricular reentrant tachycardia. To the best of our knowledge, it is the first report of Wolff-Parkinson-White syndrome associated with Kartagener's syndrome. Situs inversus and mirror image dextrocardia occurred with no additional detectable cardiac structural abnormalities. Diagnostic and therapeutic electrophysiological study was carried out via transaortic approach and a left-to-right reversal of monoplane fluoroscopic image.

Radiofrequency Catheter Ablation of a Right Free‐Wall Accessory Pathway in Dextrocardia with Complete Situs Inversus

An uncommon case of orthodromic atrioventricular reentrant tachycardia in a patient with dextrocardia and complete situs inversus is reported. There was no associated cardiac abnormality apart from the mirror image dextrocardia. An electrophysiological study and successful catheter ablation of a right free-wall concealed accessory pathway was performed. A simplified three-catheter technique from a femoral approach and monoplane fluoroscopy were used in a noncomplicated procedure of normal duration.

Sympathetic predominance of cardiac autonomic regulation in patients with left free wall accessory pathway and orthodromic atrioventricular reentrant tachycardia.

The aim of this study was to compare cardiac autonomic regulation in patients with a history of paroxysmal supraventricular tachyarrhythmias, such as atrioventricular nodal reentrant tachycardia and atrioventricular reentrant tachycardia, and healthy controls. Seventeen patients with paroxysmal atrioventricular nodal reentrant tachycardia (atrioventricular nodal reentrant tachycardia group), 14 patients with overt preexcitation and paroxysmal atrioventricular reentrant tachycardia caused by a left free wall accessory pathway (atrioventricular reentrant tachycardia group) and 14 healthy control subjects, were studied. The patients and the controls were age and gender matched. Cardiac autonomic regulation was assessed by means of frequency domain analysis of heart rate variability at rest, during head-up tilt, active standing, treadmill exercise and after exercise. The high frequency component (0.15-0.5 Hz) of heart rate variability tended to be lower and the low frequency component (0.04-0.15 Hz) tended to be higher among the atrioventricular reentrant tachycardia patients than in atrioventricular nodal reentrant tachycardia patients and controls. The difference reached statistical significance at rest (P < 0.05) and during standing (P < 0.05 atrioventricular reentrant tachycardia vs atrioventricular nodal reentrant tachycardia and P < 0.01 atrioventricular reentrant tachycardia vs controls). Accordingly, the low-to-high frequency ratio--the marker of cardiac sympathetic regulation--was higher in atrioventricular reentrant tachycardia patients than in atrioventricular nodal reentrant tachycardia patients (P < 0.05 at rest and during standing) and controls (P < 0.01 during standing). The cardiac autonomic status in atrioventricular reentrant tachycardia patients was suggestive of a higher sympathetic tone than in atrioventricular nodal reentrant tachycardia patients or healthy controls. This may be related to inhomogeneous ventricular activation in the presence of antegrade conduction via the accessory atrioventricular pathway.

Overdrive atrial stimulation during transesophageal electrophysiological study: usefulness of post-pacing VA interval analysis in differentiating supraventricular tachycardias with 1:1 atrio-ventricular relationship

