Single Ventricular Extrastimuli Research Articles

Response to single ventricular extrastimuli during a wide complex tachycardia: What is the mechanism?

A 29-year-old woman with recurrent palpitations was referred for electrophysiological study of wide QRS complex tachycardia. She had no structural heart disease. Baseline ECG showed no ventricular pre-excitation, and baseline HV interval was 40 ms. Dual atrioventricular (AV) nodal physiology was demonstrated. This article is protected by copyright. All rights reserved.

Reduced heart rate response after premature ventricular contraction depending on severity of atrial fibrillation symptoms – Analysis on heart rate turbulence in atrial fibrillation patients

BackgroundThe severity of symptoms during atrial fibrillation (AF) may be influenced by heart rate and blood pressure variation, due to irregular beats and the related adaptations in baroreflex sensitivity. This study investigated whether heart rate turbulence (HRT) as a reflection of baroreflex sensitivity is related to symptom severity during AF. MethodNinety-seven patients (pts) who underwent electrophysiological study were enrolled. Consecutive 56 pts had paroxysmal AF (21 with milder symptoms [EHRA I or II; Group-M], 35 with severe symptoms [EHRA III or IV; Group-S]), and 41 age-matched controls without AF were included. After delivering a single ventricular extrastimulus during sinus rhythm and repeating the process 10 times, the quantification of HRT was performed by measuring turbulence onset (TO: heart rate acceleration) and turbulence slope (TS: rate of heart rate deceleration). ResultsGroup-M pts showed significantly diminished TO as compared to controls and Group-S pts (P = 0.012). There was no significant difference of the TS between the 3 groups. Given that a TO ≥ 0% or TS ≤ 2.5 ms/RR was considered abnormal, Group-M pts showed significantly higher incidences of abnormal HRT as compared to controls and Group-S pts (71% vs 40% vs 21%, respectively, P = 0.0012). Regression analysis demonstrated an independent and significant association between a diminished TO and milder AF symptoms (P < 0.05). ConclusionsThe usual heart rate acceleration after premature ventricular contraction is significantly diminished in pts with milder AF symptoms as compared to pts with severe AF symptoms. The mechanism of association between this diminished response and symptoms should be further investigated.

Unusual Termination by Single Ventricular Extra-Stimulus Applied during Atrioventricular Reciprocating Tachycardia: What Is the Mechanism?

Pacing and Clinical ElectrophysiologyVolume 37, Issue 6 p. 774-776 EP ROUNDS Unusual Termination by Single Ventricular Extra-Stimulus Applied during Atrioventricular Reciprocating Tachycardia: What Is the Mechanism? YUKINORI IKEGAMI M.D., YUKINORI IKEGAMI M.D. Department of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, JapanSearch for more papers by this authorSEIJI TAKATSUKI M.D., Corresponding Author SEIJI TAKATSUKI M.D. Department of Cardiology, Keio University School of Medicine, Tokyo, JapanAddress for reprints: Seiji Takatsuki, M.D., Department of Cardiology, Keio University Hospital, 35 Shinanomachi, Shinjukuku, Tokyo, 160-8582 Japan. Fax: 81-3-5363-3875; e-mail: [email protected]Search for more papers by this authorTAKUO YOSHIDA M.D., TAKUO YOSHIDA M.D. Department of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, JapanSearch for more papers by this authorYUKIHIKO MOMIYAMA M.D., YUKIHIKO MOMIYAMA M.D. Department of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, JapanSearch for more papers by this author YUKINORI IKEGAMI M.D., YUKINORI IKEGAMI M.D. Department of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, JapanSearch for more papers by this authorSEIJI TAKATSUKI M.D., Corresponding Author SEIJI TAKATSUKI M.D. Department of Cardiology, Keio University School of Medicine, Tokyo, JapanAddress for reprints: Seiji Takatsuki, M.D., Department of Cardiology, Keio University Hospital, 35 Shinanomachi, Shinjukuku, Tokyo, 160-8582 Japan. Fax: 81-3-5363-3875; e-mail: [email protected]Search for more papers by this authorTAKUO YOSHIDA M.D., TAKUO YOSHIDA M.D. Department of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, JapanSearch for more papers by this authorYUKIHIKO MOMIYAMA M.D., YUKIHIKO MOMIYAMA M.D. Department of Cardiology, National Hospital Organization Tokyo Medical Center, Tokyo, JapanSearch for more papers by this author First published: 15 February 2014 https://doi.org/10.1111/pace.12364 Conflict of interest: None. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Volume37, Issue6June 2014Pages 774-776 RelatedInformation

