Influence of tachycardia cycle length and antiarrhythmic drugs on pacing termination and acceleration of ventricular tachycardia

We examined the influence of ventricular tachycardia (VT) cycle length and antiarrhythmic drugs on the frequency of VT termination and acceleration by single and double extrastimuli and right ventricular burst pacing. In 57 patients, 89 episodes of sustained VT (32 control, 57 drug) were induced by programmed electrical stimulation. Overall, 60 of 89 (67%) episodes of ventricular tachycardia were terminated by means of programmed electrical stimulation. In patients with relatively slow ventricular tachycardia (VT cycle length greater than or equal to 350 msec) pacing terminated 37 of 44 (84%) episodes but terminated only 24 of 45 (51%) episodes of more rapid VT (VT cycle length less than or equal to 349 msec, p less than 0.005). Pacing successfully terminated VT in nine of 49 (18%) episodes using a single extrastimulus, 22 of 52 (42%) episodes using double extrastimuli, and 40 of 66 (61%) episodes using burst right ventricular pacing. VT acceleration occurred in none of 49 attempts with a single extrastimulus, in eight of 52 (15%) attempts with double extrastimuli, and in 12 of 66 (18%) attempts using burst right ventricular pacing. During therapy, the frequency of either ventricular tachycardia termination or acceleration did not change regardless of the pacing termination method used. However, by prolonging the mean VT cycle length from 311.1 +/- 82.2 msec to 401.9 +/- 103.5 msec (p less than 0.01), drugs increased the overall frequency of VT termination. We conclude that: (1) pacing terminates VT more frequently if the VT cycle length is long and if right ventricular bursts are used, (2) burst right ventricular pacing increases the risk of VT acceleration, and (3) drugs increase the frequency of ventricular tachycardia termination by prolonging VT cycle length but do not affect frequency of VT acceleration.     

Resetting of ventricular tachycardia with electrocardiographic fusion: incidence and significance

The incidence and significance of fusion of the QRS complex during resetting of sustained ventricular tachycardias (VTs) was determined in 53 VTs induced by programmed stimulation in 46 patients with prior myocardial infarction. All 53 VTs were reset with one or two extrastimuli delivered at the right ventricular apex (RVA); 29 (54.7%) demonstrated fusion of the VT QRS complex coincident with the extrastimulus resetting the VT. Activation time at the RVA during VT (measured from the onset of the VT QRS complex to the first rapid deflection of the RVA electrogram) was longer in VT reset with fusion compared with those without fusion (91 +/- 30 vs 33 +/- 32 msec; p less than .001). A right bundle branch block VT QRS morphology and a rightward and inferior axis were more common in VT reset with electrocardiographic (ECG) fusion. Additionally, the shortest return cycle following the extrastimulus resetting the VT was shorter in VT reset with ECG fusion compared with those without (327 +/- 66 vs 423 +/- 84 msec; p less than .001). Fusion of the endocardial electrogram recorded at the site of VT origin was noted in 11 of 15 VTs that were reset while a recording catheter was positioned at this site, including all eight VTs with evidence of surface ECG fusion and three of seven VTs without fusion. Seventeen VTs were reset from the right ventricular outflow tract as well as the RVA; eight demonstrated QRS fusion at both sites, five from the right ventricular outflow tract only, and four from neither site.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prospective comparison of right and left ventricular stimulation for induction of sustained ventricular tachycardia

