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.     

Mechanisms and management of paroxysmal supraventricular tachycardia

Paroxysmal supraventricular tachycardia (PSVT) is defined as a regular rapid heart beat, which initiates and terminates suddenly. PSVT may have a variety of electrophysiologic mechanisms, including atrial tachycardia, atrioventricular (AV) nodal reentry, and tachycardia involving an accessory AV connection. Atrial tachycardia may be reentrant or may be caused by abnormal automaticity or triggered activity. AV nodal reentry, in which the reentrant circuit is confined to the AV node or the region around the AV node, is the most common type of PSVT in adults. Orthodromic supraventricular tachycardia is the most frequently found tachycardia in patients with accessory AV connections. During orthodromic supraventricular tachycardia, antegrade conduction occurs via the AV node, and retrograde conduction occurs via an accessory AV connection. Other types of PSVT, including junctional tachycardia, are less common. A definitive diagnosis of the PSVT mechanism usually requires electrophysiologic testing, but clinical and electrocardiographic clues may be present. Understanding the mechanism of PSVT can alter therapy because the response to antiarrhythmic drugs may be somewhat different depending on the PSVT type. In addition, the risks and efficacy of catheter ablation for curing PSVT may differ depending on the PSVT type. A better understanding of PSVT mechanisms, which has developed over the past 20 years, has led to dramatic improvements in therapy.     

Diagnostic and therapeutic use of adenosine in patients with supraventricular tachyarrhythmias

Adenosine has been shown to affect both sinus node automaticity and atrioventricular (AV) nodal conduction. The effects of increasing doses of intravenous adenosine were assessed in 46 patients with supraventricular tachyarrhythmias. Adenosine reliably terminated episodes of supraventricular tachycardia in all 16 patients with AV reciprocating tachycardia, in 13 of 13 patients with AV nodal reentrant tachycardia and in 1 of 2 patients with junctional tachycardia with long RP intervals. Adenosine produced transient high grade AV block without any effect on atrial activity in six patients with intraatrial reentrant tachycardia, four patients with atrial flutter, three patients with atrial fibrillation and in single patients with either sinus node reentry or an automatic atrial tachycardia. The dose of adenosine required to terminate episodes of supraventricular tachycardia was variable (range 2 to 23 mg). Side effects were minor and of short duration. These results demonstrate that adenosine is useful for the acute therapy of supraventricular tachycardia whenever reentry through the AV node is involved. When arrhythmia termination is not affected, atrial activity may be more readily analyzed during adenosine-induced transient AV block.     

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.     

Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarrhythmic agents

The clinical, electrocardiographic and electrophysiologic determinants and effects of antiarrhythmic agents on sustained sinus node reentrant tachycardia remain poorly defined. Of 65 consecutive men undergoing electrophysiologic studies for symptomatic paroxysmal supraventricular tachycardia over a 4 year period, 11 (16.9%), who ranged in age from 39 to 76 years, demonstrated sustained sinus node reentrant tachycardia. On the surface electrocardiogram, before electrophysiologic studies, the following diagnoses were considered in the 11 patients: sinus node reentrant tachycardia on the basis of an RP'/P'R ratio of greater than 1 and P wave configuration similar to that of sinus P waves (7 patients); atrioventricular (AV) nodal reentrant tachycardia on the basis of an RP'/P'R ratio of less than 1 (3 patients); and paroxysmal atrial tachycardia with AV block (1 patient). All 11 patients had a history of recurrent palpitation, 4 had syncope, 2 had dizzy spells and 9 had organic heart disease. Sustained sinus node reentrant tachycardia could be reproducibly induced in all 11 patients during atrial pacing or premature atrial stimulation, or both, over a wide echo zone. The tachycardia could be terminated by carotid sinus massage, atrial pacing and premature atrial stimulation. Characteristics of tachycardia included: high-low activation sequence; cycle lengths of 250 to 590 ms with wide fluctuations of 20 to 180 ms in individual patients; RP'/P'R ratio of greater than 1 in 8 (73%) of the 11 patients and a ratio of less than 1 in 3 (27%). Induction of sustained sinus node reentrant tachycardia was prevented by intravenous ouabain (0.01 mg/kg body weight) in two of two patients, by intravenous verapamil (10 mg) in two of two patients and by intravenous amiodarone (5 mg/kg body weight) in four of four patients. In contrast, intravenous propranolol (0.1 mg/kg body weight) did not affect induction of sustained sinus node reentrant tachycardia in two of two patients. It is concluded that sustained sinus node reentrant tachycardia, seen in 16.9% of the study patients with paroxysmal supraventricular tachycardia, is not as benign as previously believed; it is frequently associated with organic heart disease; it demonstrates wide variations in cycle length, unlike other forms of paroxysmal supraventricular tachycardia; it can masquerade as AV nodal reentrant tachycardia and paroxysmal atrial tachycardia with AV block on the surface electrocardiogram in 36% of patients; and it is responsive to intravenous administration of ouabain, verapamil or amiodarone.     

