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)     

The Value of Electrophysiologic Testing in Patients Resuscitated From Documented Ventricular Fibrillation

EP Study and Ventricular Fibrillation. Introduction: Electrophysiologic testing is performed in patients resuscitated from ventricular fibrillation (VF) on the assumption that sustained monomorphic ventricular tachycardia (VT) may be a precursor to VF, with the former amenable to assessment by serial drug testing.
Methods and Results: We assessed the usefulness of this strategy by analyzing clinical and electrophysiologic data of 42 survivors (29 men and 13 women; mean age 54 ± 14 years) of VF without a reversible cause. All patients had VF documented on ECG and required defibrillation. Underlying heart diseases included coronary disease in 28, dilated cardiomyopathy in 3, arrhythmogenic right ventricular dysplasia in 1, and no apparent structural heart disease in 10 patients. Only 2 (4.7%) patients had a prior history of documented VT. The electrophysiologic study was performed 7 to 30 days after VF. Programmed stimulation at the right ventricular apex using at least two drive cycle lengths and up to three extrastimuli induced sustained monomorphic VT in 4 (9.5%), sustained polymorphic VT in 3 (7.1%), nonsustained monomorphic VT in 1 (2.3%), nonsustained polymorphic VT in 5 (11.9%), and VF in 13 (30.9%) patients. Two patients with documented prior VT and coronary disease had sustained VT induced during the electrophysiologic study. On the other hand, sustained monomorphic VT was induced in 53 of the 59 (90%) patients (45 men and 14 women; mean age 57 ± 16 years) with clinically documented VT concurrently studied using the same stimulation protocol.
Conclusion: We conclude that reproducible induction of sustained monomorphic VT in survivors of documented VF is uncommon. It may be more cost effective to proceed directly to treatment with implantable cardioverter defibrillators in these patients.     

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.     

Programmed ventricular stimulation in mitral valve prolapse: analysis of 36 patients

Programmed ventricular stimulation with 3 extrastimuli was performed in 36 patients with mitral valve prolapse (MVP). Among 11 patients without transient cerebral symptoms, none had inducible ventricular tachycardia (VT) or ventricular fibrillation (VF), whether or not nonsustained VT or ventricular premature complexes (VPC) were present during ambulatory electrocardiographic recordings. These patients remained well without antiarrhythmic drug therapy for 6 to 57 months (mean 23) of follow-up. Two patients with recurrent unexplained syncope and no documented ventricular arrhythmia during electrocardiographic monitoring also had no inducible VT or VF. Among 20 patients with syncope or presyncope and documented nonsustained VT or VPCs during electrocardiographic monitoring, polymorphic nonsustained VT was induced in 8, sustained unimorphic VT in 2, and VF in 3. In 1 patient who had inducible polymorphic nonsustained VT, electrocardiographic monitoring during syncope showed sinus rhythm. Among 3 patients with a history of sustained VT or VF, unimorphic VT was induced in each. Patients with MVP who have asymptomatic ventricular ectopic activity and no inducible VT may have a benign prognosis without treatment. In patients who have transient cerebral symptoms and documented nonsustained VT or VPCs, VT or VF is inducible in 65%, most often polymorphic VT. It is unclear in which patients this finding is clinically significant and in which it is a nonspecific response to programmed stimulation.     

Electrophysiological studies in patients with chronic recurrent ventricular tachycardia.