Thirty-eight patients who had sustained monomorphic ventricular tachycardia (VT) or sudden cardiac death underwent programmed ventricular stimulation. To assess the relative efficacy of right and left ventricular (RV and LV) stimulation, a tandem protocol with 1 to 4 extrastimuli and burst pacing was used. Each step of the protocol was performed in a rotating sequence at the RV apex, basal RV septum and LV apex. Sustained VT was induced from the RV apex in 26 patients, right ventricle (either site) in 27, and LV apex in 24, and spontaneous VT was reproduced from those sites in 11, 14 and 12 patients, respectively. In the 23 patients who had sustained VT induced from both ventricles, RV stimulation always required fewer or the same number of extrastimuli for induction. At every stage of the protocol, the cumulative yield of sustained VT was consistently greater from the right ventricle than from the left ventricle. After delivering 4 extrastimuli and burst pacing, LV stimulation only increased the yield of sustained VT by 1 patient, and spontaneous VT by 3 patients. Inducibility or noninducibility in the right ventricle generally predicted the same outcome in the left ventricle. Previously undocumented VT or ventricular fibrillation was induced from the right ventricle in 19 patients and from the left ventricle in 13. Thus, LV stimulation was less efficacious than RV stimulation. LV stimulation increased the yield over RV stimulation only minimally and did not reduce the number of extrastimuli required to induce sustained VT.     

Prospective comparison of a conventional and an accelerated protocol for programmed ventricular stimulation in patients with coronary artery disease

BACKGROUND. This study compared the sensitivity, specificity, and efficiency of a "conventional" and "accelerated" programmed stimulation protocol in 293 patients with coronary artery disease who had a history of sustained or nonsustained monomorphic ventricular tachycardia (VT). METHODS AND RESULTS. In the conventional protocol, one and two extrastimuli were introduced during sinus rhythm and during basic drive trains at cycle lengths of 600 and 400 msec at the right ventricular apex and then at the outflow tract or septum. In the accelerated protocol, one, two, and then three extrastimuli were introduced at each of three basic drive train cycle lengths (350, 400, and 600 msec) at the right ventricular apex; the procedure was repeated at a second right ventricular site. Six hundred thirty-four electrophysiological tests were performed using one of these two protocols either in the baseline state (293 tests) or during drug testing (341 tests). The yield of sustained, monomorphic VT was 89% with the conventional protocol and 92% with the accelerated protocol during baseline tests in patients who had a history of sustained VT (p = 0.05); 20% and 34%, respectively, during baseline tests in patients with a history of nonsustained VT (p = 0.06); and 70% and 77%, respectively, during drug testing (p = 0.2). To induce sustained, monomorphic VT, 10.1 +/- 5.0 (mean +/- SD) protocol steps and 14.4 +/- 8.7 minutes were required with the conventional protocol, compared with 4.0 +/- 3.7 steps and 5.6 +/- 6.1 minutes with the accelerated protocol (p less than 0.001 for each comparison). Among the tests in which sustained, monomorphic VT was induced, sustained polymorphic VT or ventricular fibrillation was induced more often with the conventional protocol (3.6%) than with the accelerated protocol (0.9%, p = 0.05). CONCLUSIONS. The efficiency of programmed stimulation can be improved by the early use of a basic drive train cycle length of 350 msec and three extrastimuli. Compared with a conventional stimulation protocol, the accelerated protocol used in this study reduces the number of protocol steps and duration of time required to induce monomorphic VT by an average of more than 50% and improves the specificity of programmed stimulation without impairing the yield of monomorphic VT.     

Refractoriness as a determinant of tachycardia inducibility in the right ventricle

The use of more than one right ventricular site for programmed electrical stimulation has been reported to increase the number of patients in whom ventricular tachycardia can be provoked. To determine a possible reason for these observations, programmed ventricular tachycardia studies were evaluated in 316 patients (185 men and 131 women) with a mean age of 63 +/- 7 years who presented with ventricular tachycardia or cardiac arrest. The underlying cardiac disease was atherosclerosis (81%), cardiomyopathy (15%), valvular heart disease (3%), and miscellaneous conditions (1%). Programmed electrical stimulation studies employed a six-beat pacing train, at a cycle length of 500 msec with the introduction of one to three premature stimuli at twice diastolic threshold at the right ventricular apex. If ventricular tachycardia at the right ventricular apex could not be provoked in a patient, the study was repeated at the right ventricular outflow tract. A total of 36 patients were studied at the right ventricular outflow tract. Eleven (31%) were provoked into ventricular tachycardia, while 25 (69%) were not. No difference existed between the QRS, QT, and QTc intervals between those having ventricular tachycardia provoked at the outflow tract compared to those without inducible tachycardia at the right ventricular outflow tract. The effective refractory period was 280 +/- 5 msec at the right ventricular outflow tract in those patients not inducible, and 226 +/- 4 msec in those inducible (p less than 0.05). We defined the change in ventricular refractory period as the difference in the effective refractory period at the right ventricular outflow tract minus the effective refractory period at the right ventricular apex.(ABSTRACT TRUNCATED AT 250 WORDS)     