Atypical forms of supraventricular tachycardia due to atrioventricular node reentry in children after radiofrequency modification of slow pathway conduction

Objectives. This study was performed to investigate the prevalence, mechanisms and clinical significance of supraventricular tachycardias inducible in children or adolescents after radiofrequency modification of slow pathway conduction for the treatment of atrioventricular (AV) node reentrant tachycardia.Background. Limited data have been reported with regard to the physiology of AV node reentrant tachycardia in young patients. Radiofrequency catheter ablation allows evaluation of the effects of selective modification of the different pathways involved in AV node reentrant tachycardia.Methods. Selective modification of slow pathway conduction was performed in 18 young patients (12.9 ± 3.4 years old) with typical (anterograde slow-retrograde fast) AV node reentrant tachycardia. Radiofrequency energy was applied across the posteromedial or midseptal tricuspid annulus, guided by slow pathway potentials and anatomic position. Programmed stimulation was performed after modification of slow pathway conduction defined as noninducibility of typical AV node reentrant tachycardia.Results. Modification of slow pathway conduction was achieved in each patient, with a median of four applications of radiofrequency energy. However, atypical forms of supraventricular tachycardia were inducible in 9 of 18 young patients after slow pathway modification: AV node reentrant tachycardia with 2 to 1 AV block (seven patients; anterograde fast-retrograde slow AV node reentrant tachycardia (five patients); and sustained accelerated junctional tachycardia (two patients). In comparison, atypical forms of tachycardia were inducible in only 2 of 59 adult patients with AV node reentrant tachycardia undergoing slow pathway modification in the same laboratory (p = 0.01). Additional applications of radiofrequency energy to the posteromedial tricuspid annulus rendered AV node reentrant tachycardia with 2 to 1 block and the fast-slow form of AV node reentrant tachycardia noninducible. Junctional tachycardia terminated spontaneously in both patients. During 9.8 ± 3 months of follow-up, slow-fast AV node reentrant tachycardia has recurred in one patient, whereas fast-slow AV node reentrant tachycardia has occurred in two patients, both with inducible fast-slow tachycardia after the initial modification of slow pathway conduction.Conclusions. Initial applications of radiofrequency energy may selectively modify the anterograde conduction of slow pathway fibers in young patients with AV node reentrant tachycardia. This may result in AV node reentrant tachycardia with 2 to 1 AV block or a reversal of the reentrant circuit (fast-slow tachycardia). Induction of these tachyarrhythmias indicates that further applications of radiofrequency energy are required for the successful modification of slow pathway conduction in young patients. The increased prevalence of inducible atypical arrhythmias among young patients suggests differences in the anatomic or electrophysiologic substrate of AV node reentrant tachycardia that may evolve as a function of age.     

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

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

Value of transesophageal programmed atrial stimulation in the evaluation of unexplained cerebrovascular accidents

Certain embolic cerebrovascular accidents can be explained by the development of paroxysmal atrial fibrillation. When noninvasive complementary investigations are negative, programmed atrial stimulation can be proposed to detect increased atrial vulnerability. The objective of this study was to evaluate the reliability of this method performed via a transoesophageal approach in 59 subjects presenting with an embolic cerebrovascular accident and who were in sinus rhythm at the time of the accident. Seven of these patients had a history of paroxysmal atrial fibrillation (AF) or atrial tachycardia (AT) (group I). Three of these seven patients also presented AV nodal reentrant junctional tachycardia. The other 52 patients had no history of arrhythmia and their Holter recording did not reveal any episodes of sustained atrial tachycardia (group II). Transoesophageal programmed atrial stimulation used up to 2 extrastimuli under baseline conditions and during Isuprel infusion. The following results were obtained: sustained atrial tachycardia (> 1 min) was induced in all patients of group 1, 3 of them also presented inducible junctional tachycardias. 14 patients of group II (27%) presented inducible supraventricular tachycardia: atrial tachycardia in 7 cases. Patients in group II with inducible AT presented either heart disease (n = 3) or minor abnormalities on the Holter recording (runs of atrial premature complexes or sinus pauses (n = 3). Two of these patients subsequently developed sustained atrial fibrillation during follow-up. In 25 patients with normal Holter recording and no heart disease, programmed atrial stimulation induced junctional tachycardia in 4 cases. In conclusion, transoesophageal electrophysiological investigation is a useful way to identify various forms of supraventricular tachycardia able to explain an embolic cerebrovascular accident. The considerable incidence of inducible AV nodal reentrant junctional tachycardia must be emphasized, while the incidence of atrial fibrillation is much lower than during intracardiac investigations.     

