Termination of ventricular tachycardia: Role of tachycardia cycle length

The mode of termination of ventricular tachycardia (VT) and its relation to tachycardia cycle length was evaluated in 139 patients. Tachycardia was terminated by programmed stimulation in 110 patients (79%) and cardioversion was required in 29 patients (21% ). Single, double, and triple ventricular extrastimuli terminated the tachycardia in 23 of 85 (27%), 39 of 62 (63%), and 7 of 16 patients (44%), respectively. In all patients requiring 1 extrastimulus, in 35 patients (90%) requiring 2 extrastimuli, and in 6 patients (86%) requiring 3 extrastimuli, the tachycardia cycle length exceeded 300 ms. Rapid ventricular pacing terminated tachycardia in 41 of 54 patients (76%). In 21 (51%) of these patients the tachycardia cycle length exceeded 300 ms. However, rapid ventricular pacing caused acceleration of the arrhythmia in 19 patients (35%). The ability of procainamide to modify the termination of VT was studied in 23 patients. In 7 of these patients (30%) procainamide increased the tachycardia cycle length by 49 ± 42 ms (p < 0.01) and did not modify the mode of termination. In 6 patients (26%) procainamide increased cycle length by 142 ± 108 ms (p < 0.01), but termination was more difficult. In 10 patients (44%) procainamide increased the cycle length by 138 ± 110 ms (p < 0.001) and termination was easier. We conclude that termination of VT by timed extrastimuli requires a tachycardia cycle length longer than 300 ms. Rapid pacing or cardioversion is usually required when the cycle length is less than 300 ms. Although procainamide slows tachycardia, it can unpredictably make termination more difficult in 1 of 4 patients.     

Classical response of antidromic atriofascicular tachycardia to premature atrial extrastimulus delivered during septal refractoriness

A 23‐year‐old gentleman presented with a history of palpitations. The 12‐lead electrocardiogram showed no manifest ventricular pre‐excitation. Echocardiogram was within normal limits. A retrograde study showed concentric activation of the atrium with decremental conduction. Atrial pacing from right atrial free wall showed progressive pre‐excitation. No anterograde nodal duality was documented.     

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.     

Spontaneous changes in ventricular tachycardia cycle length

Understanding spontaneous fluctuations in ventricular tachycardia cycle length is required to develop algorithms for ventricular tachycardia detection and termination. Variations in cycle length, time to stable cycle length and the range of RR intervals during ventricular tachycardia were analyzed in 74 episodes of sustained monomorphic ventricular tachycardia induced in patients not taking antiarrhythmic medication. Linear regression demonstrated cycle length variability to decrease over time (41 +/- 24 to 17 +/- 19 ms, p less than 0.001). Slower ventricular tachycardia had more cycle length variability than faster ventricular tachycardia (p less than 0.001). Ventricular tachycardia that was initially more variable tended to remain more variable (p less than 0.001). Fifty-four percent of episodes stabilized within the first 15 beats, 75% by 30 beats and 93% by 50 beats. The number of beats to stable cycle length was independent of ventricular tachycardia rate. The average range in cycle length per episode was 127 +/- 72 ms; 12% of ventricular tachycardia episodes varied by less than 50 ms and 45% by less than 150 ms. The maximal range in RR intervals from a single episode of ventricular tachycardia was 290 ms. Therefore, ventricular tachycardia demonstrates a wide range of cycle lengths and has time-dependent changes in variability and stability. These cycle length changes should be considered in the algorithms for ventricular tachycardia detection and termination by automatic antitachycardia devices.     

Alternation of atrial cycle length in supraventricular tachycardia

Nine cases of alternation of the atrial cycles during supraventricular tachycardia are presented, three of which were manifestly due to digitalis toxicity. They presented the following features: absence of 1/1 conduction, upright P waves in Lead II, atrial rates of 156-218. When alternation disappeared, the atrium adopted the longest of the previously inscribed cycles. A ventriculophasic cause was excluded. The possible mechanisms are discussed in terms of the known functional anatomy of the various forms of SVT.     