Complex ventricular ectopic activity in patients less than 20 years of age with or without syncope, and the role of ventricular extrastimulus testing

To assess the potential for ventricular tachycardia (VT), ventricular extrastimulus testing was performed in 33 young patients with complex ventricular ectopic activity defined as multiform ventricular premature complexes (VPCs), couplets or nonsustained VT, or a combination, found during electrocardiographic monitoring. There were 21 male and 12 female patients with a mean age of 11 years (range 1 to 18). Patients were divided into 2 groups based on the presence (14 patients) or absence (19 patients) of syncope. Patients with syncope had ostensibly normal hearts (9 patients) or miscellaneous heart disease (5 patients). Patients without syncope had ostensibly normal hearts (8 patients) or miscellaneous heart disease (11 patients). Ventricular stimulation protocol consisted of burst pacing and 1 to 4 programmed extrastimuli decreasing to refractoriness at 3 drive-train cycle lengths, and at 2 pacing sites (right ventricular apex and outflow tract) during the drug-free baseline state and isoproterenol infusion. No patient had VT induced with 1 or 2 extrastimuli. VT was induced in 13 of 14 patients (93%) with syncope, and in 9 of 19 patients (47%) without syncope (p less than 0.05). Using a 3-extrastimuli protocol, 8 of 14 patients (57%) with and 3 of 19 patients (16%) without syncope had VT induced (p less than 0.05). These findings suggest that VT may be the cause of syncope in young patients with complex ventricular ectopic activity.     

Influence of right ventricular site of stimulation and infarct location on the inducibility of ventricular tachycardia in patients with coronary artery disease

No prior studies have evaluated the relationship between the site of right ventricular stimulation, the site of prior infarction, and the inducibility of ventricular tachycardia (VT). This study was performed to determine if the location of pathologic Q waves influences the inducibility of VT at various right ventricular sites in patients with coronary artery disease (CAD) and a history of myocardial infarction (MI). In 30 patients with a history of sustained, monomorphic VT, CAD, prior MI, and pathologic Q waves, programmed ventricular stimulation was performed at the right ventricular apex, septum, and outflow tract, in random order. There was electrocardiographic evidence of an MI that was inferior in 11 patients, anterior in 10 patients, and both inferior and anterior in 9 patients. Sustained, monomorphic VT was induced in 27 of 30 patients (90%). There were no significant differences among the three sites in the rate of inducibility of VT. The rate of inducible VT at each of the three right ventricular sites was not affected by the location of prior infarction. In conclusion, among patients with sustained, monomorphic VT, CAD, and a history of MI, the incidence of inducible sustained, monomorphic VT is not influenced by the location of prior infarction, regardless of whether programmed ventricular stimulation is performed at the right ventricular apex, septum, or outflow tract.     

