Incidence and clinical significance of induced ventricular tachycardia

Five hundred twenty-nine patients were studied with programmed ventricular stimulation for evaluation of supraventricular and ventricular tachyarrhythmias. Eighty-six patients had clinical ventricular tachycardia. Sustained ventricular tachycardia was induced in 52 (91 percent) of the 57 patients with a sustained form of the arrhythmia clinically. Nonsustained ventricular tachycardia was induced in 18 (62 percent) of 29 patients with a symptomatic nonsustained form clinically, in 2 (4 percent) of 57 patients with a sustained form and in 3 (0.7 percent) of the 443 patients with no documented spontaneous ventricular tachycardia. Ventricular tachycardia (sustained or nonsustained) was induced by double right or left ventricular extrastimuli in 47 patients (63 percent) and by single right ventricular extrastimuli in 23 (31 percent); in 5 (7 percent), it was inducible only by rapid ventricular pacing and in 9 (12 percent) only by left ventricular stimulation.All 52 patients with induced sustained ventricular tachycardia had the sustained form clinically. Of the 23 patients with induced nonsustained ventricular tachycardia, 18 (78 percent) had the nonsustained form clinically. Four hundred fifty-four patients had no induced ventricular tachycardia; only 14 (3 percent) of these had the arrhythmia spontaneously. The morphologic features, axis and cycle length of 54 of 62 episodes of induced ventricular tachycardia in 43 patients were similar to those of the clinically observed arrhythmia. It is concluded that ventricular tachycardia resembling the clinical variety can be induced in the laboratory in almost all patients with sustained ventricular tachycardia clinically, in the majority of those with symptomatic nonsustained ventricular tachycardia clinically, and only rarely in patients with no previously documented ventricular tachycardia. Conversely, induction of ventricular tachycardia implies the likelihood of spontaneous episodes of this arrhythmia.     

Role of triple extrastimuli during electrophysiologic study of patients with documented sustained ventricular tachyarrhythmias

Electrophysiologic studies were performed in 172 consecutive patients for evaluation of documented sustained ventricular tachyarrhythmias. One hundred thirteen patients presented with sustained ventricular tachycardia that was hemodynamically stable, and 59 patients presented with cardiac arrest. Seventy-one patients without previously documented or suspected ventricular arrhythmias were also studied to determine the specificity of our electrophysiologic study protocol. The stimulation protocol included single, double, and triple right ventricular extrastimuli and rapid ventricular pacing at multiple cycle lengths performed at one or more right ventricular sites. Stimulation was performed at one or more left ventricular sites in patients with documented spontaneous arrhythmias when right ventricular programmed stimulation failed to induce sustained ventricular tachycardia. Ventricular tachyarrhythmias were induced in 110 (97%) of the patients who presented with sustained ventricular tachycardia, in 48 (81%) of the patients who presented with cardiac arrest, and in 28 (40%) of the patients without documented spontaneous arrhythmias. Right ventricular triple extrastimuli induced tachycardia in 22% of patients who presented with sustained ventricular tachycardia vs 46% of those who presented with cardiac arrest (p less than .001). Left ventricular stimulation was required for tachycardia induction in 3% of patients with stable tachycardia vs 19% of those with cardiac arrest (p less than .01). Triple extrastimuli induced 57% of tachycardias in the 28 patients without spontaneous arrhythmias, and virtually all of these tachycardias were polymorphic and nonsustained. The cycle lengths of tachycardias induced in each group by double and triple extrastimuli were similar, but the tachycardias induced in patients with cardiac arrest were significantly faster than those induced in the ventricular tachycardia group (mean cycle length 218 vs 291 msec, p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Mechanism of ventricular fibrillation in man. Observations based on electrode catheter recordings.