Seventeen consecutive patients with chronic recurrent ventricular tachycardia (VT) were studied in an attempt to delineate the reproducibility and mechanism of this arrhythmia. Six patients had nonsustained and 11 had sustained VT. The following electrophysiological techniques were utilized in an attempt to reproduce VT: 1) rapid atrial and ventricular pacing (17 pts); 2) atrial extrastimulus technique (17 pts); 3) ventricular extrastimulus technique (17 pts); 4) V1V2V3 stimulation technique (5 pts); 5) ventricular pacing from two or more sites (5 pts). Ventricular tachycardia was induced in six of 11 (54%) patients with sustained VT. However, in four there was only a single induction and only in the remaining two patients could VT be repetitively induced. In the latter two patients ventricular tachycardia was induced with both atrial and ventricular stimulation. Ventricular tachycardia could not be induced in any patient with nonsustained VT, although three had spontaneous episodes of ventricular tachycardia during study. In conclusion, in the present series of patients with chronic recurrent VT, this rhythm could not be reproducibly induced in the majority of patients in the cardiac catheterization laboratory utilizing catheter stimulation techniques.     

Decline in inducibility of sustained ventricular tachycardia from two to twenty weeks after acute myocardial infarction

To determine temporal evolution of sustained ventricular arrhythmias inducible after acute myocardial infarction (AMI), serial programmed ventricular stimulation (PVS) was performed in 27 patients 15 +/- 4 and 150 +/- 28 days after AMI. These patients did not have worsening of congestive heart failure or angina, coronary artery bypass surgery or spontaneous sustained ventricular tachycardia (VT) in the period between 2 PVS studies. During initial PVS, sustained VT or ventricular fibrillation (VF) was inducible in 17 patients (group I) and was not inducible in 10 (group II). Late PVS in group I induced sustained VT or VF in 8 patients (47%) and nonsustained VT or no VT in 9 (53%). A decrease in late inducibility of sustained VT/VF was greater for arrhythmias induced during initial PVS by triple extrastimuli and burst pacing than for those induced by double extrastimuli (88% vs 25%, p less than 0.04), but appeared to be unrelated to the morphologic characteristics or cycle length of the initially induced sustained VT or VF and to other clinical, hemodynamic or angiographic variables. During late PVS in 10 group II patients, sustained VT or VF remained noninducible in 9 (90% concordance); in 1 patient sustained VT was induced. During a mean follow-up of 14 +/- 5 months since late PVS, none of 27 patients had spontaneous sustained VT and 2 patients in group I died suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)     

Termination of sustained ventricular tachycardia by external noninvasive pacing

Cardiac pacing has proven useful in the termination of sustained ventricular tachycardia (VT). In this study, the effectiveness of external noninvasive temporary pacing was compared with traditional endocardial burst ventricular pacing for the termination of sustained and hemodynamically stable VT. In 14 patients, 16 VT morphologies induced by programmed right ventricular extrastimulation were reproducibly terminated by endocardial burst pacing (3 to 9 complexes). VT cycle lengths averaged 392 +/- 97 ms (standard deviation) and ranged from 300 to 690 ms. The endocardial burst pacing cycle length used to terminate VT averaged 298 +/- 93 ms (range 220 to 600 ms). External burst pacing terminated 14 of 16 VT morphologies (88%). The pacing cycle length used to terminate these 14 VTs averaged 282 +/- 44 ms. The number of ventricular captures ranged from 5 to 20 beats. Failure to terminate 2 VT morphologies probably represented a failure of the device to capture the ventricle. Acceleration of VT occurred in 1 patient with burst external noninvasive pacing. These observations suggest that external burst pacing may be an effective means of terminating sustained VT in some patients.     

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.     

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.     

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

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

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.     

Ventricular late potentials and induced ventricular arrhythmias after surgical repair of tetralogy of Fallot.