Prevention of ventricular tachycardia induction during right ventricular programmed stimulation by high current strength pacing at the site of origin

To determine whether high current strength pacing at the site of origin of ventricular tachycardia (VT) could prevent induction of VT, we studied 11 VTs in 10 patients with chronic coronary artery disease. The left ventricular site of origin of all VT was determined by endocardial catheter mapping. Reproducible VT induction from the right ventricular apex or outflow tract was demonstrated with a pacing current strength equal to twice diastolic threshold (less than or equal to 2.0 mA) with single (two VTs), double (eight VTs), or triple (one VT) extrastimuli following 8 beats of a drive cycle length of 400 to 600 msec. After determination of the baseline VT induction zone (range 10 to 80 msec), repeat induction was attempted while simultaneous pacing was performed during the 8 beat drive train from the left ventricular site of origin with the use of a high current strength (10 mA [two VTs] or 20 mA [nine VTs]) and from the baseline right ventricular site with a current strength equal to twice diastolic threshold. Extrastimuli were introduced only from the right ventricular site over the same range of coupling intervals that resulted in VT initiation during the baseline state. In five of the 11 trials, no VT could be initiated; in one trial, the VT induction zone was decreased from 80 to 10 msec; in three trials, only VT of a different morphology and a distinct (greater than 4 cm distant) site of origin was initiated; and in two trials, VT of the same morphology was initiated. In four of the five trials in which all VT was prevented by simultaneous pacing with a high current strength at the site of origin, simultaneous pacing at a lower current strength (twice diastolic threshold) at the site of origin (three VTs) or with equally increased current strength (10 to 20 mA) at nonsites of origin (two VTs) did not prevent initiation. We conclude that: high current strength pacing at the site of origin during the drive train can inhibit VT induction with extrastimuli and, successful prevention of VT may depend on the pacing site being the site of origin and the current strength used during pacing.     

Resetting response patterns during sustained ventricular tachycardia: relationship to the excitable gap

We analyzed the resetting response (a noncompensatory pause after electrical stimulation) during 37 hemodynamically tolerated ventricular tachycardias (VTs) induced by programmed electrical stimulation in 32 patients with chronic coronary artery disease. The mean cycle length of VT was 369 +/- 59 msec. Single extrastimuli were delivered at the right ventricular apex during all 37 VTs, and double extrastimuli were delivered at the same site during 23 VTs. The resetting response pattern was considered increasing, decreasing, or flat if the return cycle increased, decreased, or remained constant in response to progressively shorter coupling intervals of the extrastimuli. Ten VTs had an increasing pattern and nine a flat pattern. In 11 VTs the pattern was mixed (flat at longer coupling intervals and increasing at shorter ones), and in the remaining seven the pattern could not be defined. No VT had a decreasing pattern. The mean duration of the resetting interval (range of coupling intervals resulting in resetting) was 66 +/- 45 msec, or 17% of the cycle length of VT. VT with a mixed pattern had longer resetting intervals than VT with an increasing pattern (102 +/- 34 vs 64 +/- 40 msec; p less than .035); however, cycle lengths of VT were similar (370 +/- 58 vs 386 +/- 86, p = NS). An excellent correlation was observed between the shortest return cycles in response to single and double extrastimuli (r = .99), with a mean difference of 5 msec. The cycle length of VT exceeded the return cycle (measured to the QRS onset) during 15 VTs (41%).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prolongation of ventricular refractoriness by class Ia antiarrhythmic drugs in the prevention of ventricular tachycardia induction

The effects of class la antiarrhythmic drugs (procainamide, quinidine) on the right ventricular effective refractory period (VERP) and intraventricular conduction time were assessed during serial invasive electrophysiologic studies for sustained monomorphic ventricular tachycardia (VT). In 47 patients with remote myocardial infarction, sustained VT was inducible by up to two extrastimuli after the basic drive at one of two basic cycle lengths at the right ventricular apex. With oral drug administration, sustained VT was no longer inducible (group I) in 27 patients but remained inducible (group II) in 20 with the same protocol. Class la drugs prolonged the VERP in both groups, but there was greater lengthening when drugs were effective (e.g., +32 +/- 14 msec in group I vs +12 +/- 19 msec in group II; p less than 0.005, basic cycle length 600 to 700 msec). Prolongation of the VERP by greater than 30 msec had an 88% positive predictive value for prevention of sustained VT induction. In all except one patient in group I, drugs prolonged the VERP such that the coupling intervals that had resulted in sustained VT induction under control conditions were no longer attainable. In contrast, conduction time through the ventricle (surface QRS duration) in sinus rhythm and during right ventricular pacing was prolonged similarly regardless of efficacy (e.g., +33 +/- 21 msec vs +27 +/- 27 msec at a cycle length of 400 msec). The presence of similar plasma levels of drug did not imply equivalent prolongation of the VERP in the two groups. These results suggest that greater prolongation of the VERP by oral procainamide or quinidine correlates with drug efficacy against VT induction and is a better predictor of drug effect than achievement of a "therapeutic plasma level."     

