Verapamil in ventricular tachycardia

We compared the effects of verapamil to high dose procainamide on the rate of inducible and spontaneously occurring ventricular tachycardia (VT) in 10 patients. Verapamil induced a significant increase in the rate of tachycardia (R-R interval decreased from 278 +/- 54 to 233 +/- 32 ms, mean +/- SD; p less than 0.025 by paired t test) while procainamide slowed the tachycardia (mean R-R interval was 328 +/- 72 ms, p less than 0.02). Verapamil prevented the induction of sustained VT and was effective as chronic oral antiarrhythmic therapy in 2 patients. The accelerated VT culminated in ventricular fibrillation in 1 patient. It is assumed that verapamil may have either increased conduction velocity or shortened the reentrant cycle. This may be related either to a primary effect of the drug or secondary to increased catecholamine stimulation due to a vasodilatory effect.     

Idiopathic paroxysmal ventricular tachycardia with a QRS pattern of right bundle branch block and left axis deviation: A unique clinical entity with specific properties

Eiectrophysiologic evaluation before and after the serial administration of verapamil, lidocaine, propranolol, and procainamide was undertaken in 4 young, asymptomatic patients with recurrent, sustained ventricular tachycardia (VT). No patient had obvious organic heart disease. The electrocardiogram during sinus rhythm showed S-T depression and T-wave inversion over the inferior and lateral precordial leads in 3 patients. QRS morphologic characteristics during episodes of VT showed a pattern of right bundle branch block and left axis deviation. In all 4 patients, VT could be both induced and terminated with electrical stimulation. Verapamil terminated VT and prevented the induction of sustained VT in 3 patients, and markedly slowed the rate of VT in 1 patient. Procainamide effectively prevented the induction of sustained VT in 2 patients, and although ineffective in preventing induction in 2 patients, it slowed the rate of tachycardia in both. Lidocaine and propranolol did not prevent the induction of VT in any patient. These findings suggest that slow-response tissues may be involved in the genesis of VT in these patients, and that VT in these patients may represent a unique clinical entity with distinct electrocardiographic, electrophysiologic, and electropharmacologic properties.     

Efficacy of verapamil in chronic, recurrent ventricular tachycardia

Verapamil, 0.25 mg/kg, was given to 24 patients with chronic, recurrent ventricular tachycardia (VT) whose clinical tachyarrhythmias were reproduced at electrophysiologic study. Seven patients (29%) responded acutely to verapamil: VT was not inducible in 5 and spontaneously terminated within 5 seconds of induction in 2 patients in whom it was previously sustained. Four of the 7 responders had no identifiable structural heart disease, and 3 had coronary artery disease. Responders were younger and had better left ventricular function than did nonresponders. Long-term therapy with verapamil, attempted in 5 of the 7 responders, was effective in 3, ineffective in 1, and of uncertain efficacy in 1. Verapamil therapy was discontinued because of worsened congestive heart failure in 2 patients.

The short-term efficacy of verapamil in these patients compares favorably with the efficacy of other antiarrhythmic agents against VT induction in patients with long-term, recurrent, drug-refractory VT. The short-term efficacy of verapamil correlated with its long-term efficacy. These observations provide preliminary evidence that verapamil may be useful in the treatment of some patients with recurrent VT. When standard drugs are not effective, verapamil should be given a trial, especially in young patients with good left ventricular function.     

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.     

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.     

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)     

Effect of increased current, multiple pacing sites and number of extrastimuli on induction of ventricular tachycardia

Reproduction of spontaneously occurring ventricular tachycardia (VT) and induction of previously undocumented VT were studied prospectively in 98 patients: 48 with documented sustained VT or ventricular fibrillation, 25 with nonsustained or exercise-induced VT, and 25 with no documented VT. Patients received 1 to 4 ventricular extrastimuli and ventricular burst pacing at 2 right ventricular (RV) sites, first at twice late diastolic threshold, and then at 10 mA using a prospective, tandem study design. Spontaneously occurring VT was reproduced in 37 of 48 patients (77%) at twice late diastolic threshold and in 1 other patient (2%) at 10 mA. VT was reproduced at both RV sites in 17 of 48 patients (35%) and at 1 site in 20 of 48 patients (42%) at twice late diastolic threshold. A previously undocumented VT was induced in 7 of 25 patients (28%) with no documented VT at twice diastolic threshold and 14 of 25 patients (56%) at 10 mA. A previously undocumented VT was induced in 33 of 73 patients (45%) with a history of sustained or nonsustained VT at twice late diastolic threshold and in 47 of 73 patients (64%) at 10 mA. In patients with documented sustained VT, the use of up to 4 ventricular extrastimuli at multiple RV sites increases the sensitivity of the test. In patients without documented VT, the induction of previously undocumented VT with more than 3 ventricular extrastimuli limits the specificity of the test. Increased current provides only a slight advantage over 4 ventricular extrastimuli at twice late diastolic threshold in terms of reproduction of spontaneously occurring VT, but leads to a marked increase in induction of previously undocumented VT.     

