Simultaneous biphasic shocks enhance efficacy of endocardial cardioversion defibrillation in man.
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Electric Conductivity↗
Biomedical subjects
R B Krol
Publications and source records attributed to R B Krol.
Management of complications associated with a first-generation endocardial defibrillation lead system for implantable cardioverter-defibrillators.
An automatic cardioverter-defibrillator could be implanted using an endocardial defibrillation lead system (consisting of a tripolar defibrillation electrode catheter in conjunction with an epicostal patch electrode) in 9 of 10 patients with sustained ventricular tachycardia or ventricular fibrillation. Six lead system complications were observed during a follow-up period of 51 +/- 36 weeks. Three catheter electrode conductor fractures occurred and manifested as oversensing and subsequent delivery of inappropriate shocks (1 patient), inability to defibrillate during electrophysiologic testing 3 months after implant (1 patient) and sudden cardiac death (1 patient). Asymptomatic patch electrode conductor fractures were detected on a routine chest roentgenogram in 2 patients. Endocardial defibrillation threshold testing performed at the time of implantation resulted in malfunction of a previously implanted permanent pacemaker pulse generator in 1 patient. Catheter and patch electrode replacement procedures were performed in 3 consenting patients under local anesthesia. Endocardial defibrillation thresholds after lead replacement were comparable to those obtained at time of initial implant. Serial clinical, roentgenographic and electrophysiologic evaluation should be included in follow-up procedures for endocardial defibrillation lead systems. Monitoring for deleterious effects of endocardial defibrillation threshold testing on previously implanted pacemaker systems should be performed at the time of implant and during follow-up. Improved lead designs are necessary for long-term use of endocardial defibrillation electrodes, but replacement procedures are feasible without thoracotomy.
Aged↗
Initial clinical experience with endocardial defibrillation using an implantable cardioverter/defibrillator with a triple-electrode system.
We evaluated the early clinical performance of an implantable cardioverter/defibrillator with a nonepicardial lead system in patients with refractory ventricular tachycardia or ventricular fibrillation. Ten patients, mean age 67 years, mean left ventricular ejection fraction 35%, refractory to 5 +/- 2 antiarrhythmic drugs and with a history of prior cardiac surgery (7 patients), severe lung disease (2 patients), or renal failure (1 patient) underwent device and lead system implant. A tripolar electrode catheter with one sensing electrode and two defibrillating electrodes was placed in the right ventricular apex and a left thoracic submuscular patch electrode was used in an epicostal location. Defibrillation energy threshold was determined using dual- or triple-electrode configurations. Optimal patch electrode location was determined after temporary use of a cutaneous patch electrode prior to cardioverter/defibrillator implant. Electrophysiologic studies were performed before discharge and after 2 to 3 months to assess device function. Percutaneous insertion and placement of the electrode catheter was achieved in all patients. Defibrillation energy threshold testing was done using 1 to 4 (mean, 2.7) electrode configurations per patient and required 6 to 21 (mean, 13) ventricular fibrillation inductions and 8 to 56 (mean, 22) shocks per patient. In all patients, lowest reliable defibrillation energy threshold was obtained with a triple-electrode configuration (right ventricular common cathode with right atrial and thoracic patch as dual anodes) and bidirectional shocks (mean, 18 +/- 5 J). Optimal patch electrode position could be determined in 9 of 10 patients, and these 9 patients had cardioverter/defibrillator implant. Ventricular fibrillation termination with the first delivered shock at electrophysiologic study was documented in all patients. There was no perioperative mortality in device-implanted patients. Postoperative electrophysiologic studies before discharge (9 patients) and at 3 months (8 patients) continued to demonstrate successful defibrillation by the first device shock. During follow-up (range, 2 to 10 months; mean, 6 +/- 3 months), spontaneous device discharges occurred in 4 patients with inappropriate shocks due to electrode catheter fracture being documented in 1 patient. Antiarrhythmic drug therapy was withdrawn in 6 patients and reduced in 3 patients. We conclude, based on our preliminary experience, that an implantable cardioverter/defibrillator can be successfully used with a nonepicardial lead system for endocardial defibrillation in many patients. This lead system can be used with currently available pulse generators and should be considered at cardioverter/defibrillator implantation. It can be anticipated to reduce patient risk and hospital costs associated with this procedure.
Aged↗
The hemodynamic effects of ventricular pacing with and without atrioventricular synchrony in patients with normal and diminished left ventricular function.