Comparison of endocardial and epicardial programmed stimulation for the induction of ventricular tachycardia

Twenty-seven patients who had pairs of stainless steel wire electrodes placed on the right and the left ventricle during cardiac surgery underwent both epicardial and endocardial programmed ventricular stimulation to assess the inducibility of ventricular tachycardia. Twenty-six of the patients had coronary artery disease and were studied to evaluate map-guided surgery for treatment of ventricular arrhythmias. Burst ventricular pacing and up to three ventricular extrastimuli coupled to two drive train cycle lengths were delivered from the right and left ventricular epicardial wire electrodes and from endocardial catheter electrodes placed at the apex and outflow tract of the right ventricle. Ventricular tachycardia was reproducibly induced in three patients by both endocardial and epicardial stimulation. In one patient ventricular tachycardia was reproducibly induced by epicardial stimulation, but nonreproducible, nonsustained ventricular tachycardia was induced by endocardial stimulation. Ventricular tachycardia remained inducible by both endocardial and epicardial stimulation in three instances (two patients) during drug therapy. A negative study (less than 10 consecutive ventricular beats induced) was obtained in 23 patients by both endocardial and epicardial stimulation. The patients were followed up for 12 to 43 months (average 31). Sudden death or documented ventricular tachycardia occurred in two of the three patients with a positive study by both endocardial and epicardial stimulation. Nineteen (83%) of the 23 patients with concordantly negative studies remained free of arrhythmias. On the basis of concordant results of endocardial and epicardial stimulation (p = 0.001) these results suggest that epicardial stimulation of the right and the left ventricle is an acceptable method to assess the postoperative inducibility of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Discordant results of programmed ventricular stimulation at different right ventricular sites in patients with and without spontaneous sustained ventricular tachycardia: a prospective study of 56 patients

Programmed ventricular stimulation (PVS) was prospectively performed in 56 consecutive patients from both the right ventricular (RV) apex and the RV outflow tract. Thirty-seven patients had documented clinical sustained ventricular tachycardia (VT) and 19 patients had no sustained spontaneous VT in the absence of antiarrhythmic drugs. The sensitivity of VT induction was 65% from the RV apex, 76% from the RV outflow tract and was 89% with combined stimulation at both RV sites. The specificity from the RV apex, the RV outflow tract and both sites combined was 100%. When sustained VT was induced from both sites (51%), it was usually of the same morphologic characteristics, axis and cycle length. When sustained VT was induced at 1 site and nonsustained VT at the second site, the morphologic characteristics or axis usually differed. Of patients who had VT induced at both RV sites during the baseline study 37% had VT rendered noninducible during treatment with conventional antiarrhythmic agents. No patients whose VT was induced at only 1 RV site responded to conventional drugs. We conclude that programmed ventricular stimulation at a second RV site is frequently helpful in the evaluation of VT. Inducibility at only 1 of 2 RV sites predicts a poor response to conventional antiarrhythmic drugs.     