Ventricular tachycardia (VT) and sudden death are rare but recognized complications after surgical repair of tetralogy of Fallot. We prospectively studied 31 patients (19 boys and 12 girls, mean age +/- standard deviation 7 +/- 4 years) with postoperative tetralogy of Fallot, by means of right-sided cardiac catheterization, 24-hour Holter monitoring, body-surface and intracavitary signal-averaging (gain 10(5) to 10(6), filters of 100 and 300 Hz) and programmed ventricular stimulation (1 and 2 extrastimuli, 3 basic cycle lengths, right ventricular apex and outflow tract). All patients were asymptomatic and none had documented or suspected ventricular arrhythmias. Ventricular late potentials were detected in 10 of 31 patients (32%) and spontaneous ventricular arrhythmias in 12 of 31 patients (39%). No sustained VT was induced by programmed ventricular stimulation but nonsustained VT was induced in 3 patients (10%). Patients with inducible VT more often had late potentials (3 of 3 vs 7 of 28, p less than 0.01), and spontaneous ventricular premature complexes (VPCs) during Holter monitoring (3 of 3 vs 9 of 28, p less than 0.05). To predict VT inducibility, late potentials had a sensitivity of 100%, a specificity of 75%, a positive predictive value of 30% and a negative predictive value of 100%. For spontaneous VPCs, the figures were 100, 68, 25 and 100%, respectively. It is concluded that shortly after repair of tetralogy of Fallot, the presence of both spontaneous VPCs and ventricular late potentials are associated with an increased incidence of inducible VT. Conversely, the absence of VPCs and ventricular late potentials may identify patients at low risk of subsequent ventricular arrhythmias.     

Ventricular fibrillation in hypertrophic cardiomyopathy is associated with increased fractionation of paced right ventricular electrograms.

BACKGROUND. Intraventricular conduction in hypertrophic cardiomyopathy (HCM) has been characterized to test the hypothesis that myofibrillar disarray will cause dispersion of activation throughout the ventricular myocardium. METHODS AND RESULTS. Of 37 patients with HCM, four had spontaneous ventricular fibrillation (VF), five had nonsustained ventricular tachycardia (VT), 13 had no risk factors, and 15 had a family history of sudden death. These patients and four controls were studied by pacing one site in the right ventricle and recording electrograms from three other right ventricular sites. These electrograms were high-pass filtered to emphasize small deflections due to activation of small bundles of myocytes close to the electrode. Intraventricular conduction curves were obtained with S1S2 coupling intervals decreasing in 1-msec steps from 479 msec to ventricular effective refractory period (VERP). These curves were repeated by pacing each RV site in turn and were characterized by two parameters: the point at which latency increased by 0.75 msec/20 msec reduction of the S1S2 coupling interval and an increase in electrogram duration between an S1S2 of 350 msec and VERP. Patients with VF, VT, and family history of sudden death had a mean increase in electrogram duration of 12.8 (2.9-32.3) msec versus 4.6 (-4.2 to 14.0) msec in low-risk patients and controls. Electrogram latency increased at an S1S2 of 363 msec in the VF group (342-386), 269 msec in the controls (266-279), and 326 msec in the non-VF group (260-399). Discriminant analysis separated VF patients from the remainder (p less than 0.0001) and VF, VT, and family history of sudden death patients from the low-risk and control groups (p less than 10(-6)). CONCLUSIONS. Patients with HCM who are at risk of sudden death have increased dispersion and inhomogeneity of intraventricular conduction, and this may create the conditions for reentry and arrhythmogenesis.     

Determinants of induced sustained arrhythmias in survivors of out-of-hospital ventricular fibrillation

We prospectively studied 196 consecutive survivors of out-of-hospital ventricular fibrillation (VF) not associated with acute myocardial infarction and 46 consecutive, control patients without prior ventricular arrhythmias. Programmed stimulation included two extrastimuli (S3 protocol) in all patients and three extrastimuli (S4 protocol) in the last 140 study patients and in all control patients. Sustained ventricular tachycardia (VT) or VF was not induced in any control patient. In study patients, logistic regression identified two independent predictors of induced, sustained VT for both S3 and S4 protocols: prior spontaneous, sustained VT (37 patients; p less than or equal to .001) and prior myocardial infarction (113 patients; p = .005). With the S3 protocol, sustained VT was induced in 54% of patients with both prior myocardial infarction and prior sustained VT vs 4% without either; with the S4 protocol, sustained VT was induced in 91% vs 13%, respectively. Eighty-three percent of induced VT episodes had a cycle length less than 300 msec, and all required termination by cardioversion or pacing. VF was induced only in survivors of out-of-hospital VF without prior, spontaneous, sustained VT (S3 protocol, 9%; S4 protocol, 24%) but not in study patients with prior sustained VT (S3, p = .10; S4, p = .05) or control patients (S3, p = .06; S4, p = .01). The mean coupling intervals of extrastimuli that induced VF were not significantly different from the intervals that induced sustained VT.(ABSTRACT TRUNCATED AT 250 WORDS)     