Unusual Resetting Patterns in Response to Single Atrial Extrastimuli During AV Junctional Reentrant Tachycardia

Unusual Resetting Patterns in AV Junctional Reentry. Introduction : Two unusual resetting patterns were observed in two patients with slow-fast AV junctional reentrant tachycardia (AVJRT) submitted to an electrophysiologic study.
Methods and Results : After AVJRT induction, resetting was evaluated by introducing single extrastimuli at progressively shorter coupling intervals from the high right atrium (HRA) and the proximal coronary sinus (CS). An alteration in the return cycle length duration allowed demonstration of resetting. In the first patient, during an AVJRT with a large excitable gap, properly timed extrastimuli delivered both from the HRA and CS simultaneously reset the tachycardia and advanced the H electrogram of the preceding tachycardia beat. In the second patient, both HRA and CS stimulation apparently failed to reset AVJRT (return cycle length unchanged), but, at critical coupling intervals, the cycle length duration of the tachycardia beat following the return cycle was consistently shortened.
Conclusions : During slow-fast AVJRT, single atrial stimulation from sites remote to the reentrant circuit may result in unusual resetting patterns. Further studies are required to evidence the full spectrum of resetting in AVJRT.     

Intravenous flecainide acetate for supraventricular tachycardias

Flecainide acetate, 2 mg/kg body weight, given intravenously at 10 mg/min was administered to 128 (74 male and 54 female) patients whose ages ranged from 11 to 86 years (mean 44). All patients had supraventricular tachycardias (SVT) that developed spontaneously or were induced during electrophysiologic study. There were 26 patients with atrial flutter, 34 with atrial fibrillation, 7 with ectopic atrial tachycardia, 41 with atrioventricular (AV) reentrant tachycardia and 40 with AV nodal reentrant tachycardia. Twenty patients had more than 1 variety of SVT. Flecainide was administered during SVT to 9 patients with atrial flutter, 11 with atrial fibrillation, 7 with atrial tachycardia, 38 with AV reentrant tachycardia and 34 with AV nodal reentrant tachycardia. In the remaining 31 patients with inducible SVT at electrophysiologic study, flecainide was administered during sinus rhythm. Reinitiation of SVT was attempted in these patients after completion of flecainide administration. Flecainide successfully terminated atrial flutter in 2 patients (22%), atrial fibrillation in 9 (82%), atrial tachycardia in 5 (71%), AV reentrant tachycardia in 32 (84%) and AV nodal reentrant tachycardia in 30 (88%). Reinitiation of SVT was possible in 10 of 26 patients with atrial flutter (38%), 5 of 34 with atrial fibrillation (15%), 3 of 7 with atrial tachycardia (43%), 14 of 41 with AV reentrant tachycardia (34%) and 11 of 40 with AV nodal reentrant tachycardia (27%). In patients with AV reentrant tachycardia and AV nodal reentrant tachycardia, reinitiation occurred when retrograde anomalous pathway refractoriness was not significantly prolonged by intravenous flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of recurrent supraventricular tachyarrhythmias with flecainide or a flecainide and amiodarone combination