A prospective comparison of programmed ventricular stimulation with triple extrastimuli versus single and double extrastimuli during infusion of isoproterenol

This prospective study compared the yield of programmed ventricular stimulation with single and double extrastimuli during an infusion of isoproterenol with that of programmed stimulation with triple extrastimuli. The subjects of this study were 58 patients who underwent programmed stimulation and did not have inducible ventricular tachycardia (VT) with single or double extrastimuli at two basic drive cycle lengths and at two right ventricular sites; 17 patients had a history of uniform VT unrelated to exercise, and 41 had no history of documented or suspected VT or ventricular fibrillation (VF). Programmed stimulation was performed with triple extrastimuli at both right ventricular sites. Isoproterenol was infused as a dose titrated to increase the sinus rate by 25% or to a rate of 100 beats/min, whichever was greater, and stimulation then was repeated with single and double extrastimuli. Among the 17 patients with a history of uniform VT, the clinical VT was induced by three extrastimuli in five patients (29%) and by two extrastimuli during isoproterenol infusion in six patients (35%, p greater than 0.05). Among the total study population of 58 patients, nonclinical multiform VT or VF was induced by three extrastimuli in 29 patients (50%), and by two extrastimuli during isoproterenol infusion in 15 patients (26%, p less than 0.05). Therefore stimulation with two extrastimuli during isoproterenol infusion has the same probability of inducing a clinical form of VT as does stimulation with extrastimuli, but the former has a significantly lower probability of inducing nonclinical multiform VT and VF.     

Sequelae of nonsustained polymorphic ventricular tachycardia induced during programmed ventricular stimulation

The results of 206 programmed ventricular stimulation studies performed in 130 patients (100 men and 30 women, mean age 62 +/- 12 years, +/- standard deviation) were examined prospectively to determine the sequelae of nonsustained polymorphic ventricular tachycardia (VT) induced during programmed ventricular stimulation. The clinical indication for the electrophysiologic study was either documented monomorphic VT or unexplained syncope. The pacing protocol included 2 right ventricular pacing sites, 2 basic drive cycle lengths and up to 3 extrastimuli. In 111 studies, nonsustained polymorphic VT was induced and with continuation of the programmed stimulation protocol, sustained monomorphic VT was induced in 48 studies (43%) and polymorphic VT was induced in 13 studies (12%). Overall, sustained monomorphic VT was induced in 110 studies and sustained polymorphic VT in 18 studies. The incidence of nonsustained polymorphic VT preceding the induction of sustained polymorphic VT was significantly greater than the incidence of nonsustained polymorphic VT preceding the induction of sustained monomorphic VT (72 vs 44%, p less than 0.05). Nonsustained polymorphic VT is not a useful predictor of the outcome of programmed ventricular stimulation. The use of nonsustained polymorphic VT as an endpoint for stimulation would be likely to improve the specificity of programmed ventricular stimulation by limiting the induction of sustained nonclinical arrhythmias that require countershock, but at the cost of significantly impairing the yield of monomorphic VT.     

Comparison in the same patient of two programmed ventricular stimulation protocols to induce ventricular tachycardia

In 24 consecutive patients with documented ventricular tachycardia (VT) (22 patients) or fibrillation (VF) (2 patients), results of 2 programmed ventricular stimulation protocols to initiate VT/VF were prospectively studied. Seventeen patients had VT/VF after a healed myocardial infarction (MI) and 7 patients had idiopathic VT. In both protocols (designated 1 and 2), the right ventricular (RV) apex was paced at 100 beats/min, using a maximum of 2 ventricular premature complexes (VPCs) given at twice diastolic threshold. This protocol had a sensitivity of 25%. In protocol 1, the pacing site was changed to the RV outflow tract and the previous steps were repeated; in protocol 2, the pacing rate was increased to 120 and 140 beats/min at the RV apex, also using a maximum of 2 VPCs. The next step in protocol 1 consisted of increase of current strength to 20 mA and repeating previous steps at the RV apex and RV outflow tract, with a maximum of 2 VPCs; in the next step in protocol 2, three VPCs were used during sinus rhythm and pacing was performed at rates of 100, 120 and 140 beats/min. In protocol 1, therefore, only stimulation site and current strength were changed, while in protocol 2 only pacing rate and number of VPCs were modified. Protocol 1 had a sensitivity of 54% and protocol 2 a sensitivity of 83%. The sensitivity of protocol 2 was statistically higher than that of protocol 1 (p less than 0.05). In the group of patients with VT after MI, the sensitivity was 66% for protocol 1 and 93% for protocol 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of the results of programmed ventricular stimulation from the right ventricular apex and outflow tract: a randomized, prospective study