Role of SA–VA interval after resetting of the tachycardia by ventricular extra stimulus in differentiating AVNRT and OAVRT regarding sensitivity and specificity, single center study

Abstract Introduction Right ventricular entrainment represents a useful tool for differentiating atrioventricular nodal re-entrant tachycardia (AVNRT) from orthodromic re-entrant tachycardia (ORT) using an accessory pathway. However, inability to entrain PSVT by pacing can be observed in some patients. Aim of study Assessing whether the resetting response to SVT by single or double right ventricular extra-stimuli is a useful maneuver to differentiate AVNRT from OAVRT by calculating the difference between the stimulus-atrial interval during resetting of SVT and the VA interval during SVT (SA–VA). Methods Electrophysiological study was conducted with a calculation of the SA–VA interval after resetting of the tachycardia by ventricular extra stimulus and differential entrainment from RV apex and base, then comparing the two methods regarding sensitivity and specificity in differentiating AVNRT from OAVRT conducted on 25 patients. Results Measuring the SA–VA interval after resetting of the tachycardia by an extra stimulus during the His refractoriness during the tachycardia showed in AVNRT a mean of 145.76 ± 31.53 and in OAVRT a mean ± SD of 91.52 ± 12.79 with a high statistical significance, with a cutoff point of 107 ms above which the SVT is expected to be AVNRT, and below which OAVRT. Using this technique could differentiate AVNRT from OAVRT with an overall sensitivity of 100% and specificity of 76.47%, in comparison to a specificity of 81.8% when using the technique of differential entrainment from RV apex and base. Conclusion Resetting of SVT by ventricular extra-stimuli is a useful maneuver for differentiating AVNRT from ORT and is applicable even when entrainment is impossible.

Mode of Induction of Ventricular Tachycardia and Prognosis in Patients with Coronary Disease: The Multicenter UnSustained Tachycardia Trial (MUSTT)

Programmed stimulation is an important prognostic tool in the evaluation of patients with an ejection fraction <or=40% after myocardial infarction. Many believe that ventricular tachycardia (VT) requiring 3 ventricular extrastimuli (VES) for induction is less likely to occur spontaneously and has less predictive value. However, it is unknown whether the mode of VT induction is associated with long-term prognosis. We analyzed a cohort of 371 patients enrolled in MUSTT who had inducible monomorphic VT and who were not treated with antiarrhythmic drugs or an implantable cardioverter defibrillator during the trial. Patients in whom sustained VT was induced with 1 or 2 VES or burst pacing (single VES n = 15, double VES n = 127, burst n = 7, total n = 149) were compared with those in whom VT was induced with 3 VES (n = 222). Compared with the others, patients requiring 3 VES were closer to their most recent myocardial infarction (17 vs 51 months, P = 0.035) and showed a trend toward a lower ejection fraction (26% vs 30%, P = 0.057). VT requiring 3 VES had a shorter cycle length (240 vs 260 ms, P < 0.001). Despite these findings, there was no difference in the incidence of arrhythmic death or cardiac arrest (HR 1.02; 95% CI 0.69-1.51) or all-cause mortality (HR 1.03; 95% CI 0.76-1.39) according to the mode of induction in adjusted analyses. The prognostic significance of VT induced by 3 VES is similar to that of VT induced by 1 or 2 VES, or burst pacing, in patients with coronary disease and abnormal LV function.

Coronary-Subclavian Steal Syndrome Presenting with Ventricular Tachycardia

Coronary-subclavian steal through the left internal mammary graft is a rare cause of myocardial ischemia in patients who have had a coronary bypass surgery. We report a 70-year-old man who presented with sustained monomorphic ventricular tachycardia 5 years after the surgical creation of a left internal mammary to the left anterior descending artery. Cardiac catheterization illustrated that the left subclavian artery was occluded proximally and that the distal course was visualized by retrograde filling through the left internal mammary graft. Clinical ventricular tachycardia was reproducibly induced with a single ventricular extrastimulus, and antitachycardia pacing terminated the tachycardia. Restoration of blood flow by way of a Dacron graft placed between the descending aorta and the subclavian artery resulted in the total relief of symptoms. Ventricular tachycardia could not be induced during the control electrophysiologic study after surgical revascularization.

