AH Interval Research Articles

Long RP′ Tachycardia with an Initial A‐A‐V Activation Sequence: What Is the Mechanism?

A 79-year-old man with a history of multiple episodes of paroxysmal supraventricular tachycardia underwent electrophysiologic studies and a catheter ablation procedure. The 12-lead electrocardiogram during tachycardia showed a long RP′ tachycardia with negative P waves in leads II, III, and aVF. No dual anterograde atrioventricular (AV) nodal conduction was elicited by atrial extrastimulation. A narrow QRS tachycardia documented previously was reproducibly induced by atrial extrastimulation (Fig. 1A). During tachycardia, the HA and AH intervals measured 136 and 252 ms, respectively, and the earliest atrial activation was recorded at the ostium of the coronary sinus. Atrial extrastimuli delivered during the tachycardia did not reset the atrial cycle. Atrial overdrive pacing induced a second tachycardia with a similar atrial activation sequence and cycle length, and 2:1AV conduction (Fig. 1B). Ventricular overdrive pacing was delivered at a slightly shorter cycle length than the tachycardia (Fig. 2). Based upon these observations, what is the mechanism of tachycardia?

The Electrophysiological Characteristics of Slow/Fast Atrioventricular Nodal Reentrant Tachycardia with Left Posterior Nodal Extension

Introduction: In some slow/fast AVNRT patients, the left posterior nodal extension (LPNE) may form a part of antegrade slow pathway (SP) and ablation in the CS is necessary to eliminate the tachycardia. Methods and Results: We investigated electrophysiological properties of antegrade SP in 62 consecutive slow/fast AVNRT patients. In 10 patients (16.1%), ablation in the CS was necessary to eliminate the tachycardia (CS group), whereas ablation only at the conventional SP area was effective in other patients (83.9%, SP group). In CS group, AVNRT were induced with second AH jump-up phenomenon (N=6) and atrial double response (N=4) whereas, AVNRT were induced with single jump-up phenomenon in all of SP group patients. During AVNRT, there were no significant differences in tachycardia cycle length, AH and HA interval between the two groups. AH interval just before tachycardia induction (AH-t) was significantly longer in CS group than SP group (482±103 vs. 310±57 ms, p<0.01). An AH-t of 375 ms led to a sensitivity of 80% and a specificity of 84% for supposing that antegrade SP locates in CS. Conclusion: In slow/fast AVNRT patients, the long AH-t suggests that the LPNE participates the tachycardia initiation and ablation in the CS can eliminate the tachycardia.

Fast-Fast form of Atypical AV Nodal Reentrant Tachycardia: Incidence, Electrophysiological Characteristics and Results of Catheter Ablation

Background: Both typical and atypical AV nodal reentrant tachycardias (AVNRT) are usually amenable to slow pathway (SP) ablation at the inferoseptal areas. However, rare cases of unusual forms of AVNRT are resistant to SP ablation and their characteristics remain to be elucidated. Methods and Results: Total of 1252 AVNRTs induced in 950 cases were reviewed. Both anterograde and retrograde limbs of tachycardia circuit (TC) were classified into fast pathway (FP) or SP according to the A-H (AHI) and H-A intervals (HAI) during the tachycardia; the anterograde FP (AHI ⁄= 220 msec), and retrograde FP (HAI ⁄= 120 msec). Accordingly, the 1252 AVNRTs were classified into slow-fast (S/F: n=998), slow-slow (S/S: n=119), fast-slow (F/S: n=129) and fast-fast (F/F: n=6) forms. The F/F forms were induced by atrial or ventricular extrastimulation without associated jump-up in the AHI and HAI, and they were characterized by shorter tachycardia cycle length (260±55 msec), short AHI (153±39 msec) and HAI (107±19 msec) during the tachycardia and earliest retrograde atrial activation at the right superoseptum (n=2) or midseptum (n=4). The tachycardias were entrained from the RV and resumed with V-A-V sequence after cessation of entrainment pacing. SP ablation at right inferoseptum was unsuccessful in all F/F forms. Successful ablation was achieved at right superoseptum (n=2) or midseptum (n=4) without creating AV block. Conclusions: F/F forms of AVNRT not involving SP in TC were observed in 0.5% of all AVNRT. It was suggested the TC was smaller and confined to the superior part of AV nodal area in this extremely rare form of AVNRT.