Objective: The aim of this prospective study was to analysethe yield of programmed ventricular stimulation at the rightventricular apex compared with the outflow tract. Methods: A stepwise randomized cross-over protocol of programmedventricular stimulation with alternating stimulation at bothsites was used in 66 patients who were studied because of sustainedventricular tachycardia (n = 30), ventricular fibrillation (n= 7), or non-sustained ventricular tachycardia and/or syncope(n = 29). Results: There were no significant differences between the resultsof stimulation from either right ventricular site with regardto the presence or absence of structural heart disease, spontaneousarrhythmia, ejection fraction or effective refractory periods.Overall, monomorphic ventricular tachycardia was inducible in33 patients (50%); in 25 patients (75.8%), this arrhythmia wasinduced from both sites. However, in only 17 of these 25 patients(68%) did the induced monomorphic ventricular tachycardias havethe same morphologies and similar (± 50 ms) cycle lengths.Ventricular fibrillation was inducible in 11 patients (17%),mostly by three extrastimuli (n=8; 73%). Conclusions: (1) stimulation from at least two right ventricularsites is desirable because of their independent contributionto the induction of ventricular tachyarrythmias, (2) the non-inducibilityor inducibility at one ventricular site does not predict theeffect at another stimulation site, (3) the effective refractoryperiod at the right ventricular apex and outflow tract do notdiffer, (4) the inducibility of multiple ventricular tachycardiamorphologies emphasizes the importance of documenting the causeof spontaneous arrhythmias with multiple electrocardiographicleads to ensure the correct interpretation of arrhythmias inducedby programmed stimulation, (5) clinical or haemodynamic featurescannot predict whether one or more stimulation sites will berequired for induction of ventricular tachycardia. These resultsare important for the diagnostic evaluation and assessment ofpharmacological or non-pharmacological interventions.     

Electrophysiologic investigation in Brugada syndrome; yield of programmed ventricular stimulation at two ventricular sites with up to three premature beats.

INTRODUCTION: Numerous reports on the inducibility of ventricular tachyarrhythmias (VT) in patients with atypical right bundle branch block and right precordial ST-elevation (Brugada syndrome) are based on multicentre studies that have used different stimulation protocols. Therefore, we prospectively investigated the inducibility of VT in these patients using a uniform protocol. METHODS: In 41 consecutive patients (29 males) showing a pattern of right bundle branch block and ST-elevation, programmed ventricular stimulation was performed in the right ventricular apex with up to three premature stimuli at sinus rhythm and at four different paced cycle lengths (500, 430, 370, and 330 ms) until refractoriness was reached or reproducible induction of a sustained (>30s) VT occurred. If a VT was not reproducibly inducible, the same protocol was repeated in the right ventricular outflow tract. RESULTS: A history of life-threatening events defined as syncope (n=17) or aborted sudden cardiac death (n=13) was present in 30 patients (73%); 11 individuals were asymptomatic. Inducibility (68%) was similar between symptomatic (n=21, 70%) and asymptomatic patients (n=7, 64%). In 16 (39%) patients, VT were reproducibly inducible. If patients were only stimulated in the right ventricular apex, inducibility rate decreased to 39%. If only two premature beats at two sites were used it was as low as 32%. The mean coupling intervals of the second and third premature stimuli inducing sustained VT were short: 189+/-21 ms vs 186+/-22 ms, respectively. Forty-four percent of all patients (i.e. 64% of the inducible patients) had inducible VT only with coupling intervals shorter than 200 ms. CONCLUSIONS: The stimulation protocol markedly influences the extent of inducibility of VT in patients with right bundle branch block and ST-segment elevation. These findings question the significance of previous multicentre studies using different stimulation protocols and should have implications for further studies.     

