Ventriculoatrial Interval Research Articles

A conflict of evidence: AVNRT or junctional tachycardia?

Case presentation A 49-year-old woman who had previously undergone atrioventricular node (AVN) slow pathway cryoablation for typical AVN reentry tachycardia (AVNRT) presented with recurrent supraventricular tachycardia (SVT). During a transvenous electrophysiologic study, the SVT was reproducibly inducible with programmed atrial stimulation that resulted in an atrio-His (AH) interval “jump.” Other features of the SVT that were compatible with a recurrence of typical AVNRT included central atrial activation, AH interval HA (His-atrial) interval, and a septal ventriculoatrial interval of 40 ms. Despite several radiofrequency energy applications in the region between the os of the coronary sinus and the tricuspid valve annulus that caused slow junctional rhythm, the SVT remained inducible. A spontaneous premature atrial contraction (PAC) during tachycardia advanced the immediate His potential without terminating the SVT (Figure 1A). After this observation, atrial diastole in the SVT was scanned with paced PACs, and those delivered prior to His bundle depolarization had the same effect (Figure 1B). A paced PAC later in atrial diastole that was timed to His bundle refractoriness, however, advanced the subsequent His potential by 34 ms (Figure 2A), and a PAC delivered just after the His potential was still able to advance the subsequent His timing by 20 ms (Figure 2B). What is the mechanism of the SVT?

Tachycardia induction with ventricular extrastimuli differentiates atypical atrioventricular nodal reentrant tachycardia from orthodromic reciprocating tachycardia

Differentiating atypical atrioventricular nodal reentrant tachycardia (AVNRT) from septal orthodromic reentrant tachycardia (ORT(Septal)) is challenging in nonsustained tachycardia. When sustained, the postpacing interval minus tachycardia cycle length following entrainment (PPI(Entrainment) - TCL) and stimulation to atrial interval minus ventriculoatrial interval (Stim-A(Entrainment) - VA) are utilized. We hypothesized that the first tachycardia cycle after tachycardia induction with right ventricular apical extrastimulation would yield comparable information to entrainment, precluding the need for sustained tachycardia. Twenty-four patients with AVNRT (age 47 ± 18 years), 19 with ORT(Septal) (age 42 ± 17 years), and 15 with ORT over a left lateral accessory pathway (ORT(Left)) (age 41 ± 16 years) were included. The ventricular extrastimulus to atrial depolarization at tachycardia initiation (Stim-A(Initiation)) and tachycardia VA interval were measured to establish the Stim-A(Initiation) minus VA interval (Stim-A(Initiation) - VA). The ventricular extrastimulus to the subsequent right ventricular apical depolarization (postpacing interval at initiation, PPI(Initiation)) was utilized to obtain the PPI(Initiation) minus TCL (PPI(Initiation) - TCL). The AH interval associated with the PPI(Initiation) minus the AH in tachycardia was utilized to establish a corrected PPI(Initiation) minus TCL (cPPI(Initiation) - TCL). The intervals after tachycardia initiation were longer for AVNRT than for ORT: mean PPI(Initiation) - TCL (193 ± 44 vs 91 ± 73; P <.001), cPPI(Initiation) - TCL (174 ± 44 ms vs 88 ± 50 ms; P <.001), and Stim-A(Initiation) - VA (161 ± 45 ms vs 69 ± 53 ms; P <.001). The correlation coefficient for Stim-A(Initiation) minus VA against Stim-A(Entrainment) minus VA was 0.79 and for cPPI(Initiation) minus TCL against PPI(Entrainment) minus TCL was 0.71. cPPI(Initiation) minus TCL <115 ms or Stim-A(Initiation) - VA <85 ms was observed only in ORT. The converse was observed in AVNRT but also in ORT(Septal) over decremental accessory pathways and ORT(Left). Stim-A(Initiation) - VA < 85 ms or cPPI(Initiation) - TCL < 115 ms excludes AVNRT.