The acute electrophysiologic effects and therapeutic efficacy of intravenous and oral flecainide were assessed in 18 patients with recurrent supraventricular tachyarrhythmias, resistant to conventional antiarrhythmic agents. They were 22 to 76 years old (mean 50). Twelve patients underwent electrophysiologic study for the investigation of tachyarrhythmias. Of the whole four patients had functional longitudinal AH dissociation (dual AV pathways). These patients had provocable intra-AV nodal reentrant tachycardia (Group I). Six patients had a direct accessory AV pathway, that showed bidirectional conduction in 5 and retrograde conduction alone in 1 (Group II). These patients had provocable atrioventricular reentrant tachycardia using the accessory pathway as the retrograde limb of the tachycardia circuit. Two patients suffered from automatic supraventricular tachycardia (Group III). Group IV included patients with paroxysmal atrial flutter or fibrillation. The patients of this group did not discontinue chronic treatment with amiodarone. After baseline electrophysiologic evaluation, intravenous flecainide (2 mg/Kg body weight over 5 minutes) was given to patients of I and II group during induced reentrant tachycardia. Flecainide was administered to other patients during spontaneous episodes of tachyarrhythmias. Flecainide resulted in tachycardia termination in all patients of group I and in 4 patients of group II (66%). Tachycardia termination was due to block in the retrograde limb of the circuit. Before termination tachycardia cycle length increased significantly, mainly as the result of an increase in ventriculo-atrial conduction time. After intravenous flecainide therapy, reentrant SVT was non inducible in the patients of group I and in 4 patients of group II. Flecainide was successful in the acute termination of 100% of automatic supraventricular tachycardia and 75% of fibrillation. The patients with atrial flutter developed a faster ventricular rate.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise-induced uncommon atrioventricular nodal reentrant tachycardia with sick sinus syndrome: a case report.

Exercise seldom provokes tachycardia in patients with paroxysmal supraventricular tachycardia (PSVT). This report presents a case of exercise-induced uncommon atrioventricular nodal reentrant tachycardia (AVNRT) with sick sinus syndrome. Treadmill exercise testing provoked AVNRT of long RP' with good reproducibility. Uncommon AVNRT was confirmed by the lack of atrial pre-excitation during PSVT and para-Hisian pacing. The patient has been successfully treated with verapamil and DDD pacing for 5 years.     

食管心房调搏对室上性心动过速诊断的准确性评价

评价食管电生理检查对室上性心动过速诊断的准确性。方法 比较102例室上性心动过速经心内和食管电生理检查的结果。结果 102例室上性心动过速101例分型诊断一致：房室折返性心运过速（AVRT）58例,房室结折返性心运过速（AVNRT）37例,房内折返性心动过速（IART）5例,窦房结折返性心动过速（SART）1例,房性自律性心动过速（AAT）1例。6例房性心动过速（IART5例,AAT1例）起源于右房还是左房和57例房室折返性心动过速的旁路位于右侧还是左侧,两种检查结果完全一致。结论 食管心房调搏对室上性心动过速的分型诊断和初步定位诊断具有很高的准确性,这对选择射频消融术病例和简化消融术程序具有重要意义。     

Flecainide acetate for conversion of acute supraventricular tachycardia to sinus rhythm

The efficacy of intravenous flecainide acetate (maximum 2 mg/kg or 150 mg given at a rate of 15 mg/min) was assessed in patients with acute supraventricular tachycardia (SVT) (within 24 hours). Fifty patients were studied, 46 with spontaneous SVT and 4 with induced SVT at electrophysiologic assessment. Conversion to sinus rhythm was achieved within 45 minutes in 76%: in 25 patients with atrial fibrillation (76% conversion), 15 with atrioventricular (AV) nodal or AV reentrant tachycardia (100% conversion) and 10 with atrial flutter or atrial reentrant tachycardia (40% conversion). Adverse effects were noted in 21 patients (42%): paresthesia in 9, drowsiness in 8, nausea in 2, accelerated ventricular rate in 5, ventricular tachycardia in 1, sinus bradycardia in 1 and hypotension in 5. Adverse effects were associated with larger dosage and atrial flutter or atrial reentrant tachycardia. Thus, flecainide acetate is effective in converting to sinus rhythm acute atrial fibrillation and AV nodal and AV reentrant tachycardias, but not atrial flutter or atrial reentrant tachycardia.     

Paroxysmal supraventricular tachycardia initiated by a swallowing-induced premature atrial beat

We report a unique patient in whom electrophysiologic studies elucidated the mechanism of a rare form of swallowing-induced atrioventricular reentrant tachycardia, and for whom successful surgical ablation of an accessory pathway abolished intractable episodes of palpitation. A 64-year-old man was incapacitated by frequent attacks of palpitation following swallowing. Electrocardiograms documented paroxysmal supraventricular tachycardias initiated by a premature atrial beat or beats following swallowing. During electrophysiologic studies swallowing consistently induced premature atrial beats which in turn initiated a sustained atrioventricular reentrant tachycardia incorporating a retrogradely conducting left-sided concealed accessory pathway. The atrial activation sequence related to the premature atrial beats and the morphology of the premature P waves suggested that premature atrial beats originated in the right atrium. The mechanism of induction of premature atrial beats following swallowing remains obscure in our patient. Antiarrythmic drugs failed to prevent induction of sustained tachycardias during sequential electrophysiologic studies. The patient underwent successful surgical ablation of the accessory pathway and is free from palpitation 15 months after the surgery.     