A Case of Left Ventricular Noncompaction Accompanying Fasciculo-Ventricular Accessory Pathway and Atrial Flutter

Left ventricular hypertrabeculation/noncompaction (LVHT) is an uncommon type of genetic cardiomyopathy characterized by trabeculations and recesses within the ventricular myocardium. Frequently associated arrhythmias included atrial fibrillation, ventricular arrhythmias, atrioventricular block, and Wolff-Parkinson-White syndrome. A 29-year-old male presented with palpitations and shortness of breath. The ECG showed pre-excitation and anteroseptal accessory pathway was suspected. The echocardiogram revealed prominent trabeculations and deep recesses in the left ventricles. The recesses were perfused by intraventricular flow. During the echocardiographic examination, tachycardia developed spontaneously. The ECG showed wide complex tachycardia and the QRS morphology was similar to that of sinus rhythm. An electrophysiologic study was performed. Decremental atrial pacing caused prolongation of both AH and AV intervals in parallel. The HV interval and the degree of preexcitation remained unchanged from both right atrial and coronary sinus pacing with atrial extrastimuli. The His bundle pacing failed to normalize the QRS width. A diagnosis of fasciculo-ventricular accessory pathway was made. Decremental pacing on the proximal coronary sinus area induced typical atrial flutter, which was identical to the clinical tachycardia. A line of block was made across the cavo-tricuspid isthmus (CTI). A rare presentation of LVHT with fasciculo-ventricular accessory pathway and atrial flutter was successfully treated with conventional CTI block.

210 An unusual case of Mahaim fibers in hypertrophic cardiomyopathy

The coexistence of Mahaim fibbers (MF) and hypertrophic cardiomyopathy (HCM) is exceptional. We report an unusual case of a young female patient presenting with HCM and MF. A 17 y/o woman was referred in 1998 for a familial HCM screening. She had no symptoms; her surface EKG revealed a preexcitation suggesting a right anteroseptal WPW syndrome. The transthoracic echocardiogram (TTE) demonstrated an asymmetric septal HCM without LV outflow tract (LVOT) obstruction. The electrophysiological study (EPS) demonstrated the presence of MF (normal AH interval, a short and fixed HV interval and atrial pacing produced AH prolongation without change of preexcitation degree, indicating fasciculo-ventricular MF). Eight years later (25 y/o) while the patient was doing well, the ECG was similar and TEE demonstrated the same aspect of asymmetric septal HCM without obstruction. Three months later the patient was pregnant and gave birth to a healthy baby. (During pregnancy: Delta wave was present and there was no LVOT obstruction). After delivery, Surprisingly there was no more preexcitation on her ECG and the TEE demonstrated now a significant LVOT obstruction with a systolic anterior motion of the mitral valve and an LVOT gradient of 36 mmHg. A second EPS was performed in 2008 and showed no more preexcitation. We speculate the hypothesis that FV fiber played in this case a similar pathogenic role as does the apical right ventricular pacing when it is used to decrease LVOT gradient in patients with HCM. This case deserves to be reported because the association of MF and HCM is rare (only 3 cases reported in english litterature), the disappearance of MF during pregnancy has never been reported and the hypothesis that the RV preexcitation via FV Mahaim fiber played a role in decreasing LVOT gradient in this patient with HCM.