Induction of ventricular fibrillation versus monomorphic ventricular tachycardia during programmed stimulation. Role of premature beat conduction delay.

BACKGROUND. Premature stimuli can cause ventricular fibrillation (VF) during electrophysiological testing. The electrophysiological correlations associated with the onset of VF were evaluated in 40 patients who had this rhythm induced during programmed ventricular stimulation. These parameters were compared with those observed in 51 patients who had inducible sustained monomorphic ventricular tachycardia (VT) and 45 patients who had no inducible sustained ventricular tachyarrhythmias. METHODS AND RESULTS. Shortest premature coupling intervals for S2, S3, and S4 at induction of tachycardia or before achieving refractoriness, corresponding conduction latencies (defined as the time from the premature stimulus to the upstroke of the depolarization wave front recorded 35 mm away from the stimulation site), and ventricular activation times (defined as the time from the premature stimulus to the end of the depolarization wave) were compared. The mean coupling intervals were longest in the inducible VT patients: 300 +/- 30, 254 +/- 57, and 228 +/- 32 msec for S2, S3, and S4, respectively. In the inducible VF group, the coupling intervals were 260 +/- 37, 208 +/- 20, and 213 +/- 30 msec. In the group with no inducible VT or VF, these coupling intervals were 251 +/- 24 (p less than 0.01 versus inducible VT group), 209 +/- 27 (p less than 0.001 versus inducible VT group), and 194 +/- 21 msec (p less than 0.05 versus inducible VT and VF groups). The coupling interval of the last premature extrastimulus was above 200 msec in 70% of the patients in whom VF was induced. The largest increases in latency and activation times were recorded in patients in whom VF was induced. The cumulative increase in latency, defined as increased conduction time from baseline, summed for all the premature stimuli was also the greatest at initiation of VF. In contrast, the smallest increases in these parameters were noted in the patients with no inducible VT or VF. Measurements of total activation time yielded similar results as those recorded for latencies. The most important parameters distinguishing the VT patient population from the other two groups were the low ejection fractions and the longer coupling intervals at which VT was induced, whereas in the VF group, the most important discriminating factor was cumulative activation time. Sixty-three percent of the inducible VF patients presented with abnormal hearts (myocardial infarction or cardiomyopathy), whereas 88% of the inducible VT patients had abnormal hearts. In contrast, only 25% of the patients in whom no arrhythmia was induced presented with abnormal hearts. Mean ejection fraction was 32 +/- 15% for the inducible VT group, 45 +/- 13%* for the inducible VF group, and 51 +/- 17%* for patients with no inducible VT/VF (*p less than 0.001 versus VT). CONCLUSIONS. The results suggest that 1) initiation of ventricular tachycardia during programmed ventricular stimulation occurs with minimal conduction latency; 2) because of the large overlap in coupling intervals where VF or VT were induced, a single coupling interval cannot be recommended to adequately separate these groups; and 3) induction of VF was preceded by increased latency and prolongation of the local activation time. These parameters should not be allowed to prolong if VF is to be avoided during programmed stimulation. In addition, 4) the initiation of VF during electrophysiological studies is often associated with the presence of structural heart disease; such structural disease may promote conduction latency and the development of VF.     

Syncope and ventricular tachycardia in patients with ventricular preexcitation

Four patients with ventricular preexcitation whose syncope initially was attributed to an arrhythmia utilizing the accessory pathway are presented. At electrophysiologic study, the electrophysiologic characteristics of the accessory pathways were considered unlikely to support a tachycardia of a rate sufficient to result in syncope. Programmed Stimulation of the right ventricle, however, reproducibly induced ventricular tachycardia to which the syncope was subsequently attributed in 3 patients. The importance of identifying ventricular tachycardia as the cause of syncope in these patients is emphasized.     