Observations are reported on the initiation and spontaneous termination of ventricular fibrillation in man using endocardial electrode catheter recordings. The report is based on 16 patients in whom ventricular fibrillation developed during electrophysiologic study. In 11 patients ventricular fibrillation was initiated by programmed ventricular stimulation and in 5 patients ventricular fibrillation occurred spontaneously. In each patient two to five simultaneous ventricular electrograms were recorded at the onset or termination, or both, of ventricular fibrillation. In most patients ventricular fibrillation began as a rapid and accelerating ventricular rhythm in which local electrograms remained discrete and with progressively shortening coupling intervals. Degeneration of local electrograms into fibrillatory activity occurred at random and at varying times. In four patients ventricular fibrillation developed spontaneously during sustained ventricular tachycardia. In these cases there was acceleration of the ventricular tachycardia before degeneration to ventricular fibrillation. Fragmentation and disorganization in local ventricular electrograms did not appear to spread between contiguous areas, but occurred randomly in widely separated areas. In six patients ventricular fibrillation spontaneously converted to sinus rhythm. In four of these cases spontaneous conversion was preceded by sequential reorganization of the electrograms and a tendency toward increasing interelectrographic intervals. These observations are compatible with the multiple wavelet (reentrant) theory of ventricular fibrillation.     

Analysis of the resetting phenomenon in sustained uniform ventricular tachycardia: incidence and relation to termination

Although the phenomenon of resetting has been studied in several experimental and clinical rhythms, it has not been systematically analyzed in ventricular tachycardia. To define the incidence and determinants of resetting as well as its relation to ventricular tachycardia termination, the response to programmed stimulation was prospectively studied during 78 electrically induced episodes of sustained, uniform ventricular tachycardia (mean cycle length 365 +/- 59 ms) in 53 patients. Single and double ventricular extrastimuli were introduced during 78 and 39 episodes of ventricular tachycardia, respectively. Rapid ventricular pacing was performed during 27 episodes. Resetting occurred in response to single ventricular extrastimuli in 43 (55%) of 78 ventricular tachycardias, to double extrastimuli in 31 (79%) of 39 ventricular tachycardias and to rapid pacing in 23 (85%) of 27 ventricular tachycardias. No ventricular tachycardia characteristic distinguished those tachycardias that were reset from those not reset. Termination of ventricular tachycardia occurred in 7 (9%) of 78 episodes with single ventricular extrastimuli, 14 (36%) of 39 episodes with double ventricular extrastimuli and 13 (48%) of 27 episodes with rapid pacing. Termination was less frequent than resetting with both single (9 versus 55%) and double (36 versus 79%) extrastimuli, as well as rapid pacing (48 versus 85%). Resetting preceded termination in 7 of 7 ventricular tachycardias terminated with single ventricular extrastimuli, 12 of 14 terminated with double ventricular extrastimuli and 9 of 13 terminated by rapid pacing. Ventricular tachycardias that were terminated could not be differentiated from those that were reset without termination. In conclusion: Resetting with programmed extrastimuli is common in hemodynamically stable sustained ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Lack of Benefit of Very Short Basic Drive Train Cycle Length or Repetition of Extrastimulus Coupling Intervals for Induction of Ventricular Tachycardia

Stimulation Protocol for VT Induction. Introduction: There are considerable variations of uncertain importance in basic drive train cycle lengths and degree of repetition of extrastimuli used in programmed ventricular stimulation protocols in different laboratories. We compare prospectively three different stimulation protocols to examine the influence of a short basic drive train cycle length and repetition of extrastimuli on induction of ventricular tachycardia. Methods and Results: Thirty consecutive patients who had documented ventricular tachycardia or fibrillation based on underlying coronary artery disease underwent programmed ventricular stimulation with each of the three study protocols. Protocol A used a basic drive train cycle length of 400 msec with each extrastimulus coupling interval delivered only once. Protocol B used the same basic drive train cycle length, but with each extrastimulus coupling interval repeated three times before decrementing. Protocol C used 300 msec as the cycle length of basic drive trains without repetition of extrastimuli. Sixty-three percent, 67%, and 63% of the study patients bad ventricular tachycardia inducible with protocols A, B, and C, respectively (P = NS). Ventricular fibrillation was induced in 23% of the 30 patients in all three protocols. There were no significant differences in the mean cycle lengths of induced ventricular tachycardia, the number of extrastimuli used, and the coupling interval of the last extrastimulus inducing ventricular tachycardia among the three protocols. Conclusion: This study showed no clinical benefit for repetition of extrastimuli that have failed to induce a ventricular tachyarrhythmia during programmed ventricular stimulation. A short basic cycle length of 300 msec was not superior to 400 msec for induction of ventricular tachyarrhythmias. We recommend the use of basic cycle length 400 msec with delivery of each extrastimulus interval only once as the initial protocol for programmed ventricular stimulation.     