244 High incidence of AV block and prophylactic pacing in familial amyloid polyneuropathy

Familial amyloid polyneuropathy (FAP) is an autosomic dominant inherited disease. FAP cardiopathy is characterized by conduction disorders, denervation, and cardiac infiltration. Because of the risk of high degree atrioventricular (AV) block and sudden death, prophylactic pacing can be suggested when there is evidence of amyloid infiltration of the AV conduction pathways. Our purpose was to estimate prevalence of AV block and pacing dependence for high risk FAP patients. In a cohort of 51 FAP patients, we performed standard ECG and electrophysiological study. Patients with conduction disorders underwent prophylactic pacing. During follow up, AV conduction was studied by using data from the Holter memories of pacemakers. Baseline characteristics of the patients are summarized on table 1. During the follow up, permanent high degree AV block occurred in 23.5% of the patients (12/51)(cf. fig. 1). Average percentage was 23 ± 35% for ventricular pacing and 18 ± 24% for atrial pacing. Paroxystic AV block was recorded for all patients but 3 (94%). Prevalence of AV conduction disorders was 283 ± 465 events per month (epm) and was distributed in 14 ± 46 epm for third degree AV block, 195 ± 386 epm for second degree AV block, 73 ± 225 epm for first degree AV block and 0.2 ± 0.7 epm for pauses. During the study, sustained atrial arrhythmias occurred in three patients. No sustained ventricular arrhythmia was recorded. Patients with FAP cardiomyopathy present high incidence of AV blocks. For FAP patients with involvement of the AV conduction pathway, prophylactic pacemaker insertion should be performed. Incidence of permanent AV block Table 1: Baseline characteristics Mean ± SD age (years) 54 ± 13 % of men 64.7% Lenght of fu (months) 34 ± 33 % Val30 Met 64% Surface ECG Conduction disorders 74% AVB type 1 38% PR interbal (ms) 191 ± 41 QRS interval (ms) 94 ± 21 Electrophysiological study corrected sinus recovery time (ms) 546 ± 438 AH interval (ms) 117 ± 43 HV interval (ms) 68 ± 11 Anterior Wenckebach point (bpm) 128 ± 33

188 Characteristics and treatment of inducible flutter associated with typical atrioventricular reentrant nodal tachycardia in pediatric patients

Atrioventricular reentrant nodal tachycardia (AVNRT) and right atrial flutter could have a common area in the perinodal myocardium. We studied the occurrence of inducible flutter in pediatric patients with AVNRT or atrioventricular reentrant tachycardia (AVRT). Moreover we studied the effect of slowpathway ablation on flutter inducibility. We included 110 children (mean age = 12 ± 4 years), without underlying heart disease, previous ablation or history of atrial flutter or fibrillation, who were referred for supraventricular tachycardia ablation. Thirty-seven (34%) patients had AVNRT and 73 (66%) had AVRT. A standardized protocol of flutter induction was used in all these patients at baseline and after ablation. All patients with AVNRT had immediate successfull slowpathway ablation. Ninety-nine percent of patients with AVRT had immediate successfull accessory pathway ablation. Pediatric patients with AVNRT had inducible flutter in 14% of cases whereas no patient with AVRT had inducible flutter (p = 0.001). After slowpathway ablation, including a line between the low tricuspid valve and the coronary sinus ostium, no inducible flutter was found in the AVNRT and AVRT group. In the AVNRT group, patients with inducible flutter had shorter baseline AH interval (67 ± 14 vs. 88 ± 21 ms, p = 0.04), AV Wenckebach (294 ± 67 vs. 404 ± 101 ms, p = 0.02) and VA Wenckebach (298 ± 48 vs. 403 ± 98 ms, p = 0.04) compared to other AVNRT patients. These results suggest that AVNRT and right atrial flutter could share a common area located in the perinodal myocardium. However the slowpathway may not correspond to the slow conduction area during atrial flutter. Large slowpathway ablation could abolish flutter inducibilty.