We evaluated the feasibility and usefulness of overdrive atrial pacing to identify the relationship between atrial and ventricular activation in supraventricular tachycardias with a stable 1:1 atrio-ventricular (AV) conduction ratio during a transesophageal electrophysiological investigation. Overdrive atrial stimulation was performed in 42 consecutive patients (11 males and 31 females; mean age 49±17 years) during AV junctional reentrant tachycardia, orthodromic AV reentrant tachycardia and ectopic atrial tachycardia (22, 13 and seven subjects, respectively). Trains of 12 stimuli at a constant rate were introduced starting at a cycle length 10 ms shorter than the tachycardia cycle length; stimulation was repeated with a 10-ms decrement in pacing cycle length at each step until tachycardia terminated and/or second-degree AV block occurred. The difference between the VA interval duration at baseline and in the first post-pacing tachycardia beat was measured at each step and provided identification of the AV relationship. At least one post-pacing VA interval was evaluable in 90% of the cases and measured 2±4 and 1±3 ms in AV junctional and AV reentrant tachycardia groups, respectively, and 83±42 ms in the ectopic atrial tachycardia group ( P<0.0000001 ectopic atrial tachycardia group vs. others). When three or more post-pacing VA intervals were obtained during the same tachycardia, a curve was constructed by plotting their values against the corresponding pacing cycle lengths. A curve could be constructed in 36% of the cases and was flat in all patients with AV junctional and AV reentry, while it was completely irregular in the ectopic atrial tachycardia group ( P<0.003). The analysis of post-pacing VA interval behaviour in response to overdrive atrial stimulation provides a rapid and reliable differentiation between supraventricular tachycardias with 1:1 AV conduction ratio during a transesophageal electrophysiological study.

Alternation of atrioventricular nodal conduction time during atrioventricular reentrant tachycardia: are dual pathways necessary?

Alternation of atrial cycle length and AV nodal conduction time (NCT) is often observed during AV reentrant tachycardia. Both AV nodal dual pathway and rate-dependent function have been postulated to be involved in this phenomenon. This study was designed to determine the respective role of these two mechanisms in the alternation observed in an in vitro model of orthodromic AV reentrant tachycardia. The tachycardia was produced by detecting each His-bundle activation and stimulating the atrium after a retrograde delay, thereby simulating retrograde pathway conduction, in six isolated rabbit heart preparations. After a 5-minute stabilization period at a fast rate, the retrograde delay was decremented by 2 msec every minute until nodal blocks occurred. We observed a sequential alternation of the cycle length and NCT in four preparations in the short retrograde delay range. The magnitude of the alternation gradually increased as the retrograde delay was decreased and reached 4.6 +/- 0.5 msec during 1:1 conduction. The alternation increased further just prior to termination of the tachycardia by an AV nodal block. None of the preparations showed discontinuous AV nodal recovery curves. Moreover, an electrode positioned over the endocardial surface of the node showed that the alternation developed distally to the nodal inputs, which are believed to constitute a major component of dual pathways. A mathematical model predicted the alternation from known characteristics of rate-dependent nodal functional properties. NCT and cycle length alternation can arise during orthodromic AV reentrant tachycardia when the retrograde delay is sufficiently short. The characteristics of the alternation, presence of continuous recovery curves, intranodal location of the alternation, and mathematical modeling suggest that the alternation is predictable from the known functional properties of the AV node without postulating dual pathway physiology.

Variants of preexcitation--specialized atriofascicular pathways, nodofascicular pathways, and fasciculoventricular pathways: electrophysiologic findings and target sites for radiofrequency catheter ablation.