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.     

Utility of atrial and ventricular cycle length variability in determining the mechanism of paroxysmal supraventricular tachycardia

Introduction: No prior studies have systematically investigated the diagnostic value of cycle length (CL) variability in differentiating the mechanism of paroxysmal supraventricular tachycardia (PSVT).
Methods and Results : We studied 173 consecutive patients with PSVT; 86 typical atrioventricular nodal reentrant tachycardia (AVNRT), 11 atypical AVNRT, 47 orthodromic reciprocating tachycardia (ORT), and 29 with atrial tachycardia (AT). Two consecutive atrial cycles that displayed the most CL variability were selected for analysis. One hundred and twenty-six patients (73%) had ≥15 msec variability in tachycardia CL. The change in atrial CL predicted the change in subsequent ventricular CL in six of eight patients (75%) with atypical AVNRT, 18 of 21 patients (86%) with AT, in none of 66 patients with typical AVNRT, and in 32 patients with ORT. The change in atrial CL was predicted by the change in preceding ventricular CL in 55 of 66 patients (83%) with typical AVNRT, no patient with atypical AVNRT, 27 of 31 patients (87%) with ORT, and one of 21 patients (5%) with AT. The sensitivity, specificity, and positive and negative predictive values of a change in atrial CL predicting the change in ventricular CL for AT or atypical AVNRT were 83%, 100%, 100%, and 95%, respectively. The corresponding values for the change in atrial CL being predicted by the change in the preceding ventricular CL for typical AVNRT or ORT were 85%, 97%, 99%, and 65%, respectively.
Conclusion: Tachycardia CL variability ≥15 msec is common in PSVT. A change in atrial CL that predicts the change in subsequent ventricular CL strongly favors AT or atypical AVNRT. A change in atrial CL that is predicted by the change in the preceding ventricular CL favors typical AVNRT or ORT.     

经食管心房调搏诱发及终止预激综合征房室折返性心动过速的研究

目的探讨经食管心房调搏诱发和终止预激综合征阵发性房室折返性心动过速的价值.方法对30例预激综合征患者行食管心房调搏程控刺激.结果经食管心房调搏对房室折返性心动过速的诱发率,典型预激综合征A型与B型差异无显著意义(P＞0.05),典型预激综合征与詹姆斯型预激综合征差异则有非常显著意义(P＜0.05).心房刺激诱发顺向型房室折返性心动过速的关键因素是旁道有效不应期大于房室交接区有效不应期.结论典型预激综合征的类型对诱发房室折返性心动过速无明显影响;诱发的关键因素是旁道有效不应期大于房室交接区有效不应期;猝发法是终止发作的最有效方法之一,转复成功率接近100%.     

Simultaneous alterations of QRS configuration and tachycardia cycle length during radiofrequency ablation of idiopathic left ventricular tachycardia

Idiopathic left ventricular tachycardia is characterized by a QRS morphology of right bundle branch block pattern and left axis deviation. Alterations in the QRS configuration and tachycardia cycle length, as well as shifting of the earliest activation site occurred after eliminating the original tachycardia by radiofrequency current in an 18-year-old man with idiopathic left ventricular tachycardia. Activation mapping and entrainment mapping during tachycardia identified 2 putative tachycardia exits, 15 mm apart. Elimination of both tachycardias was accomplished after applying radiofrequency current to each exit separately. We proposed that the first radiofrequency application might have altered the exit site and the zone of slow conduction adjacent to the exit site, such that the ventricular tachycardia had a different QRS morphology and became slower in this patient.     