Identifying patients at risk of sudden death after myocardial infarction: Value of the response to programmed stimulation, degree of ventricular ectopic activity and severity of left ventricular dysfunction

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (≥4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study).

During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of <40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).

Thus, using the described protocol, the response to programmed ventricular stimulation is not helpful in identifying patients at risk for sudden death after MI. The presence of an LV aneurysm or EF of <40% appears to provide the greatest prognostic information with respect to risk for sudden cardiac death.     

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.     

Programmed ventricular stimulation: influence of early versus late introduction of a third extrastimulus, a randomized, prospective study.

OBJECTIVE: The aim of this prospective study was to analyze the yield of early vs late introduction of a third extra-stimulus during programmed ventricular stimulation. METHODS: Two randomized protocols of programmed ventricular stimulation were used in 94 consecutive patients with coronary artery disease who were studied because of non-sustained ventricular tachycardia (9.6%), sustained monomorphic ventricular tachycardia (46.8%), ventricular fibrillation (18.1) or syncope (25.5%). During protocol A, a third extrastimulus was introduced during a basic drive cycle length of 500 ms after completion of programmed ventricular stimulation with 1 and 2 extrastimuli during sinus rhythm and paced cycle lengths of 500, 430. 370 and 330 ms. During protocol B, the third extrastimulus was introduced early (after 1 and 2 extrastimuli during sinus rhythm and a paced cycle length of 500 ms). Both protocols began at the right ventricular apex. If sustained ventricular tachyarrhythmia had been induced, the same sequence of programmed ventricular stimulation was repeated at the right ventricular outflow tract. RESULTS: The overall incidence of induced arrhythmias did not differ between the two protocols. However, the use of the third extrastimulus (both protocols) increased the yield of ventricular fibrillation induction significantly (P < 0.04) compared with ventricular tachycardia induction. CONCLUSIONS: The introduction of the third extrastimulus should be considered only at the end of stimulation protocols (especially in those patients without previously documented sustained ventricular tachyarrhythmias) in order to prevent induction of polymorphic ventricular tachycardia or fibrillation.     

Influence of drive cycle length during programmed stimulation on induction of ventricular arrhythmias: analysis of 403 patients

The drive cycle length at which programmed ventricular stimulation is performed is a fundamental variable in all stimulation protocols, but the influence of this variable on the ability to induce ventricular arrhythmias has not been systematically analyzed. This study, which included 403 patients with prior ventricular tachycardia (VT) or ventricular fibrillation undergoing programmed ventricular stimulation with a uniform protocol that incorporated 3 basic drive cycle lengths from the right ventricular apex, was performed to examine the influence of drive cycle length on the induction of ventricular arrhythmias. The sensitivity of the protocol was 62% for nonsustained VT, 73% for ventricular fibrillation and 89% for sustained VT. Fifty-four percent (217 patients) had an arrhythmia induced with programmed ventricular stimulation during ventricular pacing. No arrhythmia was induced in 96 patients (24%), whereas induction was accomplished during sinus rhythm in 61 patients (15%) and rapid ventricular pacing in 29 patients (7%). With this protocol, the sensitivity for single and double extrastimuli during ventricular pacing increases using decremental drive cycle lengths. Although only 2 patients had induction of a ventricular arrhythmia at a drive cycle length of 700 to 650 ms using a single extrastimulus, 14, 8 and 3 patients had ventricular arrhythmias induced by single extrastimuli at drive cycle lengths of 600 to 550, 500 to 450 and 400 ms, respectively. Of 163 patients with arrhythmias induced with double extrastimuli, only 6 had an arrhythmia induced at drive cycle lengths of 700 to 650 ms.(ABSTRACT TRUNCATED AT 250 WORDS)     