Atrioventricular Nodal Reentrant Tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT) represents the most common regular supraventricular arrhythmia in humans.1 The precise anatomic site and nature of the pathways involved have not yet been established, and several attempts to provide a reasonable hypothesis based on anatomic or anisotropic models have been made.2 There has been considerable evidence that the right and left inferior extensions of the human atrioventricular (AV) node and the atrionodal inputs they facilitate may provide the anatomic substrate of the slow pathway, and a comprehensive model of the tachycardia circuit for all forms of AVNRT based on the concept of atrionodal inputs has been proposed.2 Still, however, the circuit of AVNRT remains elusive. Recently, time-honored conventional schemes for the diagnosis and classification of the various forms of the arrhythmia have been refuted in part by evolving evidence. Recognition of the various types of AVNRT is important, however, to expedite diagnosis and allow implementation of appropriate ablation therapy without complications. We present an update on AVNRT with a particular emphasis on electrophysiological criteria used for the differential diagnosis of regular, supraventricular tachycardias. Typically, AVNRT is a narrow-complex tachycardia, ie, QRS duration <120 ms, unless aberrant conduction, which is usually of the right bundle-branch type, or a previous conduction defect exists. Tachycardia-related ST depression and RR-interval variation may be seen. RR alternans in AVNRT has been attributed to the proposed model of a figure of 8 reentry with continuous crossing over of antegrade activation through an inferior input to the contralateral superior input via the node.2 In the typical form of AVNRT (slow-fast), abnormal (retrograde) P′ waves are constantly related to the QRS and in the majority of cases are indiscernible or very close to the QRS complex (RP′/RR <0.5). Thus, P′ waves are either masked by the QRS complex or …

Preexcitation unmasked after successful accessory atrioventricular connection ablation: What is the mechanism?

Case presentation A 19-year-old man with a history of palpitations and no underlying structural heart disease underwent electrophysiologic diagnostic evaluation for possible catheter ablation of the arrhythmogenic substrate responsible for the palpitations. Twelve-lead ECG showed ventricular preexcitation consistent with a left free-wall accessory atrioventricular (AV) connection (Figure 1A). Electrophysiologic study was performed using standard methodology with catheters in the right ventricular apex (RVA), high right atrium (HRA), His bundle, and coronary sinus. Basic intervals during sinus rhythm were as follows: PR interval 110 ms, AH interval 40 ms, HV interval 0 ms, and QRS duration 110 ms. Ventricular preexcitation was maximal during incremental atrial pacing (Figure 1B). Ventricular pacing showed nondecremental and eccentric retrograde ventriculoatrial (VA) conduction. HRA programmed stimulation induced a minimally preexcited AV reciprocating tachycardia with eccentric VA conduction (Figures 1B and 2A). Measurements of the tachycardia were as follows: AH interval 238 ms, HV interval 16 ms, and VA interval 151 ms. Retrograde conduction was due to a left free-wall accessory AV connection. However, during tachycardia, the HV interval was shorter than expected (Figure 2A). We performed radiofrequency catheter ablation of the left freewall accessory AV connection with subsequent VA dissociation during RVA pacing. After the successful ablation, a short HV interval and ventricular preexcitation of possible septal origin were apparent (Figures 1C and 2B). Atrial pacing showed rateependent prolongation of the AH interval with fixed HV nterval. Intravenous adenosine bolus showed blocked P aves with no change in degree of ventricular preexcitation.

Gender Differences in the Clinical Characteristics and Atrioventricular Nodal Conduction Properties in Patients With Atrioventricular Nodal Reentrant Tachycardia

The detailed electrophysiological characteristics of the gender differences associated with atrioventricular nodal reentrant tachycardia (AVNRT) have not been clarified. This study investigated the gender-related electrophysiological differences in a large series of patients undergoing radiofrequency catheter ablation. A total of 2,088 consecutive AVNRT patients (men/women 869/1,219) who underwent catheter ablation were enrolled in this study. We evaluated the gender differences in their electrophysiological characteristics. Women had a significantly younger age of onset, higher incidence of multiple jumps, shorter AH interval, atrial effective refractory period (ERP), anterograde fast pathway ERP, anterograde slow pathway ERP, and retrograde slow pathway ERP, and longer ventricular ERP than men. The incidence of baseline ventriculoatrial dissociation was lower in women than in men. Women needed less isoproterenol/atropine to induce AVNRT. No gender differences in the radiation exposure time, procedure time, complication rate, acute success rate, or second procedure rate were noted. Both typical and atypical AVNRT were more predominant in women. In the patients with atypical AVNRT, there was no significant gender difference in incidence of baseline ventriculoatrial dissociation; however, the retrograde slow pathway ERP was significantly shorter in women than in men. Women of premenopausal age (≤50 years old) had a significantly higher incidence of anterograde multiple jumps and a retrograde jump phenomenon, and a shorter anterograde slow pathway ERP and retrograde slow pathway ERP than those of women over 50 years old. Gender differences in the anterograde and retrograde AV nodal electrophysiology were noted in the patients with AVNRT.