Paroxysmal Regular Supraventricular Tachycardia: The Diagnostic Accuracy of the Transesophageal Ventriculo-Atrial Interval

To establish the diagnostic accuracy of the transesophageal ventriculo-atrial (VA) interval in patients with paroxysmal supraventricular tachycardia (PSVT) and normal baseline electrocardiogram (ECG). The transesophageal VA interval during tachycardia was recorded in 318 patients (age 45 ± 17 years, 58% female) with PSVT and a normal surface ECG between attacks. Subsequently, all patients underwent an ablation procedure establishing the correct tachycardia diagnosis. AV nodal reentrant tachycardia (AVNRT), AV reentrant tachycardia through a concealed accessory pathway (AVRT), and ectopic atrial tachycardia (EAT) were found in 213, 95, and 10 cases, respectively. Receiver operating characteristic curve analysis identified an optimal cutoff for a binary categorization of AVNRT versus AVRT/EAT at ≤80 ms (area under the curve 0.891). Owing to a biphasic distribution, AVNRT was very likely at VA intervals ≤90 ms with a sensitivity, specificity, and positive predictive value (PPV) of 87%, 91%, and 95%. In the range 91-160 ms the corresponding values for AVRT were 88%, 95%, and 88% (90%, 99%, and 98% in male patients). In the small group with VA intervals >160 ms (n = 29), the diagnosis was less clear (PPV of 67% for AVNRT). In patients with sudden onset regular tachycardia and a normal ECG during sinus rhythm, a transesophageal VA interval of ≤80 ms has the highest diagnostic accuracy to diagnose AVNRT versus AVRT/EAT. Overall, the biphasic distribution of VA intervals suggests considering AVNRT at 90 ms and below and AVRT between 91 and 160 ms (in particular in male patients) while the diagnosis is vague at VA intervals above 160 ms.

Entrainment for Distinguishing Atypical Atrioventricular Node Reentrant Tachycardia From Atrioventricular Reentrant Tachycardia Over Septal Accessory Pathways With Long-RP Tachycardia

The response to right ventricular (RV) entrainment is useful to distinguish atypical AV node reentrant tachycardia from AV reentrant tachycardia using a septal accessory pathway. Whether entrainment can differentiate between AV node reentrant tachycardia and AV reentrant tachycardia in patients with long-RP tachycardia has not been systematically validated. Twenty-four patients with concealed septal accessory pathways who had an electrophysiology study between January 1, 2000, and January 1, 2010, were included (age, 38 ± 17 years; men, 17). Entrainment was performed from the RV apex pacing at cycle length 20 to 40 ms shorter than tachycardia cycle length (TCL). The mean TCL was 390 ± 80 ms, the mean AH interval during tachycardia was 151 ± 57 ms, and the mean ventriculoatrial (VA) time was 182 ± 103 ms. Twelve patients had typical accessory pathways (VA/TCL <40%), and 12 had slowly conducting accessory pathways (VA/TCL ≥ 40%). In all patients with typical accessory pathways, the postpacing interval minus the TCL (PPI-TCL) was <115 ms and the difference in the VA interval during pacing and tachycardia (StimA-VA) was <85 ms. On the other hand, in 6 of the 12 patients in the slowly conducting group, the PPI-TCL was >115 ms, and the StimA-VA was > 85 ms. Slowly conducting accessory pathways frequently yield RV entrainment criteria traditionally attributable to AV node reentry. Distinguishing AV node reentry from AV reentry in patients with long-RP tachycardia requires other criteria.

Differences in Ventriculoatrial Intervals During Entrainment and Tachycardia: A Simpler Method for Distinguishing Paroxysmal Supraventricular Tachycardia with Long Ventriculoatrial Intervals

Usefulness of the interval between the last pacing stimulus and the last entrained atrial electrogram (SA) minus the tachycardia ventriculoatrial (VA) interval in the differential diagnosis of supraventricular tachycardias with long (>100 ms) VA intervals has not been prospectively studied in a large series of patients. Our objective was to assess the usefulness of the difference SA-VA in diagnosing the mechanism of those tachycardias in patients without preexcitation. The results were compared with those obtained using the corrected return cycle (postpacing interval-tachycardia cycle length-atrioventricular [AV] nodal delay). We included 314 consecutive patients with inducible sustained supraventricular tachycardias with VA intervals >100 ms undergoing an electrophysiologic study. Atrial tachycardias were excluded. Tachycardia entrainment was attempted through pacing trains from right ventricular apex. The SA-VA difference and the corrected return cycle were calculated for every patient. Electrophysiologic study revealed 82 atypical AV nodal reentrant tachycardias (AVNRT) and 237 AV reentrant tachycardias (AVRT) using septal (n = 91) or free-wall (n = 146) accessory pathways (APs). A SA-VA difference >110 ms identified an atypical AVNRT with sensitivity, specificity, positive and negative predictive values of 99%, 98%, 95%, and 99.5%, respectively. Similarly, these values were 88%, 83%, 77%, and 92% for SA-VA difference <50 ms in identifying AVRT through a septal versus free-wall AP. The SA-VA difference showed higher accuracy in septal AP identification than that obtained using the corrected return cycle. The difference SA-VA provides a simpler electrophysiologic maneuver that reliably differentiates atypical AVNRT from AVRT regardless of concealed AP location.