Characterization of the Effects of Single Ventricular Extrastimuli on Endocardial Activation in Human Infarct-Related Ventricular Tachycardia

The purpose of this study was to examine the resetting response in human ventricular tachycardia (VT) circuits with 3-dimensional mapping. In characterizing re-entry with the resetting response, inferences are made about interaction of single ventricular extrastimuli (SVE) with VT. Non-contact mapping was used to examine the effects of SVE from 25 sites on 10 infarct-related VT circuits. The local temporal excitable gap (EGap) was 113.8 +/- 64.3 ms, 25.8 +/- 11.2% of VT cycle length. In 7 VT circuits there was a clear difference in the EGap at different points in the circuit. All circuits could be pre-excited over a range of SVEs, resulting in either: 1) premature activation throughout the circuit resulting in reset; 2) premature activation at entry, but subsequent interval dependent conduction slowing (IDCS) resulting in a fully compensatory return cycle; or 3) change to functional lines of block and return cycle QRS morphology. The principal determinant of whether SVE resulted in reset was the degree of IDCS within the diastolic pathway (DP) of the circuit. Resetting occurred from 9 sites (7 VT) but was absent from 15 sites despite pre-excitation of a sizeable EGap in the circuit in all cases. In infarct-related VT, all circuits can be pre-excited over a range of SVEs, the effect of which is dependent on the degree of IDCS within the DP or modification of functional block defining the circuit. Failure to reset does not therefore indicate the absence of an EGap or failure of entry to the circuit. The temporal and spatial properties of the EGap vary at different sites of entry to the circuit.

Paradoxical autonomic modulation of atrioventricular nodal conduction during heart rate turbulence.

Heart rate turbulence (HRT) represents a biphasic chronotropic response of sinus rhythm to a single ventricular premature beat (VPB). It consists of early acceleration and late deceleration of heart rate and is predominantly mediated by the autonomic nervous system. The aim of this study was to investigate if autonomic perturbations after a VPB exert a significant effect on AV conduction. Both surface ECG and the high right atrial electrogram were recorded at a sampling frequency of 1000 Hz in 26 patients (24 men, mean age 49 +/- 12 years) referred for electrophysiological evaluation. The stimulation protocol consisted of series of single ventricular extrastimuli delivered from the right ventricular apex at decreasing coupling intervals. A biphasic profile of AV intervals after a single VPB was observed. The response of AV conduction to a VPB was approximately 25 times and 15 times weaker in the early and late phase, respectively, than that of R-R intervals. Thus, AV interval dynamics significantly preceded the change in R-R intervals, which is in conflict with the near to zero phase of transfer function between R-R and AV intervals described in previous studies. A significant AV turbulence was observed consisting of early shortening and later prolongation of AV intervals after VPB. Its magnitude was much smaller than that of HRT. Dynamics of AV delay has little impact on the accuracy of HRT assessment from surface ECG. The significant temporal dissociation of R-R and AV interval dynamics after a VPB remains unexplained.