Cardiac conduction disturbances and differential effects on atrial and ventricular electrophysiological properties in desmin deficient mice

Desmin mutations in humans cause desmin-related cardiomyopathy, resulting in heart failure, atrial and ventricular arrhythmias, and sudden cardiac death. The intermediate filament desmin is strongly expressed in striated muscle cells and in Purkinje fibers of the ventricular conduction system. The aim of the present study was to characterize electrophysiological cardiac properties in a desmin-deficient mouse model. The impact of desmin deficiency on cardiac electrophysiological characteristics was examined in the present study. In vivo electrophysiological studies were carried out in 29 adult desmin deficient (Des-/-) and 19 wild-type (Des+/+) mice. Additionally, epicardial activation mapping was performed in Langendorff-perfused hearts. Intracardiac electrograms showed no significant differences in AV, AH, and HV intervals. Functional testing revealed equal AV-nodal refractory periods, sinus-node recovery times, and Wenckebach points. However, compared to the wild-type situation, Des-/- mice were found to have a significantly reduced atrial (23.6+/-10.3 ms vs. 31.8+/-12.5 ms; p=0.045), but prolonged ventricular refractory period (33.0+/-8.7 ms vs. 26.7+/-6.5 ms; p=0.009). The probability of induction of atrial fibrillation was significantly higher in Des-/- mice (Des-/-: 38% vs. Des+/+: 27%; p=0.0255), while ventricular tachycardias significantly were reduced (Des-/-: 7% vs. Des+/+: 21%; p<0.0001). Epicardial activation mapping showed slowing of conduction in the ventricles of Des-/- mice. Des-/- mice exhibit reduced atrial but prolonged ventricular refractory periods and ventricular conduction slowing, accompanied by enhanced inducibility of atrial fibrillation and diminished susceptibility to ventricular arrhythmias. Desmin deficiency does not result in electrophysiological changes present in human desminopathies, suggesting that functional alterations rather than loss of desmin cause the cardiac alterations in these patients.

Functional atrioventricular conduction block in an elderly patient with acquired long QT syndrome: elucidation of the mechanism of block

The long QT syndrome (LQTS) is occasionally complicated by impaired atrioventricular (AV) conduction. This form of LQTS can manifest before birth or during neonatal life, and no previous report has demonstrated LQTS complicated by impaired AV conduction in elderly patient. This case report describes an elderly patient with an acquired form of LQTS who developed ventricular fibrillation that was successfully defibrillated during admission to the hospital. Electrophysiologic study demonstrated that HV interval was 38 milliseconds and QT interval was 635 milliseconds during sinus rhythm cycle length of 1167 milliseconds. 1:1 AV conduction was maintained to a pacing cycle length of 545 milliseconds with an AH interval of 144 milliseconds, HV interval of 44 milliseconds, and right ventricular monophasic action potential duration of 360 milliseconds. However, 2:1 HV block developed at a pacing cycle length of 500 milliseconds. Intravenous administration of mexiletine decreased the cycle length of developing HV block to 360 milliseconds.

A Case of Radiofrequency Catheter Ablation of Atrioventricular Nodal Reentrant Tachycardia Using Transseptal Approach, Guided by Electro-Anatomical Mapping System

A 65 year-old female was admitted to our hospital because of syncope. She has been previously diagnosed with dilated cardiomyopathy. Twelve-lead electrocardiogram (ECG) presented narrow QRS tachycardia. Electrophysiological study and radiofrequency catheter ablation was performed. Under isoproterenol infusion, supraventricular tachycardia (SVT) was easily induced followed by critical AH interval. The mechanism of SVT was diagnosed with slow-fast atrioventricular nodal reentrant tachycardia (AVNRT). We tried slow-pathway ablation from venous approach targeted at the triangle of Koch using electrogram guide and anatomical approach. Slow-pathway conduction was not eliminated, however, and SVT still could be easily induced. Therefore we delivered radiofrequency (RF) from the left atrial (LA) septum by transseptal approach using an electro-anatomical mapping (EAM) system. After RF application at mid-septum from the LA, the slow-pathway conduction was modified and SVT could not be induced.

