Effect of repetition of extrastimuli on sensitivity and reproducibility of mode of induction of ventricular tachycardia by programmed stimulation

This study examined the effect of repeating the delivery of a programmed extrastimulus that previously failed to induce ventricular tachycardia, without the usual practice of concurrently altering other stimulation variables such as pacing site or basic cycle length. The impact of such repetition on both sensitivity and day to day variability in mode of arrhythmia induction was assessed in 24 patients with documented sustained ventricular tachycardia or fibrillation. Programmed stimulation in the absence of drugs was performed in each patient on 3 separate days. In the first 12 patients, each extrastimulus was scanned through diastole to refractoriness four times if no ventricular tachyarrhythmia was induced (longitudinal repetition); in the second 12 patients, each extrastimulus was delivered four times at a particular coupling interval before the interval was decreased in 10 ms steps to a closer coupling interval (lateral repetition). Day to day reproducibility of the mode of arrhythmia induction was compared with reproducibility in a control group of 18 similar patients studied previously on 3 separate days without repetition. A sustained ventricular tachyarrhythmia was inducible in all studies with four or fewer extrastimuli. In the group studied with longitudinal repetition, there was a 25% increased yield of induced ventricular tachycardia due solely to repetition of each extrastimulus scan, and the 95% confidence limit for tachycardia induction with any extrastimulus was achieved by delivering that extrastimulus three times. In the group studied with lateral repetition, there was also an increased yield of induced ventricular tachycardia at any extrastimulus coupling interval achieved by repetitive delivery of that coupling interval.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of pacing drive cycle length on induction of sustained monomorphic ventricular tachycardia.

To assess the effect of pacing drive cycle length on induction of sustained monomorphic ventricular tachycardia, 40 patients were prospectively studied in the drug-free state. Ventricular extrastimuli were sequentially delivered at the same coupling interval at each of three drive cycle lengths (600, 500, and 400 ms) before the coupling interval was shortened and the process repeated. This protocol was continued until sustained monomorphic ventricular tachycardia was induced at all three drive cycle lengths or until pacing was completed through three extrastimuli. Of the 27 patients in whom sustained monomorphic ventricular tachycardia was induced, tachycardia was induced at all 3 drive cycle lengths in 12 (44%), only 2 drive cycle lengths in 11 (41%), and only 1 drive cycle length in 4 (15%) patients. Although the yield of inducible ventricular tachycardia increased with each additional extrastimulus, this yield increased even further with the use of multiple drive cycle lengths. In 10 of 11 patients, failure to induce ventricular tachycardia at any drive cycle length was not due to failure to achieve at that drive cycle length the critical extrastimulus coupling interval required to induce tachycardia at other drive cycle lengths. Induction of sustained monomorphic ventricular tachycardia is often drive cycle length specific, and failure to induce tachycardia cannot be explained by failure to achieve critically short coupling intervals. Pacing at multiple drive cycle lengths increases the yield of induced ventricular tachycardia.     

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.     

Effects of high stimulation current on the induction of ventricular tachycardia

Programmed stimulation at 2 right ventricular sites with 1 to 3 extrastimuli was performed at current strengths of twice diastolic threshold (1.0 +/- 0.2 mA, mean +/- standard deviation) and 10 mA in 41 patients undergoing an electrophysiologic study because of sustained ventricular tachycardia (VT) (11 patients), nonsustained VT (19 patients) or unexplained syncope (11 patients). In 26 patients, VT was not induced by programmed stimulation at twice diastolic threshold. Programmed stimulation at 10 mA induced VT or ventricular fibrillation in 16 of these 26 patients (62%). In 4 of 16 patients, the coupling intervals of the extrastimuli that induced VT/ventricular fibrillation at 10 mA were all equal to or longer than the shortest coupling intervals resulting in ventricular capture at twice diastolic threshold. Fifteen patients had inducible VT at twice diastolic threshold. Programmed stimulation at 10 mA induced a similar VT in 12 of these patients, but resulted in no VT induction in 3 of 15 patients (20%), despite ventricular capture at the same coupling intervals that had induced VT at twice diastolic threshold. This study shows that programmed stimulation at a high current strength may either facilitate or prevent induction of VT. Facilitation of VT induction usually is attributable to a shortening of ventricular refractoriness and the ability of extrastimuli at 10 mA to capture the ventricle at shorter coupling intervals than possible at twice diastolic threshold. However, in 25% of cases, the facilitation of VT induction by 10-mA stimuli is not explained by a shortening of ventricular refractoriness.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ventricular tachycardia induction: comparison of triple extrastimuli with an abrupt change in ventricular drive cycle length

This study compares two stimulation protocols in 47 patients not inducible with double extrastimuli administered during two paced cycle lengths at the right ventricular apex. Method I uses triple extrastimuli; method II, an abrupt short-to-long change in cycle length, single and double extrastimuli. Clinical arrhythmias included sustained ventricular tachycardia or fibrillation (11 patients; group I); nonsustained ventricular tachycardia (27; group II); and no documented ventricular arrhythmia (9; group III). Together, methods I and II rendered 21 of 47 patients inducible; seven were inducible by both methods. No group III patient became inducible. The two techniques were equally likely to produce tachycardias in groups I and II; to induce rapid, pleomorphic, or sustained tachycardias, and tachycardias greater than 10 beats. Since both methods can be applied at the right ventricular apex and increase sensitivity without producing tachycardia in patients with a low suspicion for ventricular arrhythmias, they may facilitate serial drug testing with an indwelling catheter, reducing the need for left-sided studies.     