Heart rate turbulence can be detected after atrial premature beat

Heart rate turbulence (HRT) describes a bi-phasic chronotropic response of sinus rhythm to a ventricular premature beat (VPB). The aim of the study was to investigate whether an atrial premature beat (APB) can produce HRT and whether it can be described using ventricular HRT quantifiers (turbulence onset, TO, and turbulence slope, TS). Methods: Thirty-seven subjects (54±16 years) referred for electrophysiologic evaluation for ventricular tachyarrhythmias underwent a stimulation protocol consisting of 3 series of single atrial and ventricular extrastimuli delivered from the high right atrium and right ventricular apex prior to programmed electrical stimulation. Atrial and ventricular TO and TS (ATO, ATS, VTO, VTS) were calculated separately using a dedicated computer algorithm. Results: Expressed as mean±SD, VTO -2.03±0.42%, ATO 1.37±0.35% (p <0.001); VTS 8.32±1.9 ms/RR, ATS 3.95±0.99 ms/RR (p <0.008). There was a strong correlation between VTS and ATS (r=0.71, p=0.0002; Figure, right) but not between VTO and ATO (r=0.83, p=0,074; left). Conclusions: HRT phenomenon is present after an APB, suggesting that similar baroreceptor mechanisms operate following both VPB and APB. After an APB, the late phase response (rhythm deceleration) is significantly attenuated and the early phase response is different than that after a VPB, indicating the presence of alternative mechanisms. Atrial HRT can be measured using existing technique but algorithm adjustments are desirable. ACC 2002 / 51st Annual Scientific Session March 17-20, 2002, Atlanta, Georgia, USA Page 1

Narrow complex tachycardia with VA block: diagnostic and therapeutic implications.

To review our experience with cases of narrow complex tachycardia with VA block, highlighting the difficulties in the differential diagnosis, and the therapeutic implications. Prior reports of patients with narrow complex tachycardia with VA block consist of isolated case reports. The differential diagnosis of this disorder includes: automatic junctional tachycardia, AV nodal reentry with final upper common pathway block, concealed nodofascicular (ventricular) pathway, and intra-Hissian reentry. Between June 1994 and January 1996, six patients with narrow complex tachycardia with episodes of ventriculoatrial block were referred for evaluation. All six patients underwent attempted radiofrequency ablation of the putative arrhythmic site. Three of six patients had evidence suggestive of a nodofascicular tract. Intermittent antegrade conduction over a left-sided nodofascicular tract was present in two patients and the diagnosis of a concealed nodofascicular was made in the third patient after ruling out other tachycardia mechanisms. Two patients had automatic junctional tachycardia, and one patient had atrioventricular nodal reentry with proximal common pathway block. Attempted ablation in the posterior and mid-septum was unsuccessful in patients with nodofascicular tachycardia. In contrast, those with atrioventricular nodal reentry and automatic junctional tachycardia readily responded to ablation. The presence of a nodofascicular tachycardia should be suspected if: (1) intermittent antegrade preexcitation is recorded, (2) the tachycardia can be initiated with a single atrial premature producing two ventricular complexes, and (3) a single ventricular extrastimulus initiates SVT without a retrograde His deflection. The presence of a nodofascicular pathway is common in patients with narrow complex tachycardia and VA block. Unlike AV nodal reentry and automatic junctional tachycardia, the response to ablation is poor.

2:1 Atrioventricular Block During Atrioventricular Node Reentrant Tachycardia

The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory. In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block. In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed. Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean +/- SD 312 +/- 32 vs. 353 +/- 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction. The incidence of induced 2:1 AV block during AV node reentrant tachycardia is approximately 10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.

Spectrum off electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease

Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamilsensitive VT in 32 patients (aged 38 years ± 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81 % of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p < 0.05) and adenosine sensitive (p < 0.001). However, verapamil-sensitive, catecholamine-dependent VT was no more likely to be adenosine sensitive than the catecholamine-independent form of the arrhythmia (p > 0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.

Ventricular tachycardia with narrow QRS duration, a right bundle branch block pattern, and right Axis deviation abolished by catheter manipulation

A 25-year-old woman underwent electrophysiologic evaluation for sustained normal QRS complex tachycardia with a pattern of right bundle branch block and right axis deviation. Ventricular tachycardia was diagnosed by demonstrating fusion beats, atrioventricular dissociation, and bundle of His potential activation, which began before the onset of each QRS complex. A single ventricular extrastimulus was capable of easily provoking the tachycardia. There was an inverse relationship between the coupling interval of the first extrastimulus and the interval of the first tachycardia beat, suggesting reentry as the mechanism. The tachycardia was unexpectedly abolished during catheter manipulation in the left ventricle and has never recurred during 1 year of follow-up evaluation. The tachycardia was thought to be an unusual form of interfascicular tachycardia or microreentrant fascicular tachycardia.