Anatomic and electrophysiologic correlates of ventricular tachycardia requiring left ventricular stimulation

In 108 patients with reproducible initiation of ventricular tachycardia by programmed ventricular stimulation, the ventricular tachycardia was initiated only by left ventricular stimulation in 12 (11 percent). Programmed ventricular stimulation included single and double extrastimuli at three cycle lengths and bursts of rapid pacing to cycle lengths of 250 ms. Clinical, electrocardiographic, angiographic, hemodynamic and electrophysiologic data were available in 74 of 96 patients with ventricular tachycardia initiated by right ventricular stimulation (Group A) and in all 12 patients with ventricular tachycardia initiated only by left ventricular stimulation (Group B). There were no significant differences between Groups A and B in clinical characteristics, hemodynamics or presence and site of infarction or aneurysm. Comparison of electrophysiologic variables revealed no significant differences between Groups A and B in mean A-H interval (92 ± 22 versus 89 ± 15 ms, respectively), H-V interval (59 ± 15 versus 59 ± 15 ms) or right ventricular (241 ± 38 versus 260 ± 40 ms) or left ventricular (232 ± 28 versus 251 ± 42 ms) effective refractory period. Ventricular tachycardia with right bundle branch block and superior axis was more prevalent in Group B (92 percent versus 31 percent, p <0.001) but was observed in 32 patients in Group A.It is concluded that 11 percent of patients with clinically documented sustained ventricular tachycardia will require left ventricular programmed stimulation to reproducibly initiate the tachycardia. No clinical, anatomic, electrocardiographic or electrophysiologic features can predict whether left ventricular programmed stimulation will be required. Because initiation of ventricular tachycardia by programmed ventricular stimulation has important prognostic and therapeutic implications in such patients, stimulation should be performed from the left ventricle when the tachycardia is not initiated by stimulation from the right ventricle.     

Can potentially significant polymorphic ventricular arrhythmias initiated by programmed stimulation be distinguished from those that are nonspecific?

Polymorphic ventricular arrhythmias (PVAs) initiated by programmed electrical stimulation may be a nonspecific response or evidence of ventricular electrical instability. To determine if PVAs initiated in patients with spontaneous sustained ventricular tachycardia or fibrillation differ from those which are clearly a nonspecific response in structurally normal hearts, the initiation, characteristics, and relationship to ventricular repolarization of PVAs greater than five beats in duration were evaluated in 32 patients without structural heart disease and in 36 patients with spontaneous sustained ventricular arrhythmias more than 9 days after myocardial infarction. Patients received one to four extrastimuli during sinus rhythm and right ventricular pacing. In a comparison with patients who completed the same steps (defined by the basic drive cycle length and number of extrastimuli) in the stimulation protocol, there was no difference in the cumulative risk of initiation of a PVA between the patients with and those without heart disease at any step. This risk was 51% vs 38% for patients who received two or fewer extrastimuli at four basic cycle lengths (p = NS). PVAs were initiated by the same mean number of extrastimuli (2.3 +/- 0.5 vs 2.6 +/- 0.9 p NS) with the same degree of prematurity in both groups. Forty-four percent of the PVAs in the myocardial infarction group had a cycle length greater than 250 msec or a coupling interval of the first tachycardia beat to its initiating stimulus greater than 320 msec as opposed to only one (6%) in the group without heart disease (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Comparison of bipolar and unipolar programmed electrical stimulation for the initiation of ventricular arrhythmias: significance of anodal excitation during bipolar stimulation