In the present report, the electrophysiologic findings in patients with different types of variants of preexcitation, i.e., atriofascicular, nodofascicular, and fasciculoventricular fibers, and the results of radiofrequency catheter ablation using different target sites are described. Twelve patients (mean age 36 +/- 17 years) with variants of the preexcitation syndromes underwent electrophysiologic study and radiofrequency catheter ablation. The atrial origin of atriofascicular pathways remote from the normal AV node was assessed by application of late atrial extrastimuli that advanced ("reset") the timing of the next QRS complex without anterograde penetration into the AV node. In patients with atriofascicular pathways, ablation of the accessory pathway or the retrograde fast AV node pathway was attempted. Ablation of the atriofascicular pathways was guided by a stimulus-delta wave interval mapping in the first five patients and by recording of atriofascicular pathway activation potentials in the next five patients. A nodofascicular pathway was suggested if VA dissociation occurred during tachycardia and if atrial extrastimuli failed to reset the tachycardia without anterograde penetration into the AV node. A fasciculoventricular connection was suggested if the proximal insertion of the accessory pathway was found to arise from the His bundle or bundle branches. The PR interval was expected within normal limits during sinus rhythm and the QRS complex to be slightly prolonged with a discrete slurring of the R wave, suggesting a small delta wave. Ten of the 12 patients had evidence for atriofascicular pathways and one patient each for a nodofascicular and fasciculoventricular pathway. In six patients, the atriofascicular pathways were successfully ablated, and in two patients, the retrograde fast AV node pathway. In one patient, a concealed right posteroseptal accessory AV pathway served as the retrograde limb and was successfully ablated. The nodofascicular pathway was shown to be a bystander during AV node reentrant tachycardia. After successful fast AV node pathway ablation resulting in marked PR prolongation, no preexcitation was present during sinus rhythm because of the proximal insertion of the nodofascicular pathway distal to the delay producing parts of the AV node. The proximal insertion of the fasciculoventricular pathway was suggested to arise distal to the AV node at the site of the penetrating AV bundle. The earliest ventricular activation at the His-bundle recording site indicated the ventricular insertion of this accessory connection into the ventricular summit. The fasciculoventricular connection gave rise to a fixed ventricular preexcitation and served as a bystander during orthodromic AV reentrant tachycardia incorporating a left-sided accessory AV pathway. The majority of patients with variants of the preexcitation syndrome present with specialized atriofascicular pathways that seem to originate from remnants of the specialized AV ring tissue. Nodofascicular and fasciculoventricular pathways exist and may give rise to preexcitation, although their functional role in participation of clinical arrhythmias still needs to be elucidated. In the present study, both a fasciculoventricular pathway and a nodofascicular pathway acted as a bystander.

Common varieties of supraventricular tachycardia: Differentiation and dangers

Two major types of supraventricular tachycardia (SVT) commonly seen in acute care situations are atrioventricular nodal reentrant tachycardia (AVNRT), and orthodromic atrioventricular reentrant tachycardia (AVRT). Intranodal reentry via fast and slow conduction pathways within the atrioventricular junction is the mechanism by which AVNRT develops. In contrast, reentrant tachycardia across accessory pathways is associated with preexcitation and AVRT. In the setting of Wolff-Parkinson-White syndrome, inappropriate treatment of AVRT may result in a potentially lethal type of atrial fibrillation. Electrocardiographic cues that differentiate between AVNRT and AVRT are discussed. Treatments range from emergency cardioversion to administration of intravenous agents such as adenosine. The tachycardias may be cured with radiofrequency catheter ablation.

Efficacy and safely of long-term oral flecamide acetate in patients with responsive supraventricular tachycardia

In 102 patients with inducible supraventricular tachycardia (SVT), 56 women and 46 men aged 20–86 (mean, 52) years, underwent electrophysiologic study. SVTs observed at electrophysiologic study were atrial flutter or atrial fibrillation (32%), the “slow-fast” form of atrioventricular (AV) nodal reentrant tachycardia (45%), orthodromic AV reentrant tachycardia (25%), and atrial tachycardia (9%). More than 1 SVT occurred in some patients. Spontaneous symptomatic SVT frequency prior to oral flecainide varied from 3/day to 1/3 months (mean, 3/month). At electrophysiologic study and during SVT, intravenous flecainide, 2 mg/kg body weight, was given at an infusion rate of 10 mg/min up to a maximum dose of 150 mg. Patients were commenced on oral flecainide if SVT termination occurred during intravenous flecainide administration and if reinitiation was not possible after the total dose of flecainide had been given. In patients with AV nodal reentrant tachycardia and AV reentrant tachycardia further criteria for commencing oral flecainide were SVT termination by ventricularatrial conduction block and persistent ventricularatrial block after intravenous flecainide administration. Initial oral flecainide dosage was determined by assessing ability to reinitiate SVT after 50 mg, 100 mg, and the total dose of intravenous flecainide had been given. Eighty-nine patients (87%) remained free of symptomatic SVT over a mean follow-up period of 3.9 years (range, 3 months to 6.5 years). Two thirds were still taking the original dosage of flecainide and the rest were SVT-free on a higher dosage. Oral dosages ranged from 50 to 300 mg/day (median dosage, 100 mg twice daily) Nine patients experienced minor side effects, including lethargy, dizziness, headache, and blurred vision. There were no deaths and no reports of major proarrhythmic events or other major adverse effects.