Use of Double Ventricular Extrastimulation to Determine the Preexcitation Index in Atrioventricular Nodal Reentrant Tachycardia

The ability of single paced ventricular beats during tachycardia to penetrate the tachycardia circuit and reset the subsequent atrial depolarization (atrial preexcitation), enabling calculation of the "preexcitation index," can be helpful in analyzing supraventricular tachycardias. However, the ventricular refractory period often prevents ventricular capture of beats with the necessary prematurity to demonstrate atrial preexcitation, particularly in atrioventricular nodal reentrant tachycardia (AVNRT). We hypothesized that the use of double premature stimuli could overcome this limitation. In 25 consecutive patients with either AVNRT or atrioventricular reciprocating tachycardia (AVRT) we attempted to demonstrate atrial preexcitation with single and double ventricular extrastimuli. Whereas atrial preexcitation with a single extrastimulus could only be achieved in 3 of 11 patients with AVNRT, all but 1 patient demonstrated atrial preexcitation with the use of double ventricular extrastimuli. On the other hand, in all but 1 patient with AVRT, atrial preexcitation could be achieved with single and double extrastimuli. A formula was derived for obtaining a preexcitation index with double extrastimuli and shown to correspond closely with the preexcitation index obtained with a single extrastimulus in the 16 patients in whom atrial preexcitation could be achieved with single and double extrastimuli. Thus, this technique significantly enhances the ability to achieve atrial preexcitation and to calculate the preexcitation index in patients with AVNRT, and thus may be useful in deciphering tachycardia mechanism in some patients, as well as being a useful technique in studying the electrophysiological properties of the antegrade and retrograde limbs of AVNRT.

Systematic characterization of the reentrant circuit during atrioventricular nodal reentrant tachycardia

This study was conducted to systematically characterize the excitable gap and conduction properties of the reentrant circuit during atrioventricular nodal reentrant tachycardia (AVNRT). Previous studies have attempted to analyze these properties by introducing single ventricular extrastimuli during tachycardia. These studies have been limited, however, by the inability of single extrastimuli to engage the circuit in the majority of patients studied. Thus, in most cases, the nature of the excitable gap and the conduction properties of the anterograde and retrograde limbs of the circuit during tachycardia remain undefined. In this series, 11 patients with typical AVNRT were studied. During tachycardia, both single and double ventricular extrastimuli (the first extrastimulus acting as a conditioning stimulus) were used to scan diastole. The resetting response of the reentrant circuit, as well as the conduction properties f the retrograde fast and anterograde slow pathways, was recorded and analyzed. Whereas atrial preexcitation and resetting of the reentrant circuit could be demonstrated in only 1 patient with single ventricular extrastimuli, resetting was achieved in all 11 patients with closely coupled double ventricular extrastimuli. Over the full range of coupling intervals used, no retrograde delay in fast pathway conduction could be demonstrated before tachycardia termination or ventricular refractoriness. Penetration of the reentrant circuit resulted in a progressive increasing delay in the anterograde portion of the subsequent return cycle and an increasing resetting response pattern in all cases. Thus, the reentrant circuit during AVNRT demonstrates heterogeneous excitability. While the fast pathway remains fully excitable during tachycardia, the slow pathway uniformly demonstrates decrementai conduction, resulting in an increasing resetting response pattern. An increasing resetting response pattern does not preclude the presence of fully excitable tissue within a reentrant circuit.

Multiple supraventricular tachycardia mechanisms in a single patient treated with radiofrequency catheter ablation