Evaluation of bepridil efficacy by electrophysiologic testing in patients with recurrent ventricular tachycardia: Comparison of two regimens

Summary The purpose of the study was to evaluate this effect of different doses of intravenous and oral bepridil on the induction of ventricular tachycardia. Thirty-eight patients underwent electrophysiologic evaluation for recurrent ventricular tachycardia (VT). Sustained monomorphic VT was induced by programmed ventricular stimulation, using up to three extrastimuli in all patients. The effects of intravenous bepridil (2 mg/kg) were evaluated during the initial study. Intravenous bepridil prevented the induction of sustained VT in eight patients (21%). Electrophysiologic study was repeated after oral bepridil. In six patients the study was stopped because of adverse effects or VT recurrence. Thirty-two patients underwent repeat study 7 days later, taking oral bepridil, 500 mg/day (n=16) or 900/day (n=16). A dose of 500 mg/day of bepridil prevented the induction of sustained VT in only one patient. A dose of 900 mg/day of bepridil prevented the induction of sustained VT in eight patients. There were no significant clinical adverse effects, except in one patient receiving intravenous bepridil. The response to intravenous bepridil did not predict the response to oral bepridil. The response to intravenous or oral bepridil was not related to the plasma level of bepridil but was related to a higher left ventricular ejection fraction. Eight patients (21%) in whom VTs were noninducible on oral bepridil were discharged on 300 mg/day of bepridil if their initial loading dose was 500 mg/day or on 600 mg/day if their initial loading dose was 900 mg/day. They remained free of VT during a follow-up of at least 6 months. In conclusion, this study suggests that oral bepridil at the dose of 600 mg/day may be of value in patients with recurrent VT.     

Programmed ventricular stimulation using up to two extrastimuli and repetition of double extrastimulation for induction of ventricular tachycardia: a new highly sensitive and specific protocol

The sensitivity and specificity of a new protocol of programmed ventricular stimulation were evaluated in 71 consecutive patients who were divided into 2 groups: group 1 included 41 patients, of whom 25 had sustained ventricular tachycardia (VT) not associated with cardiac arrest and 16 had ventricular fibrillation (VF) not precipitated by any obvious factor; group 2 included 30 patients without demonstrable heart disease and no suspected or documented sustained ventricular tachyarrhythmias. The study consisted of a standard protocol (up to 2 extrastimuli given only once for each extrastimulus prematurity, 2 right ventricular sites and 3 basic pacing cycle lengths, as well as rapid ventricular pacing) in which double extrastimulation at the shortest coupling intervals that allowed ventricular capture was repeated 10 times. A stimulus current of 3 mA was used. Sustained ventricular tachyarrhythmias were induced in 23 of 25 (92%) patients who presented with sustained VT, 14 of 16 (88%) patients who presented with VF and 2 of 30 (7%) group 2 patients. Eighteen of 25 (72%) patients with sustained VT but only 4 of 16 (25%) with VF had arrhythmias inducible at "immediate" trials of single or double extrastimulation (p less than 0.01). Repetition of double extrastimulation increased the yield of inducible sustained ventricular tachyarrhythmia to 92% in patients with sustained VT (+20%, p = 0.14) and 75% (+50%, p = 0.013) in patients with VF. Rapid right ventricular pacing added a 13% increase in the overall yield in patients with VF. This new protocol of programmed ventricular stimulation has both high sensitivity (90%) and specificity (93%) for induction of sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

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)     

Frequency and significance of induced sustained ventricular tachycardia or fibrillation two weeks after acute myocardial infarction