Significance of cycle length alternation during orthodromic atrioventricular reentrant tachycardia

These data confirm that modest cycle length alternation is frequently seen in orthodromic AV reentrant tachycardia, even when dual AV node pathway physiology cannot be demonstrated.

Radiofrequency catheter ablation of accessory pathways during entrainment of AV reentrant tachycardia.

Radiofrequency ablation of accessory pathways must sometimes be done during orthodromic atrioventricular reentrant tachycardia when manifest anterograde accessory pathway conduction is absent or retrograde fusion obscures accessory pathway location during ventricular pacing. Unfortunately, abrupt heart rate slowing upon radiofrequency induced termination of atrioventricular reentrant tachycardia often causes catheter dislodgment. We report our experience in circumventing this problem during radiofrequency ablation by using entrainment of atrioventricular reentrant tachycardia. The latter maintains retrograde activation pattern over the accessory pathway while preventing abrupt ventricular rate change. Eight patients (4 men and 4 women, mean age 37.3 +/- 17.9) with eleven left-sided accessory pathways were included. Ablation during entrainment was used as the first approach in three patients with concealed accessory pathways and one patient with a bidirectional accessory pathway. In another four patients, ablation during entrainment was used after technical difficulties in ablating during tachycardia. Only 1-3 radiofrequency applications were required to eliminate the accessory pathway using the entrainment technique. The catheter remained stable when accessory pathway conduction was interrupted by radiofrequency current. In conclusion, entrainment of atrioventricular reentrant tachycardia during radiofrequency application is useful for maintaining catheter position for accessory pathway ablation during atrioventricular reentrant tachycardia.

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

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. 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 relating 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. 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.

Unmasking of left free wall ventricular preexcitation by His bundle ablation.

His bundle ablation was performed in a 48 year old man with drug refractory orthodromic atrioventricular reentrant tachycardia and paroxysmal atrial fibrillation. Reentry was caused by a left free wall concealed accessory pathway. Interruption of the His bundle by low energy direct current shock (25 J) was quickly followed by anterograde conduction via the accessory pathway, with various forms of advanced block. The combined effect of unfavourable anterograde conduction (prolonged anterograde effective refractory period and decremental conduction), the left lateral location of the accessory pathway and intra-atrial conduction delay on one side, and normal conduction via the atrioventricular node and His bundle with retrograde concealed conduction into the accessory pathway on the other side resulted in masking of the anterograde conduction capability of the anomalous pathway. This observation does not seem to invalidate the choice of His bundle ablation in similar cases.

Atrioventricular junctional and orthodromic atrioventricular reentrant tachycardia in Wolff-Parkinson-White syndrome

The existence of two or more types of reentrant tachycardias in the same patient with Wolff-Parkinson-White syndrome has been emphasized, and the occurrence of orthodromic atrioventricular (AV) reentrant tachycardia and AV junctional reentrant tachycardia have been well documented. This report describes a patient with Wolff-Parkinson-White syndrome in whom the phenomena of spontaneous transition from AV reentry to AV junctional reentry and adenosine-induced conversion from AV junctional reentry to AV reentry were observed.