The incidence of atrioventricular (AV) nodal reentrant tachycardia in patients with accessory AV connection is 5 % or 1ess.l The occurrence of either accessory AV pathways or AV nodal reentrant tachycardia with ectopic atria1 tachycardias is even more uncommon.” This article reports the previously undocumented occurrence of sustained ectopic atria1 tachycardia, AV nodal reentry, and AV reciprocating tachycardia in a single patient. The successful treatment of all three tachycardia mechanisms with radiofrequency catheter ablation techniques is described. A 20-year-old man from Turkey was referred for treatment of medically refractory paroxysmal tachycardia. Symptoms of paroxysmal palpitations with dyspnea had been present for 4 years. These episodes occurred almost every evening in the absence of medical therapy. His symptoms were inadequately controlled by digoxin, metoprolol, propafenone, and amiodarone (200 mg/day). Ambulatory ECG monitor tracings suggested a diagnosis of ectopic atria1 tachycardia. Amiodarone therapy was discontinued 10 days before admission to the hospital. His echocardiogram and ECG were normal. According to electrophysiologic testing there was no evidence of antegrade ventricular preexcitation with atria1 pacing. Retrograde AV conduction was eccentric and nondecremental, with the earliest site of atria1 activation in the distal coronary sinus (CS), which was consistent with a concealed left lateral accessory pathway. No tachycardias were induced until after a continuous isoproterenol infusion at 2 pg/min was started. Single atria1 and ventricular extrastimuli induced both sustained orthodromic AV reciprocating tachycardia, utilizing the concealed left lateral accessory pathway, and sustained AV nodal reentrant tachycardia. The AV reciprocating tachycardia had a cycle length of 320 msec with local ventriculoatrial conduction times as follows: distal CS = 90 msec, mid CS = 100 msec, proximal CS = 130 msec, His atrium = 160 msec, and right atria1 appendage = 188 msec (Figs. 1 and 2). With the use of the retrograde transaortic approach, the reciprocating tachycardia

The excitable gap in atrioventricular nodal reentrant tachycardia. Characterization with ventricular extrastimuli and pharmacologic intervention.

Our purpose was to characterize the excitable gap during atrioventricular nodal reentrant tachycardia (AVNRT) to elucidate the electrophysiologic substrate of this clinically familiar microreentrant arrhythmia. Accordingly, in 11 patients with classic slow-fast AVNRT (mean cycle length, 342 +/- 41 msec), a single ventricular extrastimulus (V2) was periodically delivered after a spontaneous tachycardia beat (V1) until ventricular refractoriness was reached. With this technique, an excitable gap was considered present when atrial preexcitation of at least 20 msec could be achieved along with tachycardia resetting (noncompensatory pause after V2). The range of V1V2 intervals that resulted in atrial preexcitation constituted the preexcitation zone. Five patients (45%) showed evidence of an excitable gap at baseline, with a maximal atrial preexcitation achievable of 33 +/- 6 msec, representing 9 +/- 1% of the tachycardia cycle length. Verapamil was then administered to all 11 patients with the purpose of slowing the anterograde tachycardia wavefront before arrival of V2. This resulted in widening of the preexcitation zone in three patients by a mean of 50 +/- 37 msec, with a corresponding increase in maximal atrial preexcitation to 70 +/- 32 msec, or 16 +/- 4% of AVNRT cycle length, and the appearance of atrial preexcitation in two patients who lacked it during baseline. In the remaining six patients, AVNRT was not sustained after verapamil or was too unstable for evaluation. During baseline, V2A2 conduction time increased by only 5 +/- 3 msec throughout the preexcitation zone, with values at the outer border unchanged after verapamil, implying a fully excitable gap in the retrograde limb. In all patients with a preexcitation zone, AVNRT was consistently reset by V2, both at baseline and after verapamil, with a "flat" but mainly "increasing" response pattern as V1V2 was shortened. Hence, a significant number of patients with AVNRT have evidence of an excitable gap whose demonstrability can be facilitated by pharmacologic intervention; documentation of an increasing resetting response pattern, most apparent after verapamil, provides new evidence for a reentrant mechanism in AVNRT; and while not definitively proven, the presence of a fully excitable gap during AVNRT is most consistent with a microreentry circuit that incorporates an anatomic obstacle.

Coupling intervals of ventricular extrastimuli causing resetting of sustained ventricular tachycardia secondary to coronary artery disease: Relation to subsequent termination