Electrophysiologic study, 24-hour ambulatory electrocardiographic monitoring, treadmill exercise test and angiographic evaluations were performed in 45 patients 14 +/- 3 days (mean +/- standard deviation) after acute myocardial infarction. Electrophysiologic study protocol included burst ventricular pacing and 1 to 3 ventricular extrastimuli at 2 cycle lengths from right ventricular apex, right ventricular outflow and left ventricle. Sustained monomorphic ventricular tachycardia (VT) (13 patients) or ventricular fibrillation (VF) (7 patients) was induced in 20 patients (44%) (group I). In these 20 patients, VT/VF was inducible with 2 extrastimuli in 10 patients, 3 extrastimuli in 9 patients and burst pacing in 1 patient. In the remaining 25 patients (56%), induction of no fewer than 7 ventricular beats were noted (group II). Severe left ventricular (LV) wall motion abnormalities occurred in 70% of group I patients and 22% of group II patients (p less than 0.005). There was no difference in the site of infarction, frequency and grade of ventricular ectopic rhythm on ambulatory electrocardiographic monitoring, double product on submaximal exercise, LV ejection fraction, and number of obstructed coronary arteries (70% or greater) (p greater than 0.1) between group I and group II patients. During a mean follow-up of 10 +/- 3 months, 1 patient in each group died suddenly, and in 1 group I patient spontaneous sustained VT developed which was identical in morphologic configuration to that induced during electrophysiologic study. In conclusion, electrical induction of sustained VT or VF during electrophysiologic study is common in patients 2 weeks after acute myocardial infarction.(ABSTRACT TRUNCATED AT 250 WORDS)     

Availability of electrophysiological approach to the selection and assessment of antiarrhythmic drugs for recurrent ventricular tachycardia

We performed serial electrophysiological-pharmacological studies on 21 patients with recurrent sustained or non-sustained ventricular tachycardia (VT). In 8 of 11 patients with recurrent sustained VT, VT could be induced repeatedly by programmed electrical stimulation and terminated by ventricular burst pacing. In 13 of the 21 patients, repetitive ventricular response (RVR) was successfully induced. In the 8 patients with induced VT, the efficacy of several antiarrhythmic drugs intravenously administered was assessed. Procainamide prevented the initiation of VT in 57%, disopyramide in 50% and mexiletine in 40%. However, lidocaine, propranolol and verapamil could not prevent VT in any of 5, 3 and 6 patients, respectively. Verapamil in combination with quinidine prevented the initiation of VT in one case. Each of disopyramide, propranolol and verapamil increased the VT zone in 2 patients. The drugs belonging to the same group classified by their electrophysiological properties were not interchangeable in 2 patients. Their ability to terminate induced VT did not always correlate with that to prevent its initiation in 2 patients. The effects of specific drugs were rather variable and unpredictable in each patients, and especially those of combination regimens using more than 2 antiarrhythmic drugs were more unpredictable. In all patients, the induced VT was morphologically identical to the spontaneously occurring VT and its rate was ranged within 13% of that of the spontaneously VT. In 10 of 13 patients with RVR, QRS configuration of RVR was not similar to the spontaneously occurring arrhythmia. The pharmacological suppression of RVR as an index for prevention against spontaneous VT remains controversial. This study concludes that the serial electrophysiological-pharmacological study provides a rapid prediction of effectiveness of a particular regimen and combination and a rapid identification of the deleterious effects of certain drugs in patients with recurrent sustained VT.     

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.     

The Use of Fontaine Leads in the Diagnosis of Arrhythmogenic Right Ventricular Dysplasia

We report a case of a 68‐year‐old man admitted to the emergency department with syncope preceded by rapid palpitations. His admission ECG demonstrated a sustained ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT). This report highlights the importance of distinguishing ventricular tachycardia caused by arrhythmogenic right ventricular dysplasia (ARVD) from the more benign idiopathic RVOT‐VT. Furthermore, we demonstrate the utility of the Fontaine leads placement in increasing the sensitivity for uncovering epsilon waves, a highly specific electrocardiographic feature that increases diagnostic accuracy in patients with ARVD.     

Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity

Catecholamine-induced triggered activity is thought to be caused by intracellular calcium overload mediated by elevation of intracellular cyclic AMP (cAMP). Although shown to occur in isolated preparations, evidence supporting its clinical existence has been lacking. Electrophysiologic studies were performed in four patients with structurally normal hearts who had exertionally related sustained ventricular tachycardia (VT). Programmed stimulation reproducibly initiated and terminated VT in all patients. Induction of tachycardia was also facilitated by infusion of isoproterenol. Adenosine, an endogenous nucleoside, whose only known electrophysiologic effect on ventricular myocardium and Purkinje fibers is antagonism of catecholamine-induced stimulation of intracellular cAMP production, reproducibly terminated all episodes of VT. The tachycardia was also terminated by intravenous verapamil and by the Valsalva maneuver and/or carotid sinus massage. Beta-Adrenergic receptor blockade with propranolol either terminated or prevented induction of VT during programmed stimulation or catecholamine challenge. Adenosine was also administered during VT to 14 patients whose arrhythmias fulfilled standard criteria for reentry, two of whom also had exercise-induced VT. Adenosine, at a dose (112.5 to 225 micrograms/kg iv) sufficient to cause either sinus slowing/arrest or ventriculoatrial block during ventricular pacing, failed to slow or terminate any episode of VT in these patients. Verapamil and autonomic modulation were also ineffective in this group of patients. Adenosine, verapamil, vagal maneuvers (acetylcholine), and beta-adrenergic receptor blockade are all known to decrease the slow-inward calcium current either directly by modulating calcium channels or indirectly by inhibiting production of cellular cAMP. Therefore the observation in this study that interventions that lower intracellular cAMP either terminate or prevent induction of VT in patients with structurally normal hearts and exercise-induced VT suggests that the mechanism of tachycardia may be cAMP-mediated triggered activity.     

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.     

Analysis of programmed stimulation methods in the evaluation of ventricular arrhythmias in patients 20 years old and younger

The purpose of this study was to systematically evaluate programmed ventricular stimulation in patients less than 21 years of age undergoing electrophysiologic testing. A standardized protocol was applied in 55 consecutive patients (mean age 14 years) with the following clinical presentations: sustained ventricular tachycardia (VT) (n = 17); ventricular fibrillation (VF) (n = 7); syncope with heart disease (n = 10); nonsustained VT (n = 6); and syncope with an ostensibly normal heart (n = 15). The stimulation protocol consisted of 1 and 2 ventricular extrastimuli during sinus rhythm, followed by 1 to 4 (S2, S3, S4, S5) extrastimuli during pacing at 2 ventricular sites. Of the 17 patients with sustained VT, 12 had induction of the arrhythmia (sensitivity = 71%). Overall, 18 of 55 patients had inducible sustained VT, with this response significantly enhanced by use of S4 or S5 protocols (p = 0.02). Although no syncope patients with an ostensibly normal heart had inducible sustained VT, 7 had polymorphic nonsustained VT in response to ventricular stimulation. The mean number of extra-stimuli preceding the induction of nonsustained or sustained VT or VF did not differ. The induction of VF in 5 cases during this study was preceded in each case by extrastimuli intervals less than or equal to 190 ms. Thus, data indicate that aggressive stimulation protocols appear to be required for induction of sustained VT in most young patients, nonsustained polymorphic VT as a response to aggressive programmed stimulation is of uncertain significance, and that coupling intervals less than or equal to 190 ms may correlate with the induction of VF.     

Clinical significance of the electrophysiologic study (EPS)-guided therapy for the secondary prevention of ventricular tachycardia.

BACKGROUND: Although electrophysiologic study (EPS) is one of the most reliable methods for selecting preventive therapy for patients with sustained ventricular tachycardia (VT), VT may recur during EPS-guided effective therapy; therefore, the importance of implantable cardioverter-defibrillator (ICD) has been emphasized. In this study, the prognoses of VT patients were evaluated to clarify the importance of EPS-guided therapy for the secondary prevention of VT. METHODS AND RESULTS: The study population consisted of 99 consecutive patients with a history of sustained VT, which was inducible in EPS. The VT induction protocol used 1-3 extrastimuli and rapid ventricular pacing at 2 right ventricular sites and included additional isoproterenol infusion. ICD implantation was applied to all patients with an episode of hemodynamically unstable VT, regardless of the result of preventive therapy. For preventive therapy, an antiarrhythmic drug and/or catheter ablation were selected, and they were defined as being effective in the EPS-guided therapy when the induction of VT was completely prevented. When no therapy was effective for prevention, an antiarrhythmic drug was prescribed under ICD implantation. During the follow-up period of 19+/-20 months, VT recurred in 17 of 32 patients (53%) in the ineffective group and in 10 of 67 patients (15%) in the effective group (p=0.0001). The therapies used in the effective group were class I antiarrhythmic drug in 9, class III in 15, and catheter ablation in 35 patients. Between the patients with and without VT recurrence, there were no significant differences in the left ventricular ejection fraction and the maximum number of repetitive ventricular responses that remained in VT induction in EPS. CONCLUSIONS: Although VT may recur in up to 15% of patients with EPS-guided effective therapy, the recurrence rate was significantly reduced in comparison to that in the ineffective group. EPS-guided therapy may be useful to reduce the clinical recurrence of VT, as well as the action of ICD.