Diastolic forward flow in the fetal main pulmonary artery and its implication for fetal cardiac cycle evaluation

To examine if the fetal main pulmonary artery diastolic forward flows (MPADFs) are detected consistently, if the waves from fetal MPADFs coincide with those from atrial contractions, and the reproducibility of the cardiac cycle measurements using this technique. Two examiners performed a fetal pulsed Doppler echocardiography of the four chamber (4CV), ductal arch (DA) and short axis (SA) views on 44 women with singleton pregnancies. Time intervals between atrial contraction peaks and those between MPADF peaks were compared. Atrioventricular (AV) and ventriculoatrial (VA) intervals were measured from MPADF waves in DA and SA views and compared between observers. Intraclass correlation coefficients (ICCs) were calculated as a measure of inter-observer reproducibility. In all observations, MPADFs were demonstrated. The mean time intervals between atrial contraction peaks from 4CV and those between MPADF peaks from DA and SA views were not significantly different. The mean AV and VA intervals were not significantly different between observers. Comparison of measurements of two observers had substantial agreements. Our data show that MPADFs can be found consistently and coincide with atrial contractions. As cardiac cycle measurements can be done with considerable reproducibility, this technique may be useful in assessing fetal cardiac cycle.

A supraventricular tachycardia with two atrial activation sequences: What is the mechanism?

Case presentation A 62-year-old woman presented with a history of paroxysmal regular palpitations. She did not have any structural heart disease. Treatment with antiarrhythmic drugs was stopped 5 half-lives before the electrophysiological study. Basic intervals were normal. On right ventricular (RV) apical pacing 500 ms in the basal state, the ventriculoatrial (VA) conduction pattern was distal to proximal in the coronary sinus (CS) and the earliest atrial signal (A) was in the His bundle electrogram (Figure 1A). The VA block cycle length was 410 ms. During isoprenaline infusion, the VA block cycle length was 300 ms, with the earliest A at the His and a CS atrial activation pattern that was proximal to distal (Figure 1B). During infusion of isoprenaline, a sustained narrow-QRS tachycardia with 1:1 VA relationship started spontaneously. The initiation was with a spontaneous atrial premature depolarization (Figure 2), and termination was with a ventricular signal (V). The tachycardia cycle length (VV) and HH interval were constant at 320 ms. However, the CS activation sequence was distal to proximal at times and proximal to distal at other times. The VA interval changed from 130 to 156 ms as the CS activation pattern switched from a distal-to-proximal pattern to a proximal-to-distal one (Figure 3). What is the tachycardia mechanism?

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.

Narrow Complex Tachycardia: What is the Mechanism?

This article reports an interesting case of a narrow complex tachycardia presenting the diagnostic dilemma of differentiating atrioventricular nodal reentrant tachycardia (AVNRT) from junctional tachycardia. It proposes delivering late-coupled premature atrial complexes during the tachycardia with short ventriculo-atrial interval as a diagnostic maneuver to differentiate AVNRT from junctional tachycardia in the electrophysiology laboratory. Treatments of these arrhythmias vary, and making the appropriate diagnosis of supraventricular tachycardia is essential to providing effective arrhythmia management.