Electrocardiographic and electrophysiologic characteristics of anterior, midseptal and right anterior free wall accessory pathways

Objectives. The objective of this study was to define the electrocardiographic (ECG) and electrophysiologic characteristics of midseptal, anteroseptal and right anterlor free wall accessory pathways.Methods. The fully pre-excited 12-lead surface ECGs and ECGs during orthodromic atrioventricular (AV) reentrant tachycardia were compared for 13 patients with an anteroseptal, 7 with a midseptal and 7 with a right free wall accessery pathway. Routine electrophysiologic studies were performed in all and stimulation of the right ventricular summit during tachycardia was accomplished in 10 patients.Results. Differences in the surface ECGs were not sufficiently sensitive to distinguish among accessory pathway locations. Premature ventricular complexes induced from the right ventricular septal summit during ventricular activation either advanced the succeeding atrial depolarization or terminated the tachycardia in three of six patients with a septal pathway and in none of the four with a right anterior pathway. The change in ventriculoatrial (VA) interval with the development of right bundle branch block during orthodromic AV tachycardia proved most helpful in distinguishing these pathways. Patients with a right anterior free wall pathway showed a change in VA interval ≥ 40 ms, whereas those with an anteroseptal pathway showed changes of 20 to 30 ms and those with a midseptal pathway showed no change.Conclusions. Anteroseptal, midseptal and right anterior free wall pathways may be distinguished by using programmed stimulation of the summit of the right ventricular septpm and especially With changes in the VA interval with development of right bundle branch block during orthodromic AV reentrant tachycardia.

Electrophysiologic effects and efficacy of cibenzoline in patients with supraventricular tachycardia.

Electrophysiologic effects of intravenous (i.v.) cibenzoline were evaluated in 18 patients with accessory pathways or dual atrioventricular (AV) nodal pathways (12 men and 6 women with a mean age of 44 +/- 18 years). Twelve patients had accessory AV pathways, including 6 patients with a manifest accessory pathway. Six patients had AV nodal reentrant tachycardia (AVNRT). Electrophysiologic studies were performed before and after cibenzoline (1.4 mg/kg i.v.) infusion for 5 min. Sinus cycle length did not change significantly after cibenzoline administration. Cibenzoline increased both the AH (85 +/- 20 vs. 91 +/- 21 ms, p less than 0.05) and HV intervals (41 +/- 10 ms vs. 53 +/- 11 ms, p less than 0.001). Neither the atrial nor ventricular effective refractory period (ERP) was altered by cibenzoline. Complete block in the accessory pathway occurred antegradely in 4 patients and retrogradely in 1 patient. Cibenzoline prevented induction of AV reentrant tachycardia (AVRT) in 3 of 8 patients with sustained orthodromic AVRT by abolishing retrograde accessory pathway conduction or prolonging the retrograde accessory pathway ERP. Of 5 patients who continued to have inducible AVRT before and after cibenzoline administration, the tachycardia cycle length was increased in 3, mainly due to the increase in retrograde accessory pathway conduction time. Cibenzoline prevented induction of sustained AVNRT in 4 of 5 patients by prolonging the minimum pacing cycle length, maintaining 1:1 ventriculoatrial (VA) conduction through the retrograde fast AVN pathway or shortening the antegrade fast AVN pathway ERP equal to the slow AVN pathway. In one patient who had an uncommon type of AVNRT, sustained tachycardia was induced by cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Significance of ventricular pacing site in manifest entrainment during orthodromic atrioventricular reentrant tachycardia with left-sided accessory pathway.

We examined entrainment by ventricular pacing in six patients during orthodromic atrioventricular reentrant tachycardia (AVRT) utilizing a left-sided lateral accessory pathway. Constant fusion and progressive fusion were demonstrated in all patients by left ventricular pacing during tachycardia, but in none of the patients by right ventricular pacing. When left ventricular pacing was performed during AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous pacing beat (n - 1) within the ventricle, therefore, constant fusion and progressive fusion were demonstrated in the surface electrocardiographic QRS complexes. On the other hand, when right ventricular pacing was performed during orthodromic AVRT, the antidromic wave front from the pacing impulse (n) collided with the orthodromic wave front of the previous paced beat (n - 1) within the normal atrioventricular pathway, and constant fusion and progressive fusion were therefore not demonstrated. These phenomena were explained by the relationship of the ventricular pacing site and the reentrant circuit. This study demonstrates the importance of the pacing site in manifest entrainment of orthodromic AVRT during ventricular pacing.