Efficacy of automatic multimodal device therapy for ventricular tachyarrhythmias as delivered by a new implantable pacing cardioverter-defibrillator. Results of a European multicenter study of 102 implants.

BACKGROUND. Third-generation implantable cardioverter-defibrillators are devices designed to treat ventricular tachycardia (VT) and ventricular fibrillation (VF) by means of overdrive pacing, cardioversion, or defibrillation. So far, the efficacy of tiered therapy has been documented only in small series. Therefore, a European multicenter clinical evaluation study of a new tachyarrhythmia control device, the Medtronic PCD pacer-cardioverter-defibrillator with epicardial patch-lead configuration, was undertaken. METHODS AND RESULTS. We report on 102 patients (mean age, 55 +/- 13 years) from 11 European centers. PCD devices implanted between May 1989 and February 1991 were included. The patients suffered from hemodynamically significant ventricular tachyarrhythmias not suppressed by antiarrhythmic drug therapy and unrelated to acute myocardial infarction; one patient had nonsustained VT and severely depressed left ventricular function. Seventy patients had coronary artery disease with old myocardial infarctions, 23 had cardiomyopathies of various etiologies, and nine patients had no detectable heart disease. Mean ejection fraction was 36 +/- 14% (range, 10-76%). Mean intraoperative defibrillation threshold (51 patients) was 10.6 +/- 5.1 J (range, 2-18 J). The documented follow-up ranged from 1 to 21 months (mean, 9.4 +/- 5.8 months), or 79.9 cumulative patient-years. Perioperative mortality was 3.9%. The actuarial survival rate at 12 months was 91%. One sudden arrhythmic death occurred. Sixty patients (58%) received device therapy. Seventeen patients had therapies only for "VF" episodes, 16 patients only for VT, and 28 patients for VT and "VF" episodes. Based on device memory data, 1,235 spontaneous VT episodes were detected and treated in 43 patients. Twelve hundred four of these VT episodes received painless initial antitachycardia pacing therapy, restoring sinus rhythm in 91%. The 108 ongoing episodes received 209 multiple therapeutic attempts. Eighty-five additional overdrive pacing therapies restored sinus rhythm in 30%. Initial ineffective antitachycardia pacing therapies received 51 cardioversion pulses. The success rate was 61%. Seventy-three additional cardioversion pulses were delivered to backup ineffective pacing therapy as well as ineffective secondary cardioversion pulses. Their success rate was only 40%. Two hundred eighty-six spontaneous episodes were detected in 44 patients as "VF." Overall defibrillation efficacy was 97.6%. CONCLUSIONS. The implanted device nearly eliminates sudden arrhythmic death in patients with documented, potentially fatal ventricular tachyarrhythmias. Automatic tiered therapy is highly effective to restore sinus rhythm, provided that an integrated two-zone tachycardia detection algorithm is used, assigning lower tachycardia rates to overdrive pacing and/or cardioversion and higher tachycardia rates to defibrillation. In general, spontaneous VTs can be terminated by automatic overdrive pacing, and painful or disturbing countershock therapies are not required to terminate the majority of spontaneous VT episodes.     