Fetal arrhythmia: Prenatal diagnosis and perinatal management

The importance of managing fetal arrhythmia has increased over the past three decades. Although most fetal arrhythmias are benign, some types cause fetal hydrops and can lead to fetal death. With the aim of improving the outcome in such cases, various studies for prenatal diagnosis and perinatal management have been published. Detailed analysis of the type of arrhythmia in utero is possible using M-mode and Doppler echocardiography. In particular, a simultaneous record of Doppler waveform at the superior venous cava and the ascending aorta has become an important and useful method of assessing the interval between atrial and ventricular contractions. Common causes of fetal tachycardia (ventricular heart rate faster than 180 bpm), are paroxysmal supraventricular tachycardia (SVT) with 1:1 atrioventricular (AV) relation and atrial flutter with 2:1 AV relation. Of fetal SVT, short ventriculo-atrial (VA) interval tachycardia due to atrioventricular reentrant tachycardia is more common than long VA interval. Most fetuses with tachycardia are successfully treated in utero by transplacental administration of antiarrhythmic drugs. Digoxin is widely accepted as a first-line antiarrhythmic drug. Sotalol, flecainide and amiodarone are used as second-line drugs when digoxin fails to achieve conversion to sinus rhythm. Fetal bradycardia is diagnosed when the fetal ventricular heart rate is slower than 100 bpm, mainly due to AV block. Approximately half of all cases are caused by associated congenital heart disease, and the remaining cases that have normal cardiac structure are often caused by maternal SS-A antibody. The efficacy of prenatal treatment for fetal AV block is limited compared with treatment for fetal tachycardia. Beta stimulants and steroids have been reported as effective transplacental treatments for fetal AV block. Perinatal management based on prospective clinical study protocol rather than individual experience is crucial for further improvement of outcome in fetuses with tachycardia and bradycardia.

A single atrial extrastimulus during a short RP tachycardia

A 26-year-old female underwent electrophysiological study for recurrent palpitations. She was in sinus rhythm at baseline with cycle length (CL), atrial-His (AH), and His-ventricular (HV) intervals of 802, 87, and 48 ms, respectively. Ventricular pacing showed decremental ventriculoatrial (VA) conduction with concentric atrial activation. Parahisian pacing showed VA prolongation with loss of His capture consistent with nodal conduction. Rapid atrial pacing induced a short RP tachycardia with a CL of 580 ms that corresponded to the tachycardia documented clinically (Figure 1). The VA interval was 30 ms during the tachycardia with the earliest atrial activation at the proximal coronary sinus. The short VA interval is not consistent with atrioventricular reentrant tachycardia, but atrial tachycardia (AT), atrioventricular nodal reentrant tachycardia (AVNRT), and junctional tachycardia (JT) are possible differential diagnoses. During tachycardia, a single premature atrial complex (PAC) was introduced from the proximal coronary sinus (Figure 2). Based on the response to the extra stimulus, what is the most likely mechanism of the tachycardia? Commentary The short RP tachycardia with a very short VA interval can represent AT with a long atrioventricular (AV) delay, typical slow-fast AVNRT, or JT. Although JT is an uncommon tachycardia mechanism in this setting, it becomes a distinct possibility due to the long CL of the tachycardia.

Influence of Ventriculoatrial Timing on Hemodynamics and Symptoms During Supraventricular Tachycardia

Patients with reentrant supraventricular tachycardia (SVT) are often highly symptomatic and the mechanism of symptoms is not well understood. We hypothesized that variation in ventriculoatrial interval (QRS to P) modulates the left atrial pressure and symptoms during tachycardia. Three hundred twenty-six patients awaiting electrophysiological study completed a questionnaire regarding "neck pounding" or "shirt flapping" during tachycardia. Mean left atrial pressure was measured during simulated atrioventricular reentry tachycardia (AVRT) and atrioventricular nodal reentry tachycardia (AVNRT) in 18 patients. Pulmonary venous flow reversal was assessed using transesophageal echocardiography in 12 dogs when pacing at 220 bpm with different VA delays (0 to 250 ms). "Shirt flapping" is present more often during AVNRT than during AVRT (58.6% vs 43.8%, respectively, P < 0.05). Simulated AVNRT is associated with higher left atrial pressure compared with AVRT (19.4 +/- 4.8 mmHg vs 13.7 +/- 3.9 mmHg, respectively, P < 0.05). In dogs, pulmonary venous flow reversal during atrial systole was observed with significantly decreasing amplitude as VA delays increased: 668 +/- 167% at 0 ms; 492 +/- 138% at 100 ms; 278 +/- 148% at 180/ms; and 134 +/- 91% at 220 ms. "Shirt flapping" and "neck pounding" frequently occur during AVNRT. LA contractions during AV valve closure increase left atrial pressure and may explain differences in certain symptoms between AVNRT and AVRT.