不同部位右室起搏对心功能的影响

目的:比较右室心尖部起搏与右室间隔部起搏对心功能的影响. 方法:将48例高度房室传导阻滞患者随机分为右室心尖部起搏组(25例)或右室间隔部起搏组(23例).随访术后的超声心动图左室舒张末期内径和射血分数变化以及临床的NYHA心功能分级变化. 结果:24个月后,右室间隔部起搏组左室舒张末期内径,射血分数及NYHA分级较术前无明显变化.但右室心尖部起搏组与术前相比,左室舒张末期内径有增大趋势,射血分数显著减低,NYHA心功能分级级别增高.结论:右室间隔部起搏较右室心尖部起搏更有利于双心室电激动的同步性,且不产生对心功能的不良影响.     

不同部位右室起搏对心功能的影响

目的：比较右室心尖部起搏与右室间隔部起搏对心功能的影响。方法：将48例高度房室传导阻滞患者随机分为右室心尖部起搏组（25例）或右室间隔部起搏组（23例）。随访术后的超声心动图左室舒张末期内径和射血分数变化以及临床的NYHA心功能分级变化。结果：24个月后,右室间隔部起搏组左室舒张末期内径,射血分数及NYHA分级较术前无明显变化。但右室心尖部起搏组与术前相比,左室舒张末期内径有增大趋势,射血分数显著减低,NYHA心功能分级级别增高。结论：右室间隔部起搏较右室心尖部起搏更有利于双心室电激动的同步性,且不产生对心功能的不良影响。     

Limited value of programmed electrical stimulation from multiple right ventricular pacing sites in clinically sustained ventricular fibrillation or ventricular tachycardia associated with coronary artery disease

One-hundred and fifty patients with coronary artery disease and a documented history of sustained ventricular tachyarrhythmias were studied to determine if programmed electrical stimulation (PES) from a second right ventricular (RV) pacing site optimizes the induction of such sustained arrhythmias. The first PES test was performed from 2 RV pacing sites (apex and outflow tract or septum) using the apex first in each patient. All patients underwent a second PES within 6 to 24 hours of the first; both studies used up to 4 ventricular extrastimuli, in the absence of antiarrhythmic treatment. The second PES was performed from a single RV apical site using a pacing catheter retained from the first study. During the first day's study, 74 patients (49%) had sustained ventricular tachycardia induced from the RV apex. Only 11 of the remaining 76 patients (7% of the total group) were inducible exclusively from a second RV pacing location during the first day's testing. Seven of these 11 patients, as well as 15 additional patients who did not have ventricular tachycardia induced from either site on the first day's study, were inducible from the RV apex during the second drug-free study. Among patients with sustained ventricular tachyarrhythmias, limiting PES to a single RV site, with the option of performing a second study in those who are initially noninducible is more effective in inducing sustained ventricular tachyarrhythmias than is PES performed from 2 RV pacing sites.     

右心室不同位点起搏对QRS时限的影响

目的 观察右心室不同起搏位点的QRS时限,为临床导线放置提供参考依据.方法 选择216例符合Ⅰ类或Ⅱa类起搏器植入适应证的患者,在放置心室导线过程中,分别在右心室心尖部、流入道、中位间隔部、高位间隔部和流出道等不同位点起搏右心室,记录起搏时的体表心电图,比较不同位点QRS时限和形态的差异.结果 与基础心电图QRS波比较,所有右心室起搏部位心电图QRS时限均明显增宽(P＜0.001);以心尖部起搏QRS时限增宽(168±16) ms,其次为流入道(166±15) ms和流出道(165±15) ms;三者比较差异无统计学意义(P＞0.05).间隔部起搏QRS时限明显缩短(P＜0.001),且QRS波形态和电轴正常.中间隔部最短(139± 19) ms,高位间隔部次之(153±14) ms,二者相比差异有统计学意义(P＜0.01).结论 在所有右心室起搏位点中,中间隔部起搏QRS时限最窄,且形态和电轴正常.中间隔部可能是右心室最理想起搏选择位点.     

Characterization of the effects of single ventricular extrastimuli on endocardial activation in human infarct-related ventricular tachycardia.

OBJECTIVES: The purpose of this study was to examine the resetting response in human ventricular tachycardia (VT) circuits with 3-dimensional mapping. BACKGROUND: In characterizing re-entry with the resetting response, inferences are made about interaction of single ventricular extrastimuli (SVE) with VT. METHODS: Non-contact mapping was used to examine the effects of SVE from 25 sites on 10 infarct-related VT circuits. RESULTS: 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. CONCLUSIONS: 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.     