Electrophysiologic effects of ethmozin in patients with ventricular tachycardia

Ten patients with recurrent episodes of ventricular tachycardia (VT) had electrophysiologic studies in the basal state and on chronic oral ethmozin (12.1 ± 0.6 SE mg/kg/day). Ethmozin significantly prolonged the AH interval (basal: 75 ± 8 SE msec; ethmozin: 91 ± 10 msec, p < 0.05), the HV interval (51 ± 3; 66 ± 5 msec, p < 0.01), and the QRS duration (101 ± 4; 118 ± 4 msec, p < 0.001). Atrial and ventricular refractory periods and the corrected QT interval were not significantly affected by ethmozin. VT was induced in 7 of 10 patients in the basal state by means of programmed right ventricular extrastimulation or rapid burst ventricular pacing. On oral ethmozin nine patients had inducible VT. VT cycle length was consistently prolonged on ethmozin (250 ± 13; 326 ± 14 msec, p < 0.001). Four of the seven patients with VT on basal ambulatory monitoring had total abolition of spontaneous VT on ethmozin. Ethmozin failed to prevent induction of VT in most patients despite significant reductions in ventricular arrhythmia on ambulatory monitoring. Further studies comparing VT induction with ambulatory monitoring in patients on ethmozin are needed to confirm these findings and to define the clinical significance of this dissociation.     

Comparison of coupling intervals that induce clinical and nonclinical forms of ventricular tachycardia during programmed stimulation

Coupling intervals of extrastimuli that induced 57 previously documented unimorphic ventricular tachycardias (VTs) were compared with coupling intervals that induced 57 episodes of polymorphic VT or ventricular fibrillation (VF) in patients without a documented or suspected history of polymorphic VT or VF. Programmed stimulation was performed with the patient in the drug-free state, with 1 to 3 extrastimuli and 2 basic drive cycle lengths (600 or 500 ms, and 400 ms) at 2 right ventricular sites; stimuli were twice diastolic threshold. The mean coupling intervals of the first, second and third extrastimuli that induced nonclinical VT/VF (241 +/- 19, 185 +/- 19 and 173 +/- 24 ms, respectively, mean +/- standard deviation) were significantly shorter than the corresponding coupling intervals that induced the clinical VTs (266 +/- 25, 228 +/- 32 and 214 +/- 27 ms, respectively, p less than 0.001 for each). Regardless of the basic drive cycle length, the shortest coupling interval required to induce a clinical VT was 180 ms. Depending on the drive cycle length, 29 to 70% of nonclinical VT/VF induced by 3 extrastimuli required a coupling interval of less than 180 ms to induce. Therefore, a lower limit of coupling intervals may be identified below which only nonclinical VT/VF is induced by programmed stimulation. Restriction of coupling intervals to this lower limit may allow for significant improvement in specificity without compromise in the sensitivity of programmed ventricular stimulation protocols.     

Prognostic usefulness of programmed ventricular stimulation in idiopathic dilated cardiomyopathy without symptomatic ventricular arrhythmias

Twenty-four patients, mean age 42 years, with idiopathic dilated cardiomyopathy (DC) and no history of symptomatic ventricular arrhythmias underwent right ventricular programmed stimulation with up to 3 extrastimuli. Ventricular tachycardia (VT) was induced in 8 patients and ventricular fibrillation (VF) in 2. The VT was unimorphic in 2 and polymorphic in 6. No significant differences were noted between patients in whom arrhythmias were inducible and and those in whom they were not with regard to age, symptomatic class, arrhythmia severity or hemodynamic indexes. Over a mean follow-up of 12 months, 4 patients died, 3 suddenly and 1 with progressive heart failure. Only 1 of the 3 who died suddenly had inducible VT. One other patient with induced sustained unimorphic VT later presented with spontaneous sustained VT similar in rate and configuration to induced VT. In conclusion, VT or VF may be induced in approximately 40% of patients with DC and no history of symptomatic VT or VF. Inducibility of polymorphic VT or VF does not correlate with clinical or hemodynamic variables or with the risk of sudden death. However, induction of unimorphic VT may predict later occurrence of spontaneous unimorphic VT.     

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)