Single and double ventricular extrastimuli (VE) delivered during sustained, uniform ventricular tachycardia (VT) are able to reset or terminate the tachycardia. The relation between the coupling intervals of single and double VE resetting VT and those terminating it was examined in 80 uniform, morphologically distinct VT occurring in 52 patients. Of the 80 tachycardias receiving single VE, 41 were reset and 8 terminated. The corrected coupling interval of single VE first causing resetting was 0.81 ± 0.08 compared with 0.66 ± 0.06 for termination (p < 0.001). Forty-two tachycardias received double VE with 33 being reset and 13 terminating. The corrected coupling interval of double VE at which resetting was first seen was 0.86 ± 0.08 compared with 0.73 ± 0.05 for termination (p < 0.001). If the longest corrected coupling interval causing resetting was ≥0.75, then 7 of 34 tachycardias terminated with single VE and 13 of 31 terminated with double VE compared with only 1 of 46 terminating with single VE and 0 of 10 with double VE if resetting was not observed by a corrected coupling interval of 0.75 (p < 0.01 and p < 0.02, respectively). If the longest corrected coupling interval at which resetting occurred was ≥0.75, the predictive value for VT termination was 21% with single VE and 42% with double VE compared with only 2% with single VE and none with double VE if resetting was not observed by this corrected coupling interval. Thus, critical coupling intervals can be identified during the delivery of premature extrastimuli where if resetting has not occurred, termination is unlikely. Potential applications of these findings in algorithms for antitachycardia pacemakers exist.

The resetting response of ventricular tachycardia to single and double extrastimuli: Implications for an excitable gap

To evaluate the influence of local tissue refractoriness and delay in intervening tissue on the ability of single ventricular extrastimuli to reset and characterize a resetting response pattern in ventricular tachycardia (VT), single ventricular extrastimuli were delivered during 81 VTs and double ventricular extrastimuli in 45 of the 81 VTs. Resetting of VT was recognized as a less than fully compensatory pause after stimulation and was seen in 43 of 81 VTs (53%) with single ventricular extrastimuli and 35 of 45 (78%) with double ventricular extrastimuli. Double ventricular extrastimuli reset 16 VTs not reset by single ventricular extrastimuli. The return cycle, the interval from the extrastimulus to the first VT beat after extrastimuli, has 1 of 3 distinct response patterns: flat, increasing, and flat plus increasing. In 19 VTs, resetting was seen with both single ventricular extrastimuli and double ventricular extrastimuli; 4 flat responses with single ventricular extrastimuli became flat plus increasing with double ventricular extrastimuli. All other patterns were unchanged. In the 19 VTs reset by both single and double ventricular extrastimuli, the estimate of both the total reset zone (94 ± 36 vs 56 ± 32 ms) and the flat portion of the reset zone (52 ± 42 vs 42 ±28 ms) was significantly longer with double ventricular extrastimuli (p < 0.001 and p < 0.02, respectively). In conclusion: (1) when single ventricular extrastimuli failed to reset a VT, double ventricular extrastimuli from the same site may reset the VT; (2) single ventricular extrastimuli underestimate the size of the excitable gap; (3) double ventricular extrastimuli better characterize the VT circuit; and (4) the finding of a flat curve with both single and double ventricular extrastimuli suggests that the fixed returned cycle seen in a flat curve is due to fully excitable tissue within the circuit with a fixed entry into the VT circuit.

Influence of the site of stimulation on the resetting phenomenon in ventricular tachycardia

Uniform, sustained ventricular tachycardia (VT) in the setting of prior myocardial infarction is believed to be due to reentry. The ability to reset VT with programmed extrastimuli requires that the premature impulse reach and enter the reentrant circuit. To evaluate the importance of the site of pacing on the ability to reset VT, single ventricular extrastimuli were delivered during 32 morphologically distinct, uniform VTs from both the right ventricular (RV) apex and RV outflow tract. Single ventricular extrastimuli resulted in resetting of VT from the RV apex only in 6 VTs, from the RV outflow tract only in 2, from both sites in 11 VTs and neither site in 13. When VT reset at both RV sites, 1 RV site or neither RV site was compared, a left bundle branch block VT QRS morphologic pattern was found to be more common in VT reset at both sites than at neither site (8 of 11 vs 4 of 13, p less than 0.05). No other differences in VT characteristics analyzed were found between these groups. Multiple ventricular extrastimuli were delivered in 16 VTs; in 6 of these, resetting was shown from at least 1 additional site, as compared to the response with single ventricular extrastimuli. In summary, site of stimulation can influence the ability of premature extrastimuli to reset uniform VT, and site dependence of VT resetting diminishes when multiple extrastimuli are used. This suggests that refractoriness or conduction delay in tissue between the pacing site and tachycardia circuit are important determinants of ability to reset VT from a particular site.