Differential ventricular entrainment: A maneuver to differentiate AV node reentrant tachycardia from orthodromic reciprocating tachycardia

Distinguishing atrioventricular node reentry (AVNRT) from orthodromic reentrant tachycardia (ORT) utilizing an accessory pathway (AP) can sometimes be challenging. A pacing maneuver that reliably distinguishes between the two would be of value. This study sought to assess the utility of differential entrainment for the diagnosis of supraventricular tachycardia. Consecutive patients underwent prospective electrophysiological study of regular paroxysmal supraventricular tachycardia. Overdrive pacing with entrainment of tachycardia from each of the right ventricular apex and right ventricular base was performed. The post-pacing interval (PPI), PPI minus the tachycardia cycle length and corrected for AV node decrement (cPPI-TCL), and the ventriculoatrial (VA) interval (last RV pacing stimulus to last entrained high right atrial signal) were calculated at each site. Entrainment at both RV sites was achieved in 35 patients, 16 with typical AVNRT, 1 with atypical AVNRT, and 18 with ORT (13 left free wall, 3 right free wall, and 2 septal APs). The cPPI-TCL and VA intervals were significantly longer from base than apex in AVNRT (cPPI-TCL 61 ms longer, VA 38 ms longer, both P < .0001). There was no significant difference in differential entrainment intervals in patients with ORT. A differential cPPI-TCL >30 ms or VA interval >20 ms identified patients with AVNRT with a positive predictive value, negative predictive value, sensitivity, and specificity of 100%. Differential ventricular entrainment is a useful tool for diagnosing between AVNRT and ORT. A differential cPPI-TCL >30 ms or VA interval of >20 ms reliably predicts AVNRT.

Reversal of the Activation Sequence along the Coronary Sinus during RF Application with a Single Left Lateral Pathway:

A 16-year-old girl with a 4-year history of recurrent supraventricular tachycardia was referred for catheter ablation. A standard 12-lead electrocardiogram (ECG) during sinus rhythm revealed no abnormalities. Invasive electrophysiologic study was performed. Two quadripolar catheters were inserted via femoral venous access and placed in the high right atrium and right ventricle. A decapolar catheter was inserted via the right internal jugular vein into the coronary sinus with the proximal bipole at the os. Programmed atrial stimulation revealed a continuous atrioventricular (AV) node function curve. Right ventricular pacing at different cycle lengths (CLs) showed nondecremental ventriculoatrial (VA) conduction and the earliest atrial activation at the distal coronary sinus (CS). Rapid ventricular stimulation easily and repeatedly induced a regular narrow QRS complex tachycardia with a CL of 300 ms. The activation sequence on the CS leads during tachycardia is distal to proximal (Fig. 1). A diagnosis of orthodromic AV reentrant tachycardia (AVRT) using a left-sided free-wall accessory pathway (AP) was made. The retrograde transaortal approach was used. Due to difficulty in reaching a left anterolateral position beneath the mitral valve, the ablation catheter was positioned supra the mitral valve in a left anterolateral location. Radiofrequency (RF) energy was delivered to the earliest atrial activation site 4 mm above the distal CS catheter electrode at the mitral annulus. After 3 times RF energy application (10 second × 3) during sinus rhythm, another type of tachycardia was induced (Fig. 2). The catheter in CS were placed 1.5-cm distal to the original site. During tachycardia, CS3–4 electrodes showed double atrial potentials with an interval of 40 ms (Fig. 3). What has happened in Figures 2 and 3 and what is the mechanism of the changed tachycardia? Before ablation, tachycardia with a CL of 300 ms and the activation sequence on the CS leads was distal to proximal. After RF energy application, the earliest atrial activation was at the proximal CS electrogram with a reversal of activation sequence along the coronary sinus during tachycardia. The catheter in CS was placed 1.5-cm distal to the original site. CS3–4 electrodes showed double atrial potentials (↑↑) with the earliest atrial activation at the distal CS electrogram (↑) during tachycardia. During left lateral AP ablation, AVRT remained inducible with a change in the retrograde atrial activation sequence after application of radiofrequency energy can suggest a second AP. In our case, a reversal of activation sequence along the coronary sinus with the earliest atrial activation at the proximal CS electrogram was noted after three RF energy deliveries that did not eliminate AVRT. This phenomenon could be explained by the existence of a second septal or right side AP. The arguments against this mechanism are that the tachycardia CL and the VA interval at the ablation catheter remained unchanged during AVRT. This indicated the targeted AP has not been interrupted and there may be conduction block made by RF energy between the lateral AP insertion site and the distal CS electrode. Additionally, the CS3–4 electrodes presented double atrial potentials with the earliest atrial activation at the distal CS electrogram when more lateral positioning of the CS catheter. The double atrial potentials with an interval of 40 ms during AVRT provided direct evidence of intra-atrial conduction block along the mitral valve annulus. Luria et al. reported the phenomenon of intra-atrial conduction block in 11 patients during left AP ablation. They postulated that the area between the left inferior pulmonary vein and the inferolateral mitral annulus might serve as an mitral isthmus.1 Cheng et al. suggested a circumferential bundle of myocardial fibers with the minimum width of 0.8 cm in the inferoposterior left atrium may serve as the underlying anatomic substrate.2 Since the width was in the same order of magnitude as the typical RF lesion size, it is not surprising that a complete mitral isthmus block was made by a limited number of RF energy application, resulting a reversal of activation sequence along the coronary sinus as in this case. The ablation catheter was repositioned lateral to the site of the former attempts with atrial activation 25 ms earlier than the distal CS electrogram. A single application of radio frequency energy interrupted the tachycardia. Ventricular pacing at different CLs showed no VA conduction. Tachycardia could not be induced by programmed electrical stimulation both from the right atrium and ventricle.