Prenylamine-induced ventricular tachycardia and syncope controlled by ventricular pacing.

We describe eight patients treated for angina with prenylamine who developed life-threatening ventricular arrhythmias after QT interval prolongation. When prenylamine administration was stopped QT interval shortened to within normal values, while the ventricular arrhythmias were controlled by a temporary ventricular pacemaker and disappeared after several days. We stress the importance of surveillance of the QT interval and ventricular arrhythmias in patients receiving long-term treatment with prenylamine.     

Termination of ventricular tachycardia with bursts of rapid ventricular pacing

Bursts of rapid ventricular pacing used during 573 episodes of ventricular tachycardia in 23 patients terminated 5 12 episodes (89 percent), with burst rates averaging 56 beats/min above the ventricular tachycardia rate, for 5 to 10 captures. Tachycardia was accelerated by pacing bursts to rates below 300 beats/min in 16 episodes (3 percent); 10 of these terminated spontaneously or responded to further bursts. Acceleration of heart rate to more than 300 beats/min or ventricular fibrillation occurred six times (1 percent), each episode requiring direct current cardioversion. Pacing bursts had no effect in 38 instances (7 percent), mostly in patients with terminal cardiogenic shock. Implantable pacemakers delivering bursts of rapid ventricular pacing were placed in two patients who have used these units at home. No deaths were associated with bursts of rapid ventricular pacing, which is an effective, rapid, pleasant alternative to repeated direct current cardioversion and a useful tool during electrophysiologic testing in patients with recurrent tachycardia.     

Effects of atrial pacing, isoprenaline and lignocaine on experimental polymorphous ventricular tachycardia

In 22 anaesthetised dogs, iv, administration of quinidine sulphate (30 mg X kg-1) over 5 min produced bradycardia and marked prolongation of the QT interval. Right ventricular extrastimulations, four times diastolic threshold, provoked polymorphous ventricular tachycardia in 18 dogs, and typical torsade de pointes was observed in four of these 18 dogs. Ventricular flutter was induced in another four dogs. In one of these 22 dogs, double stimuli were required to induce ventricular tachyarrhythmias, in 19 dogs triple stimuli, and in two dogs quadruple stimuli. Using this experimental model, effects of interventions including atrial pacing, isoprenaline, and lignocaine on the QT interval and induction of polymorphous ventricular tachycardia by extrastimuli were studied. Atrial pacing shortened QT interval only slightly and did not prevent induction of polymorphous ventricular tachycardia in nine dogs studied. Isoprenaline infusion definitely shortened QT interval, and in four out of nine dogs triple stimuli could not elicit polymorphous ventricular tachycardia. By contrast, although the QT interval was not shortened, lignocaine was effective in preventing induction of polymorphous ventricular tachycardia by triple stimuli in three out of nine dogs. These results indicate atrial pacing is an ineffective means of preventing induction of polymorphous ventricular tachycardia by extrastimuli in dogs with a long QT interval, but that isoprenaline and lignocaine are effective in some dogs.     

Permanent radiofrequency ventricular pacing for management of drug-resistant ventricular tachycardia

Three patients with frequent episodes of symptomatic, sustained ventricular tachycardia that often required physician intervention were treated with a permanent patient-activated radiofrequency ventricular pacemaker for self-termination of ventricular tachycardia. Before pacemaker implantation, electrophysiologic testing revealed the tachycardia to be resistant to all approved and several investigational antiarrhythmic drugs. In all three patients, ventricular tachycardia was reliably and reproducibly terminated with brief bursts of rapid right ventricular apical pacing over several hundred trials. No patient had rapid ventricular pacing-induced acceleration of ventricular tachycardia or pacing-induced ventricular fibrillation. Since the implantation of a radiofrequency ventricular pacemaker an average of 13.7 months ago, all episodes of ventricular tachycardia (average 43/patient) have been terminated successfully by radiofrequency pacing, and no patient has required hospitalization for an arrhythmia-related problem.     

Repetitive beating after single ventricular extrastimuli: Incidence and prognostic significance in patients with recurrent ventricular tachycardia

The incidence of repetitive ventricular beating in response to programmed single ventricular extrastimuli delivered during spontaneous rhythm was tabulated in 59 patients with recurrent ventricular tachycardia. Repetitive beating occurred in only nine patients (15 percent). The repetitive response seemed to be a result of bundle branch reentry in four subjects and possibly a result of other mechanisms in five. There was no difference in the incidence of repetitive beating or type of repetitive response in patients with and without ischemic heart disease. During an average patient follow-up period of 13.6 months, there were eight sudden and six nonsudden deaths. Life table analysis revealed a significantly greater incidence of sudden death in patients with ischemic than in patients with nonischemic heart disease. There was no significant difference in the incidence of sudden death in patients with and without repetitive beating. It is concluded that the repetitive response to single ventricular extrastimulation is infrequent in patients with recurrent ventricular tachycardia, and that repetitive beating is not a prognostic indicator or an indicator of vulnerability to ventricular tachycardia.