The relative hemodynamic effects of heart rate, inotropic state, and atrioventricular (AV) synchrony during ventricular pacing were evaluated in 10 patients with normal left ventricular ejection fraction (LVEF) (0.66 +/- 0.07, mean S.D.) and in eight patients with a diminished LVEF (0.34 +/- 0.18). Hemodynamics were measured at AV intervals of 130, 0, and -130 msec during ventricular pacing at a baseline rate that was 10 pulses/min greater than the resting heart rate, at 130 pulses/min alone, and at 130 pulses/min during continuous intravenous infusion of dobutamine. During baseline ventricular pacing and during ventricular pacing at 130 pulses/min with and without dobutamine, both groups of patients had a significant decrease in cardiac index, stroke volume index, and stroke work index when the AV pacing interval was decreased from 130 to 0 msec. The observed decrease in these three hemodynamic variables was similar when patients with diminished LVEF were compared to patients with normal LVEF. No further significant decrease in cardiac index, stroke volume index, and stroke work index occurred in either group when the AV interval was changed from 0 to -130 msec during baseline ventricular pacing or during ventricular pacing at 130 with and without dobutamine. Beneficial hemodynamic effects occur during ventricular pacing when AV synchrony is maintained at resting heart rates and during increases in heart rate and inotropic state in patients with normal and diminished LVEF.
Adult↗
Electrophysiologic testing in patients with unexplained syncope: clinical and noninvasive predictors of outcome.
To assess whether the level of risk of having significant electrophysiologic abnormalities can be determined, 29 clinical variables were analyzed in 104 patients with unexplained syncope who underwent electrophysiologic testing. A positive electrophysiologic study was defined as: a sinus node recovery time greater than or equal to 3 seconds; HV interval greater than or equal to 100 ms; infranodal block during atrial pacing; unimorphic ventricular tachycardia; and supraventricular tachycardia associated with hypotension. Thirty-one patients had a positive study, with inducible ventricular tachycardia being the most common finding (71% of positive studies). A left ventricular ejection fraction less than or equal to 0.40 was the most powerful predictor of a positive electrophysiologic study (p less than 0.00001), followed by the presence of bundle branch block (p less than 0.00003), coronary artery disease (p less than 0.0003), remote myocardial infarction (p less than 0.00006), use of type 1 antiarrhythmic drugs (p less than 0.00003), injury related to loss of consciousness (p less than 0.01) and male sex (p less than 0.01). A negative electrophysiologic study was associated with an ejection fraction greater than 0.40 (p less than 0.00001), the absence of structural heart disease (p less than 0.00001), a normal electrocardiogram (ECG) (p less than 0.0001) and normal ambulatory ECG monitoring (p less than 0.0001). The probability of a negative study increased as the number and duration of syncopal episodes increased.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Role of myocardial ischemia during programmed stimulation in survivors of cardiac arrest with coronary artery disease.
The role of ischemia in the induction of ventricular tachycardia during programmed stimulation was studied in 19 patients who survived a cardiac arrest and were found to have a significant stenosis in at least one branch of the left coronary artery. The arterial-coronary sinus lactate difference was measured during electrophysiologic testing, before the induction of ventricular tachycardia. Ventricular tachycardia was induced in 15 patients; it was sustained and unimorphic in 6 patients and polymorphic in 9. Myocardial ischemia, as reflected by net myocardial lactate production, was present within 60 seconds before the induction of ventricular tachycardia in 8 of the 15 patients with inducible ventricular tachycardia. In 9 of the 15 patients, programmed stimulation was repeated after a 15 minute rest period, with the same coupling intervals that had induced ventricular tachycardia previously. Net myocardial lactate production was not present in any patient during this repeat attempt. In three patients without evidence of ischemia during the first induction of ventricular tachycardia, the arrhythmia was induced again by the specific coupling intervals that had induced it previously. However, in five of six patients with net myocardial lactate production during the first induction of ventricular tachycardia, the same coupling intervals that had induced the arrhythmia in the presence of ischemia no longer induced it in the absence of ischemia. The results of this study suggest that myocardial ischemia may be a requirement for the induction of ventricular tachycardia in some patients with coronary artery disease who survive a cardiac arrest.
Angioplasty, Balloon↗
Supraventricular tachycardia induced by swallowing: a case report and review of the literature.
A 64-year-old man who complained of palpitations brought on by swallowing was found to have short runs of paroxysmal supraventricular tachycardia (SVT) induced by swallowing. Electrophysiology studies suggested that the SVT was an automatic atrial tachycardia. An esophageal manometric study demonstrated that the tachycardia was coincident with relaxation of the upper esophageal spincter and preceded peristaltic activity in the esophageal body. Atropine and bethanechol did not affect the swallow-induced tachycardia. The patient's symptoms were controlled by verapamil and quinidine. After five months, these medications were discontinued, with no recurrence of symptoms. Based on analysis of ten prior cases and the present case, it appears that swallow-induced SVT generally occurs in men between the ages of 45-75 years who have no evidence of structural heart disease or an esophageal disorder. The SVT is usually either a nonsustained automatic atrial tachycardia or atrial fibrillation. The mechanism is conjectural, but the most likely possibility is a vagally-mediated neural reflex, probably involving a neurotransmitter other than acetylcholine.