Use of electroanatomic mapping in the assessment of atrial tachycardia aetiology

The present case report is of a 36-year-old man who had been symptomatic for frequent palpitations for 4 years after a prolonged febrile episode. The electrocardiogram on admission revealed an iterative supraventricular tachycardia at rate of 110 bpm, with ventriculoatrial interval of 180 ms and superior P-wave axis. Electroanatomic mapping showed substantially normal values in the right atrium other than an area along the posteroseptal region of the tricuspid annulus, with a low-voltage region that correlated with the area of earliest activation.

Differentiating Junctional Tachycardia and Atrioventricular Node Re-Entry Tachycardia Based on Response to Atrial Extrastimulus Pacing

The purpose of this study was to differentiate non-re-entrant junctional tachycardia (JT) and typical atrioventricular node re-entry tachycardia (AVNRT). JT may mimic AVNRT. Ablation of JT is associated with a lower success rate and a higher incidence of heart block. Electrophysiologic differentiation of these tachycardias is often difficult. We hypothesized that JT can be distinguished from AVNRT based on specific responses to premature atrial complexes (PACs) delivered at different phases of the tachycardia cycle: when a PAC is timed to His refractoriness, any perturbation of the subsequent His indicates that anterograde slow pathway conduction is involved and confirms a diagnosis of AVNRT. A PAC that advances the His potential immediately after it without terminating tachycardia indicates that retrograde fast pathway is not essential for the circuit and confirms a diagnosis of JT. This protocol was tested in 39 patients with 44 tachycardias suggesting either JT or AVNRT based on a short ventriculo-atrial interval and apparent AV node dependence. Tachycardias were divided into 3 groups: clinically obvious AVNRT, clinically obvious JT, and clinically indeterminate rhythm. In the 26 cases of clinically obvious AVNRT, the sensitivity and specificity of the test were 61% and 100%, respectively. In the 9 cases of clinically obvious JT, the sensitivity and specificity were 100% and 100%, respectively. In the 9 cases of clinically indeterminate rhythm, the technique indicated AVNRT in 1 patient and JT in 7 patients, and the test was indeterminate in 1 patient. The response to PACs during tachycardia can distinguish JT and AVNRT with 100% specificity in adult patients.

Abstract 637: Utilization of Retrograde Right Bundle Branch Block to Differentiate Atrio Ventricular Nodal from Accessory Pathway Conduction