To determine if anodal excitation during bipolar stimulation facilitates the initiation of sustained monomorphic ventricular tachycardia, nonsustained polymorphic ventricular tachycardia, or repetitive ventricular responses, both bipolar and cathodal unipolar programmed ventricular stimulation with one to three extrastimuli delivered during ventricular pacing at two rates from the right ventricular apex were performed in 28 patients evaluated for spontaneous sustained ventricular tachycardia or ventricular fibrillation (11 patients), nonsustained tachycardia (eight patients), or syncope (nine patients). In 25 patients a hexapolar pacing catheter was used to record local endocardial activation times adjacent to the cathode and anode and ventricular excitation during bipolar stimulation was defined as predominantly anodal, cathodal, or simultaneous at both anode and cathode. When bipolar and unipolar stimulation were compared there was no difference in the incidence of initiating sustained monomorphic ventricular tachycardia (57% vs 57%), nonsustained polymorphic ventricular tachycardia (14% vs 14%), or repetitive ventricular responses (21% vs 21%), although the response to bipolar vs unipolar stimulation was not concordant in every patient. Evidence of anodal excitation was observed in 11 (44%) patients but did not indicate increased risk of initiation of any ventricular arrhythmia, despite the fact that it was associated with shortening of the ventricular effective refractory period by 5.2 +/- 8.7 msec (p less than .05) during bipolar as opposed to unipolar stimulation. We conclude that unipolar and bipolar stimulation produce a similar incidence of initiation of arrhythmia, despite the frequent occurrence of anodal excitation during bipolar stimulation. Thus, the risk of initiation of nonspecific ventricular arrhythmias during programmed stimulation is unlikely to be reduced by the use of unipolar stimulation.     

Inducible multiform ventricular tachycardia in Wolff-Parkinson-White syndrome.

The induction of ventricular tachycardia by ventricular stimulation was investigated in 46 patients with isolated Wolff-Parkinson-White syndrome (10 concealed) and 36 control patients with normal electrocardiograms and conduction systems. None of those studied had spontaneous ventricular arrhythmias or myocardial or valve disease. Single and double ventricular extrastimuli were delivered at 3 cycle lengths (sinus, 600 ms, 400 ms). In the controls ventricular simulation induced one episode (3%) of non-sustained ventricular tachycardia. Ventricular stimulation in patients with Wolff-Parkinson-White syndrome induced two episodes of ventricular fibrillation and 15 episodes of non-sustained multiform ventricular tachycardia (37%). Ventricular arrhythmias were induced only in patients with overt Wolff-Parkinson-White syndrome. In 14 patients the conformation of the electrocardiogram at the start of ventricular tachycardia resembled that of major pre-excitation. The absence of inducible ventricular tachycardia in patients with concealed Wolff-Parkinson-White syndrome suggests that anterograde conduction via an atrioventricular accessory pathway is required to initiate the ventricular arrhythmias: the ventricular tachycardia may be associated with reentry of impulses via atrioventricular connection during the phase of ventricular vulnerability. The similarity between the start of ventricular tachycardia and pre-excitatory complexes may also indicate local reentry into the ventricular area occupied by the bypass tracts. Patients with Wolff-Parkinson-White syndrome and anterograde pre-excitation are more likely to have inducible multiform ventricular tachycardia than individuals without Wolff-Parkinson-White syndrome.     

Inducible multiform ventricular tachycardia in Wolff-Parkinson-White syndrome

The induction of ventricular tachycardia by ventricular stimulation was investigated in 46 patients with isolated Wolff-Parkinson-White syndrome (10 concealed) and 36 control patients with normal electrocardiograms and conduction systems. None of those studied had spontaneous ventricular arrhythmias or myocardial or valve disease. Single and double ventricular extrastimuli were delivered at 3 cycle lengths (sinus, 600 ms, 400 ms). In the controls ventricular simulation induced one episode (3%) of non-sustained ventricular tachycardia. Ventricular stimulation in patients with Wolff-Parkinson-White syndrome induced two episodes of ventricular fibrillation and 15 episodes of non-sustained multiform ventricular tachycardia (37%). Ventricular arrhythmias were induced only in patients with overt Wolff-Parkinson-White syndrome. In 14 patients the conformation of the electrocardiogram at the start of ventricular tachycardia resembled that of major pre-excitation. The absence of inducible ventricular tachycardia in patients with concealed Wolff-Parkinson-White syndrome suggests that anterograde conduction via an atrioventricular accessory pathway is required to initiate the ventricular arrhythmias: the ventricular tachycardia may be associated with reentry of impulses via atrioventricular connection during the phase of ventricular vulnerability. The similarity between the start of ventricular tachycardia and pre-excitatory complexes may also indicate local reentry into the ventricular area occupied by the bypass tracts. Patients with Wolff-Parkinson-White syndrome and anterograde pre-excitation are more likely to have inducible multiform ventricular tachycardia than individuals without Wolff-Parkinson-White syndrome.     