Reentrant ventricular tachycardia originating in the right ventricular outflow tract: slow conduction identified by right coronary artery ostium pacing.

A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was designated as the exit for the stable VT. Intriguingly, entrainment pacing from the ostium of the right coronary artery showed that the post-pacing interval was identical to VTCL. The stimulus to QRS interval was very long (340 ms) during entrainment with concealed fusion, and the right coronary artery ostium was therefore consistent with the VT reentry circuit inner loop or the upper portion of the VT reentry circuit exit. These findings suggest that the stable VT reentry circuit had a slow conduction zone from the ostium of the right coronary artery to the exit in the anterior septum RVOT. When radiofrequency catheter ablation was performed at the 2 exits of the anterior septum RVOT, both VTs then could not be induced.     

Late ventricular potentials and spontaneous and electric stimulation-induced ventricular tachycardia

The purpose of this study was to compare the relation of signal averaged variables of the QRS complex to spontaneous and to inducible sustained ventricular tachycardia. Signal averaging of the surface QRS complex was performed in 96 patients with coronary artery disease and ventricular arrhythmias. Twenty eight of them were evaluated by programmed electrical stimulation. Signal average variables were considered abnormal as: 1) the QRS duration as the time from the onset to end point of the QRS vector complex greater than 120 ms, 2) the maximal amplitude of the terminal 40 ms of the QRS vector complex less than 25 microV, 3) the duration of low (less than 40 microV) amplitude signal of QRS vector complex less than or equal to 40 ms. The ventricular late potentials were defined as the pressure of 2 or 3 abnormal averaged variables. Programmed electrical stimulation was performed using single and double extrastimuli at sinus rhythm and at ventricular pacing rates 100, 120, 140 bpm, followed by ventricular burst pacing (3 and 10 consecutive beats) at sinus rhythm. If stimulation of the right ventricular apex did not initiate ventricular arrhythmias (sustained ventricular tachycardia, ventricular fibrillation or two repetitive nonsustained ventricular tachycardias) right ventricular outflow tract stimulation was performed. Sustained ventricular tachycardia was defined as ventricular tachycardia lasting 30 s or requiring termination because hemodynamic compromise. Quantitative comparison of signal averaged variables was performed in patients with inducible versus noninducible ventricular tachycardia and in patients with spontaneous versus non-spontaneous ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of basic drive cycle length on the yield of ventricular tachycardia during programmed ventricular stimulation

The yield of sustained, monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation was compared, using basic drive trains of 400 ms, 600 ms and sinus rhythm, to identify the most efficient sequence of basic drive trains to use during programmed stimulation. Fifty-five patients with coronary artery disease and inducible sustained monomorphic VT not requiring countershock to terminate underwent 81 electrophysiology tests in which 1 to 3 extrastimuli were introduced during sinus rhythm and after basic drive trains of 600 and 400 ms. In 72 electrophysiology tests, sustained, monomorphic VT was induced at the right ventricular apex. The yield of VT using a drive cycle length of 400 ms was 63 of 72 (88%), compared to 46 of 72 (64%) when the drive cycle length was 600 ms, and 23 of 72 (32%) when the extrastimuli were introduced during sinus rhythm (p less than 0.001 for all pairwise comparisons). In 14 electrophysiology tests in which VT was not induced using a 400 ms basic drive cycle length at the apex, the yield of VT was higher using a 400 ms drive cycle length at a second right ventricular site (12 of 14) than with a 600 ms drive cycle length (3 of 12) or sinus rhythm (4 of 12) at the apex (p less than 0.05). The yield of sustained, monomorphic VT induced by 1 to 3 extrastimuli increases as the basic drive cycle length shortens. Whereas programmed stimulation is conventionally started during sinus rhythm or with a drive cycle length of 600 ms, the present results suggest that starting with a drive cycle length of 400 ms may be more efficient.