Recurrent syncope associated with a distinct ECG pattern consisting of short QT interval, early repolarization and atrioventricular block

A 17-year-old apparently healthy individual with recurrent syncopal episodes during walking was referred to our institution for further evaluation. Baseline ECG showed sinus rhythm with prominent J-waves and ST-segment elevation and a short QT interval of 320 ms (Fig. 1). The corrected QT (QTc) interval was 283, 295 and 288 m using the Bazett’s, the Fredericia’s and the Framingham’s formula, respectively. There was no family history of sudden cardiac death. Transthoracic echocardiography revealed a structurally normal heart. Exercise treadmill test failed to induce any arrhythmic or ischemic events, while the early repolarization features (J-waves and ST-segment elevation) were normalized. A drug-free tilt table test was negative for neurocardiogenic syncope. Holter monitoring revealed several asymptomatic episodes of abrupt advanced AV block during day and night, with a maximum pause of 4.2 s (Fig. 2). No episodes of atrial or ventricular arrhythmic events were recorded. Late potentials (RMS-40, LAS-40) as detected and calculated by signal-averaged ECG were positive. Sodium channel blocking test with procainamide (10 mg/kg) failed to induce the diagnostic type 1 ECG pattern of Brugada syndrome (BS) in the right precordial leads. Quinidine administration (900 mg) normalized the absolute QT and QTc values to 380 and 425 m, respectively. Electrophysiological study (EPS) demonstrated normal AH (110 ms) and HV (49 ms) intervals. Right ventricular programmed stimulation at three basic cycle lengths (600, 500 and 430 m) with up to three extra stimuli failed to induce any ventricular arrhythmias. The atrial and ventricular refractory periods were 190 and 200 ms, respectively. No atrial arrhythmias were induced and no episodes of AV block were documented during EPS. A dual-chamber cardioverter defibrillator (ICD) was implanted. The patient was asymptomatic after a 12-month follow-up period. Genomic DNA was prepared from peripheral blood lymphocytes using standard methods. The entire open reading frame of the KCNQ1, KCNH2 and SCN5A genes was analyzed. The following non-coding genetic variants were identified: KCNQ1 (1638 G [ A S546S), KCNH2 (G3152 ? 22 G [ A) and SCN5A (5457 C [ T D1819D, 3183 G [ A E1061E). The KCNJ2, CACNA1C and CACNB2 genes were not screened for mutations.

Cardiac electrophysiological effects of remifentanil: study in a closed-chest porcine model

Remifentanil has been implicated as causing intraoperative bradyarrhythmias, but little information is available regarding its cardiac electrophysiological effects. Thus, we evaluated the cardiac electrophysiological properties before and after remifentanil in a closed-chest porcine model. Eighteen Landrace-Large pigs were premedicated with ketamine and anaesthetized with propofol (4.5 mg kg(-1) bolus followed by 13 mg kg(-1) h(-1)). After instrumentation, an electrophysiological evaluation was performed under propofol and repeated after remifentanil (bolus of 1 microg kg(-1), followed by an infusion of 0.5 microg kg(-1) min(-1)). We evaluated sinus node function [sinus node recovery time (SNRT) and sinoatrial conduction time (SACT)], atrioventricular (AV) nodal function [AH intervals during sinus rhythm (SR) and atrial pacing, Wenckebach cycle length (WCL), and effective refractory periods (ERP)], atrial, His-Purkinje, and ventricular conduction and refractoriness. Significant changes between 'propofol protocol' and 'propofol+remifentanil protocol' were evaluated. Remifentanil caused a significant increase in sinus cycle length (21%, P=0.001) and a significant prolongation of SNRT (43%, P=0.001), corrected SNRT (136%, P=0.003), SACT (40%, P=0.005), AH interval during SR (17%, P=0.02), AH interval during atrial pacing (25%, P=0.01), and ventricular ERP (12%, P=0.004). There was a tendency towards a prolongation of WCL and AV nodal refractoriness. Similar significant changes were observed in a reference group of seven animals in which sevoflurane was used instead of propofol. No significant changes were observed in atrial parameters, His-Purkinje function, parameters of intraventricular conduction, and QT intervals. Remifentanil depresses sinus node function and most parameters of AV nodal function. This contributes to an explanation for clinical observations of remifentanil-related severe bradyarrhythmias.