Late induction of tachycardia in patients with ventricular fibrillation associated with acute myocardial infarction

A prospective study was made of 57 asymptomatic patients, 1 to 24 months after acute myocardial infarction, 17 with (Group I) and 40 without (Group II) ventricular fibrillation during the acute event. None of the 57 patients had symptomatic arrhythmias, uncontrolled heart failure or unstable angina. There was no significant difference between the two patient groups in time from acute myocardial infarction, medication used or left ventricular ejection fraction. Repetitive forms of arrhythmia (Lown grade 4) were more prevalent (29 versus 16%, not significant) during 24 hour ambulatory monitoring in patients in Group I (ventricular fibrillation group). Programmed extrastimulation was performed using 1 to 3 twice-threshold, 2 ms decremental extrastimuli delivered during right ventricular drive. Of the 17 patients in Group I, 8 had no induced arrhythmia (less than or equal to 4 extra responses), 4 had nonsustained ventricular tachycardia and 5 had sustained ventricular tachycardia (degenerating into ventricular fibrillation requiring electrical reversion in 4). None of the 40 patients in Group II had induced sustained ventricular tachycardia (p less than 0.005), although 9 had nonsustained ventricular tachycardia. Patients with ventricular fibrillation during acute myocardial infarction may have an increased risk for ventricular tachycardia or ventricular fibrillation that may be exposed by programmed electrical stimulation even when not yet clinically manifest.     

Efficacy of a tiered therapy defibrillator system used to treat recurrent ventricular arrhythmias refractory to drugs.

OBJECTIVE--To evaluate an implantable tiered therapy defibrillator system that delivered antitachycardia pacing treatment for slower well tolerated ventricular tachycardias and cardioversion or defibrillation for fast tachycardias or ventricular fibrillation. METHODS--A tiered treatment device (Ventritex Cadence V-100) was implanted in 30 patients with ventricular tachycardia that was refractory to drugs. Efficacy was evaluated by the responses of induced or spontaneous arrhythmias to the treatments delivered. RESULTS--Antitachycardia pacing successfully terminated 80% of episodes of ventricular tachycardia induced by non-invasive programmed stimulation, but acceleration was brought about by pacing in six patients in 10% of episodes. During a follow up of two to 17 (mean seven) months, 18 patients (60%) had recurrence of ventricular arrhythmias. Antitachycardia pacing terminated ventricular tachycardia in 17 of 18 patients in 87% of episodes. Twelve patients received shocks for ventricular tachycardia or fibrillation. Failure of pacing, with subsequent cardioversion, occurred in nine patients (50%) in one or more episodes. Acceleration of tachycardia by pacing occurred in 10 patients in 5% of episodes. Only two of these patients had experienced acceleration of previously induced arrhythmia. Five patients had spontaneous fast ventricular tachycardia or fibrillation treated by cardioversion or defibrillation. Spurious treatment was delivered in nine patients (30%), during atrial fibrillation in five, sinus tachycardia in two, and because of fracture of the sensing lead system in two patients. The retrieval of stored intracardiac electrograms was of clinical value in assessing spurious treatment. CONCLUSIONS--Tiered treatment was effective in terminating recurrent ventricular arrhythmias in these selected patients. Most episodes were treated successfully by pacing, and resistant tachycardias, pacing induced acceleration, or haemodynamically compromising arrhythmias were treated by shocks.     