Facilitation of ventricular tachycardia induction with abrupt changes in ventricular cycle length

The effect of abrupt short-to-long changes in cycle length (CL) on the postulated reentrant circuit of ventricular tachycardia (VT) was evaluated. This was performed using single and double ventricular extrastimuli in a group of 21 patients clinically suspected of having VT in whom VT could not be induced at comparable or shorter constant CLs. A second group of 10 patients without suspected VT was similarly studied. Compared with constant CLs of equal or shorter duration preceding the single or double ventricular extrastimuli, abrupt short-to-long CL changes resulted in (1) initiation of sustained VT in 13 of 21 patients in whom VT could not be induced at constant CLs despite the use of shorter S1S3 by 66 +/- 17 ms; (2) increased incidence of initiation of sustained VT after the V3 phenomenon resulting from macroreentry within the His-Purkinje system (Re-HPS); (3) a small but higher incidence of sustained VT due to sustained Re-HPS; and (4) no induction of sustained or nonsustained VT with either method in the second group of patients. These results provide additional support for reentry as the basis for sustained ventricular tachyarrhythmias. Abrupt short-to-long CL changes may be effective for initiating sustained VT in patients at risk for these arrhythmias.     

Cycle length change during reciprocating tachycardia in patients with Wolff-Parkinson-White syndrome

Cycle Length (CL) changes during reciprocating tachycardia (RT) were examined in 82 consecutive patients with Wolff-Parkinson-White syndrome (WPW) during electrophysiological studies. The significant CL changes (sudden and greater than 30 msec.) were found in 21 of 82 patients (26%). Thirteen patients had a manifest WPW and eight had a concealed WPW. An accessory pathway (AP) was located in the left side in 14 patients, the right side in four patients and the septum in two patients. One patient had multiple AP's. The development of ipsilateral bundle branch block during RT was responsible for CL changes in 11 patients. The sudden shift between fast and slow pathways in atrioventricular node (AVN) during RT was responsible for CL changes in two patients. Alternating CL changes during RT were found in eight patients. In five of them, alternating CL changes could be explained by physiological properties of a single AVN pathway. In the remaining three patients, the onset of 2:1 block in a fast pathway with 1:1 conduction in a slow pathway of the AVN may be responsible for CL changes. In one patient with multiple AP's the shift from one re-entrant circuit to the other was responsible for CL changes. In conclusion: 1) CL changes during RT are not uncommon in patients with WPW. 2) Several different mechanisms are responsible for CL changes.     

Effects of sotalol on the signal-averaged electrocardiogram in patients with sustained ventricular tachycardia: relation to suppression of inducibility and changes in tachycardia cycle length.

OBJECTIVES. This study examines the effects of sotalol on the signal-averaged electrocardiogram (ECG) in patients with spontaneous and inducible sustained ventricular tachycardia and correlates these findings with the effect of sotalol on tachycardia inducibility and tachycardia rate. BACKGROUND. Standard electrocardiography generally does not detect any change in the duration of the QRS complex resulting from sotalol therapy. However, the signal-averaged ECG is more sensitive than the standard ECG for detecting changes in QRS duration induced by antiarrhythmic drugs and can also detect changes in late potential duration. METHODS. Signal-averaged electrocardiography was performed before therapy in 30 patients with spontaneous and inducible ventricular tachycardia, and both electrophysiologic study and a signal-averaged ECG were repeated during therapy with d,l-sotalol. RESULTS. During sotalol therapy the signal-averaged QRS duration decreased by 2.6 +/- 6.6 ms in the 11 patients with no inducible tachycardia during therapy, whereas it increased by 3.8 +/- 5.8 ms (p = 0.01) in the 19 patients with inducible tachycardia during therapy. In the latter group there was a significant positive correlation between prolongation of tachycardia cycle length and prolongation of late potential duration by sotalol (r = 0.56, p = 0.01). CONCLUSIONS. Sotalol can alter QRS and late potential duration as measured by the signal-averaged ECG. Prolongation of QRS duration or late potential duration may reflect a slowing of conduction by sotalol that may interfere with this agent's antiarrhythmic efficacy and slow ventricular tachycardia.