Determining whether retrograde ventriculoatrial (VA) conduction is through the AV node (AVN) or an accessory pathway (AP) is critical for successful ablation of supraventricular tachycardia (SVT). With introduction of ventricular extrastimuli (VEST), retrograde right bundle branch block (retro RBBB) may occur and result in abrupt VH interval prolongation. We hypothesized when retrograde conduction is via an AP, VA interval change is less than VH interval change, whereas with retrograde AVN conduction, VA interval change is equal to or greater than VH interval change. We retrospectively reviewed the electrophysiology (EP) studies of patients undergoing ablation for AVNRT (n=55) or AVRT (n=50). The intracardiac electrograms were reviewed for induction of retro RBBB and change in VH and VA intervals during VEST. Parahisian pacing, decremental pacing, arrhythmia diagnosis and ablation outcomes were reviewed. All results were found to be reproducible between two independent observers with inter and intra observer reliability scores of 1.00 for identification of retro RBBB and greater than 0.85 for measurement of VH and VA intervals. Of 105 patients, 84 (80%) had evidence of induced retro RBBB during VEST. The average VH interval increase with induction of retro RBBB was 53.7 ms for patients with retrograde AP conduction and 54.4 ms for patients with AVN conduction (p=ns). The average VA interval increase with induction of retro RBBB was 13.6 ms with AP conduction and 70.1 ms with AVN conduction (P &lt; 0.001). All patients with a greater VH than VA interval change had a final diagnosis of AVRT and those with a VH change less than VA change had AVNRT, yielding sensitivity and specificity of 100%. Using a cutoff of 50 ms for change in VA interval with onset of retro RBBB to diagnose AVNRT accurately identified AVNRT in 100% and AVRT in 95%. Induction of retro RBBB during VEST is common during EP studies for SVT. The relative change in the VH and VA intervals during retro RBBB accurately differentiates retrograde AVN from retrograde AP conduction with strong predictive accuracy. The use of retro RBBB based intervals is a useful technique facilitating the diagnosis of SVT in the EP laboratory, even in the absence of inducible tachycardia.

Entrainment from the para-Hisian region for differentiating atrioventricular node reentrant tachycardia from orthodromic atrioventricular reentrant tachycardia

The difference between the stimulus-atrial and ventriculo-atrial intervals (SA-VA) and between the post-pacing interval and the tachycardia cycle length (PPI-TCL) during entrainment from the right ventricular apex distinguishes atrioventricular node reentrant (AVNRT) from orthodromic atrioventricular reentrant tachycardia (AVRT). We hypothesized that these features still apply when entrainment is performed from the para-Hisian region. Forty-seven supraventricular tachycardias (34 AVNRT/13 AVRT) were included. The SA-VA and PPI-TCL were obtained in all patients by using two right-sided diagnostic catheters. In 24 of them, these measurements were also performed upon His-bundle capture during entrainment. A paced QRS widening of >or=40 ms during entrainment, when compared with the tachycardia QRS width, identified absence of His-bundle capture, P < 0.001. A SA-VA >75 ms distinguished AVNRT from AVRT, P < 0.001 (sensitivity/specificity 97%/100%). A PPI-TCL >100 ms was diagnostic of AVNRT, P < 0.001 (sensitivity/specificity 97%/92%). Upon His-bundle capture, the SA-VA and PPI-TCL shortened in AVNRT (121 +/- 23 to 66 +/- 24 ms; 139 +/- 30 to 85 +/- 31 ms, respectively, P < 0.001) and no longer differentiated AVNRT from AVRT. Para-Hisian entrainment without His-bundle capture distinguishes AVNRT from AVRT with the advantage of using only two diagnostic catheters.

Orthodromic Atrioventricular Reentrant Tachycardia Masquerading as Atrial Fibrillation

A 17-year-old boy with a heart rate of 210 beats per minute was referred to our department for catheter ablation to treat his paroxysmal supraventricular tachycardia. The 12-lead electrocardiogram (ECG) was normal at baseline. Cardiac electrophysiologic study was performed after the informed consent was obtained. There was retrograde conduction via the atrioventricular (AV) node and the bypass tract. Irregular narrow QRS tachycardia was induced by programmed electrical stimulation (Fig. 1). During the tachycardia, there was a stable 1:1 ventriculoatrial (VA) relation and the same retrograde atrial activation sequence was seen with a fixed VA interval of 100 ms at the distal coronary sinus. Variations in the AH interval preceded the respective changes in the subsequent ventricular cycle length [the relative risk (RR) interval]. Catheter ablation of the concealed left free wall bypass tract was successfully done. Because there were AH jump and two AV nodal echo beats with the patient under isoproterenol infusion, ablation of the slow pathway was also performed. He remained free of palpitations during a 6-months follow-up period after the procedure. The differential diagnosis of irregular narrow QRS tachycardia includes atrial fibrillation, atrial tachycardia or flutter with variable AV block and a sinus rhythm with a double ventricular response. The dual AV node physiology and changes in the AV node refractoriness in this patient were attributed to the cycle length alternation during the atrioventricular reentrant tachycardia. Orthodromic AV reentrant tachycardia with marked cycle length alternations can mimic atrial fibrillation and it should be included in the differential diagnosis of irregular narrow QRS tachycardia.