External cardiac programmed stimulation for noninvasive termination of sustained supraventricular and ventricular tachycardia

To examine the feasibility of using a noninvasive temporary pacemaker for termination of well-tolerated supraventricular (SVT) and ventricular tachycardia (VT), a standard external demand pacemaker was modified to allow stimulation with single or multiple extrastimuli and overdrive pacing. To evaluate the efficacy, safety and tolerance of external cardiac programmed stimulation, a standard arrhythmia termination protocol was used in 223 tachycardias in 22 patients. The technique of external cardiac programmed stimulation was used in 209 episodes of SVT in 13 patients. It terminated 95% of the episodes with success in 19 of 20 episodes of atrioventricular nodal reentrant tachycardia and 179 of 189 episodes of atrioventricular reciprocating tachycardia. Of 198 episodes of SVT terminated by the technique 168 (85%) were terminated by a single extrastimulus and 28 (14%) by double extrastimuli. Only 2 episodes of SVT required overdrive pacing for termination. External cardiac programmed stimulation did not result in atrial fibrillation or arrhythmia acceleration. Of 14 episodes of sustained monomorphic VT 5 were terminated by external cardiac programmed stimulation. One tachycardia was terminated by a single extrastimulus, 1 by double extrastimuli and 3 by overdrive pacing. Arrhythmia acceleration occurred once and was terminated by endocardial pacing. On 27 separate occasions patient evaluation of maximal discomfort included 4 ratings of mild, 10 of moderate, 11 of severe and 2 of intolerable discomfort. External cardiac programmed stimulation is effective and safe in patients with well-tolerated sustained supraventricular or ventricular arrhythmias.     

Diagnostic value of the isoproterenol test in effort tachycardia

An isoproterenol test was performed in 69 patients during electrophysiological investigation to assess its diagnostic value in adrenergic supraventricular or ventricular tachycardia. Sixteen control subjects had no symptoms on exercise and routine exercise stress testing did not trigger any hyperexcitability. Sixteen patients had reproducible documented supraventricular tachycardia induced by exercise (13 paroxysmal junctional tachycardias, 3 focal atrial tachycardias). Eight patients had ventricular hyperexcitability related to effort. Twenty-nine patients had supraventricular and/or ventricular hyperexcitability only at rest. Electrophysiological investigations included paired atrial stimulation during sinus rhythm and paced rhythm followed by programmed ventricular stimulation using one and then two extrastimuli delivered during sinus rhythm and paced ventricular rhythm. These stimulation studies were carried out under basal conditions and then during low dose isoproterenol infusion (10 to 40 micrograms) which accelerated the heart rate to 130/mn. Electrophysiological and conduction parameters and the mode of induction of the tachycardia (defined as at least 5 successive echos with a configuration similar to the clinical tachycardia) were studied. We observed an acceleration of anterograde and retrograde conduction and a shortening of the effective atrial and ventricular refractory periods but these changes were found equally in the different groups of patients and were not related to the induction of tachycardias. The induction of paroxysmal junctional tachycardia by isoproterenol was a very sensitive (92%) and specific (100%) diagnostic method. Its diagnostic value was much greater than Holter monitoring (25%) and exercise stress testing (12.5%). Induction of ventricular tachycardia by isoproterenol was also very sensitive (75%) and specific (95%). The diagnostic value was higher than exercise stress testing (71%) and Holter monitoring (62%). Isoproterenol did not affect the induction of spontaneous tachyarrythmias unrelated to effort and even suppressed the triggering of some episodes. In conclusion, the induction by atrial or ventricular pacing or spontaneous supraventricular or ventricular tachycardia during isoproterenol infusion was very specific and correlated with the concept of tachycardia induced by exercise and therefore of adrenergic nature. The sensitivity of this test was excellent in patients with supraventricular tachycardia (95%) and very good in ventricular tachycardia (75%). On the other hand, the changes in the electrophysiological parameters were not specific for a group of patients.