YIA Abstracts: Best abstracts on clinical studies

YIA Abstracts: Best abstracts on clinical studies

Abstract 5678: Fast-Fast Form of Atypical AV Nodal Reentrant Tachycardia: Incidence, Electrophysiological Characteristics and Results of Catheter Ablation

Both the typical (slow-fast (S/F)) and atypical (slow-slow (S/S) and fast-slow (F/S)) forms of the AV nodal reentrant tachycardias (AVNRT) are usually amenable to the classical slow pathway (SP) ablation at the inferoseptal atrial region. However, rare cases of unusual forms AVNRT do not involve an SP in the tachycardia circuits (TC), and they are resistant to the classical SP ablation. The characteristics of the atypical AVNRTs not involving an SP in the TCs remain to be elucidated. A total of 1252 AVNRTs induced during the electrophysiological study in 950 cases were analyzed. Both the anterograde and retrograde limbs of the TC were classified into the fast pathway (FP) or SP according to the A-H (AHI) and H-A intervals (HAI) during the tachycardia; the anterograde FP: AHI of &lt;220 ms, anterograde SP: AHI of ≥220 ms, retrograde FP: HAI of &lt;120 ms, and retrograde SP: HAI of ≥120 ms. Accordingly, each tachycardia was classified into one of the S/F, S/S, F/S and fast-fast (F / F) forms . There were 998 S/F forms (79.7%), 119 S/S forms (9.5%), 129 F/S forms (10.3%) and 6 F / F forms (0.5%). The F / F forms were induced by atrial or ventricular extrastimulation without an associated jump-up in the AHI and HAI, and they were characterized by a shorter tachycardia cycle length (260±55 ms), short AHI (153±39 ms) and HAI (107±19 ms) during the tachycardia, earliest retrograde atrial activation (ERAA) at the right superoseptum (n=2) or midseptum (n=4), and 2nd degree AV block without a tachycardia interruption. The retrograde atrial activation sequence during the F / F forms was identical to that during ventricular pacing. The tachycardias could be entrained from the RV, and they resumed with a V-A-V sequence after the cessation of the entrainment pacing. The classical SP ablation at the right inferoseptal region was unsuccessful in all 6 cases with the F / F forms . The successful ablation was achieved at the right superoseptum (n=2) or midseptum (n=4) without creating AV block in all 6 cases. The F / F forms of atypical AVNRT not involving a classical SP in the TC were observed in 0.5% of all AVNRT cases. The results of this study suggested that the TC was smaller and confined to the superior part of the AV nodal area in this extremely rare form of AVNRT.

Antifibrillatory Actions of Cisatracurium: An Atrial Specific M2 Receptor Antagonist

Muscarinic receptor antagonists are proposed to prevent atrial fibrillation (AF), but also facilitate AV conduction, limiting clinical usefulness. Cisatracurium, a neuromuscular blocker, was administered to anesthetized dogs (0.05-0.8 mg/kg IV) and was administered to superfused pulmonary vein (PV) tissues in vitro. Dose-dependent suppression of AF induced by premature atrial stimuli was observed under control conditions (n = 3), right vagus nerve stimulation (n = 7), and anterior right ganglionated plexus stimulation (n = 3). AF was prevented (P < 0.0001) concurrent with suppression of the decreased atrial MAP duration/ERP accompanying vagus nerve stimulation without altering AH intervals or sinus cycle length. Although atropine (0.001-0.016 mg/kg, n = 4) suppressed AF (P < 0.04) in association with suppression of atrial MAP shortening induced by vagus nerve stimulation, atropine also prevented sinus cycle length and AH interval prolongation with vagus nerve stimulation, and decreased AV effective and functional refractory periods. In vitro, both cisatracurium and atropine prevented (1) action potential shortening produced by acetylcholine administration and (2) action potential shortening and arrhythmia triggering within PV sleeves produced by local autonomic nerve stimulation, atropine producing competitive inhibition, and cisatracurium producing noncompetitive M(2) muscarinic receptor blockade. Cisatracurium demonstrates a dose-dependent (1) suppression of AF and atrial action potential shortening accompanying vagus nerve stimulation without facilitating sinus or atrioventricular nodal function and (2) noncompetitive blockade of action potential shortening and triggered firing induced in isolated PVs by local autonomic nerve stimulation. The data are consistent with allosteric binding of cisatracurium to the M(2) muscarinic receptor in canine atrium.