Automatic pacemaker termination of two different types of supraventricular tachycardia

A new antitachycardia pacemaker system was used in a 58 year old woman to terminate two different types of supraventricular tachycardia by a single automatic pacing mode. During the invasive electrophysiologic study before pacemaker implantation (in the absence of medication), sustained episodes of atrioventricular (AV) nodal reentrant tachycardia and two short-lasting episodes of nonsustained atrial tachycardia were induced. After implantation, sustained episodes of both AV nodal tachycardia and atrial tachycardia were initiated. Both arrhythmias could be terminated reproducibly by a single pacing mode.     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

Atrioventricular nodal reentrant tachycardia initiated by catecholamine-induced ventricular tachycardia. A case report

The authors describe a patient who experienced recurrent wide-complex and narrow-complex tachycardias during exercise. Electrophysiologic testing in the resting state revealed dual atrioventricular (AV) nodal pathways. AV nodal reentrant tachycardia was inducible by ventricular premature stimulation but was always nonsustained, terminating with block in the anterograde slow pathway. During isoproterenol infusion, runs of ventricular tachycardia occurred frequently, and spontaneously initiated sustained AV nodal reentrant tachycardia. Exercise testing also provoked ventricular tachycardia and sustained AV nodal reentrant tachycardia. The patient was effectively treated with a combination of atenolol and verapamil. This case is an unusual example of a catecholamine-induced arrhythmia, possibly due to triggered activity (exercise-induced ventricular tachycardia), initiating an arrhythmia due to reentry (AV nodal reentrant tachycardia).     

Curative surgery for atrioventricular junctional ("AV nodal") reentrant tachycardia

A new surgical approach was studied prospectively in 10 consecutive patients with atrioventricular (AV) junctional reentrant tachycardia. The aim was to abolish tachycardia yet preserve normal AV conduction. On the basis of electrophysiologic study before operation, patients were classified as type A (ventriculoatrial [VA] intervals during tachycardia less than or equal to 40 ms) (seven patients) or type B (VA intervals greater than 40 ms) (three patients). Dual AV junctional pathways were demonstrable with single extrastimulus testing in seven patients before operation. Endocardial mapping during tachycardia at surgery revealed earliest atrial activation anteromedial to the AV node in type A patients and posterior to the node in the type B patients. The perinodal atrium in the region of earliest atrial activation during tachycardia was carefully disconnected from the AV node. After operation, AV junctional reentrant tachycardia was not inducible at comprehensive electrophysiologic study in any patient, and no clinical recurrences have occurred during a follow-up period of 2 to 14 months (mean 8 +/- 4). Normal AV conduction was preserved in all cases. Anterograde slow AV junctional pathway conduction was abolished in five of seven cases. Retrograde His to atrium conduction time was prolonged in type A patients but the capacity for retrograde VA conduction remained excellent. Retrograde His to atrium conduction was interrupted or severely compromised in the type B patients. These data show that there are at least two types of AV junctional reentry. Perinodal atrium appears to be part of the reentrant circuit in human AV junctional reentry. Although the most consistent effect of surgery was on the retrograde limb of the circuit, anterograde slow pathway conduction was also modified. AV junctional reentry is surgically curable with a high success rate.     

腺苷终止房室结和房室旁道折返性心动过速的心内电生理评价

探讨腺苷对阵发性室上性心动过速 (PSVT)的终止效果 ,观察PSVT终止后出现的心律失常。 2 5例患者 ,其中房室结折返性心动过速 (AVNRT) 11例、房室折返性心动过速 (AVRT) 14例 ,于心内电生理检查时 ,由前臂静脉注射(简称静注 )腺苷 6～ 12mg ,观察其终止心动过速的疗效和作用部位。结果 :11例AVNRT患者静注腺苷后 ,10例恢复窦性心律 ,其中 9例终止AVNRT于慢径前传 ,1例于快径逆传 ;14例AVRT患者静注腺苷后 ,14例均恢复窦性心律 ,终止AVRT 12例于房室结前传 ,2例于旁道逆传。心动过速终止后最常出现的心律失常是房性早搏和一过性Ⅰ和Ⅱ度房室阻滞 ;此外 ,室性早搏也很常见 ,部分患者可出现短阵室性心动过速 ,1例患者出现预激综合征伴心房颤动。结论 :腺苷终止PSVT有较高的成功率 ,但有潜在的促心律失常作用。