Junctional rhythm associated with ventriculoatrial block during slow pathway ablation in atypical atrioventricular nodal re-entrant tachycardia

We assessed responses to slow pathway ablation with respect to the appearance of ventriculoatrial (VA) block during junctional rhythm in both typical and atypical types of atrioventricular nodal re-entrant tachycardia (AVNRT). The 31 subjects included 16 patients with slow-fast type of typical AVNRT and 15 patients with atypical AVNRT (9 patients with fast-slow type and 6 patients with slow-slow type). During atypical AVNRT, the HA interval was prolonged (>70 ms) and the earliest atrial activation was located around the coronary sinus (CS) ostium. The difference in atrial activation times at the CS ostium and His-bundle area [A(CS-His)] during AVNRT was measured. Slow pathway ablation was performed using a classical electro-anatomical approach. In typical AVNRT, A(CS-His) was -21.3 +/- 3.4 ms, and the HA interval was 34 +/- 14 ms. During slow pathway ablation, all patients with typical AVNRT had junctional rhythm with retrograde atrial conduction. In contrast, in patients with atypical AVNRT, A(CS-His) was 12 +/- 19.3 ms and the HA interval was 189 +/- 77 ms. In 13 of the 15 patients with atypical AVNRT, slow pathway ablation induced junctional rhythm, which was not associated with retrograde atrial conduction. After ablation, AVNRT became non-inducible and antegrade atrioventricular (AV) conduction was preserved in all patients. In patients with atypical AVNRT, junctional rhythm with VA block during slow pathway ablation is commonly observed and indicates the success of the ablation of retrograde slow pathway conduction, but has no relation to the risk of subsequent AV block. During junctional rhythm, occasional appearance of the sinus beats with intact antegrade AV conduction is essential for safety of ablation.

Association of Sinus Node Dysfunction, Atrioventricular Node Conduction Abnormality and Ventricular Arrhythmia in Patients With Kawasaki Disease and Coronary Involvement

This study was performed to investigate the incidence of arrhythmias in patients with Kawasaki disease (KD). Electrophysiologic studies (EPS) were performed in 40 patients (mean age: 10.3+/-5.1 years; 30 males, 10 females) with KD who had severe to moderate coronary artery disease. Clinical arrhythmias were documented in 4 patients (premature ventricular contractions, ventricular tachycardia, atrioventricular block, and ventricular fibrillation). Dual atrioventricular nodal pathways were demonstrated in 3 patients. Nonsustained atrial fibrillation was induced in 1 patient. The AH interval was prolonged in 2 patients. The Wenckebach rate was 164+/-37 beats/min, and 4 of the patients had a decreased Wenckebach rate. The maximum and corrected sinus node recovery times were 997+/-257 ms and 281+/-130 ms, respectively, and 7 patients were thought to be abnormal. The sino-atrial conduction time was 108+/-64 ms, and 2 patients had prolonged conduction times. Although there was no relationship between coronary stenosis or obstruction and the EPS parameters, the incidence of abnormal sinus node and atrioventricular node function is apparently higher in KD patients than in the normal population. These functional abnormalities may possibly be caused by myocarditis or an abnormal microcirculation in the sinus node and atrioventricular node artery. In some patients, myocardial ischemia may provoke malignant ventricular arrhythmia.