Deglutition↗
Immediate reproducibility of clinical and nonclinical forms of induced ventricular tachycardia.
This prospective study assessed the immediate reproducibility of clinical and nonclinical forms of ventricular tachycardia (VT) induced by programmed ventricular stimulation. Twenty-three clinical VTs were unimorphic and previously documented and 22 nonclinical VTs (17 polymorphic and 5 unimorphic) were induced in patients with either no documented or suspected history of VT, or documented VT that had a configuration different from that of the induced VT. The stimulation protocol included 1 to 3 ventricular extrastimuli, 2 drive cycle lengths, and 2 right ventricular stimulation sites. Each VT was induced on the first attempt, then the stimulation protocol was repeated twice in the drug-free state. After the first VT induction, 21 of 23 clinical VTs (91%) and 17 of 22 nonclinical VTs (77%) were reinduced on the second attempt. After 2 VT inductions, 21 of 21 clinical VTs (100%) and 15 of 17 nonclinical VTs (88%) were reinduced on the third attempt. The reinduction rates of the clinical and nonclinical VTs were not significantly different. Among the clinical VTs, the reproducibility of the induction technique was 81% after 1 induction and 88% after 2 inductions with the same technique. These results imply that acute drug testing can be reliably performed after 2 inductions but not 1 induction of clinical VT; reproducibility is not helpful in determining whether an induced VT is clinical or nonclinical; and changes in induction technique during drug testing should be interpreted with caution because changes may occur in the absence of drugs.
Adult↗
Effect of programmed ventricular stimulation on myocardial lactate extraction in patients with and without coronary artery disease.
The arterial-coronary sinus lactate difference was measured in 17 patients after each step of a programmed ventricular stimulation protocol consisting of single, double, and triple extrastimuli, first at a basic drive cycle length of 600 msec, then at 400 msec, with an inter-train interval of 4 seconds. Four patients had no structural heart disease, four had an idiopathic dilated cardiomyopathy, and nine had coronary artery disease with a significant stenosis in at least one branch of the left coronary artery. Net myocardial lactate production during programmed ventricular stimulation was observed in three patients with coronary artery disease, but not in any patient without coronary artery disease. Among the patients who had coronary artery disease, net myocardial lactate production generally occurred in the patients who had more severe coronary artery disease. Exercise-induced ischemia, as demonstrated by a stress thallium-201 test, did not correlate with myocardial lactate production during programmed ventricular stimulation. Programmed ventricular stimulation, with a stimulation protocol typically used in many electrophysiology laboratories, is capable of inducing myocardial ischemia in at least some patients who have coronary artery disease. This finding suggests that myocardial ischemia may potentially influence the results of programmed ventricular stimulation in some patients with coronary artery disease.
Adult↗
Effects of magnesium sulfate on cardiac conduction and refractoriness in humans.
Magnesium has been used empirically for several decades in the treatment of atrial and ventricular arrhythmias in patients with normal and decreased serum magnesium levels. However, a systematic evaluation of the effects of magnesium on cardiac conduction and refractoriness in humans has not been described. In this study, the electrocardiographic and electrophysiologic effects of magnesium were determined in 10 patients with normal baseline serum magnesium and other electrolyte levels. Six grams of magnesium sulfate was administered intravenously over 6 minutes followed by a continuous infusion of 1 additional gram over 1 hour. Serum magnesium levels rose significantly from a baseline of 2.0 +/- 0.2 to 5.4 +/- 0.4 mg/dl (p less than 0.001). No significant change occurred in heart rate at rest, or in duration of the QRS complex or QT or QTc intervals during sinus rhythm. There were significant increases in sinus node recovery time (1,000 +/- 211 to 1,106 +/- 223 ms, p less than 0.01) and corrected sinus node recovery time (279 +/- 87 to 336 +/- 104 ms, p less than 0.05). Significant increases occurred in atrioventricular (AV) node conduction time during sinus rhythm (82 +/- 22 to 97 +/- 17 ms, p less than 0.02), in the atrial paced cycle length at which AV node Wenckebach block occurred (350 +/- 46 to 419 +/- 65 ms, p less than 0.01) and in the AV node relative refractory period (397 +/- 27 to 422 +/- 18 ms, p less than 0.05), functional refractory period (395 +/- 41 to 415 +/- 33 ms, p less than 0.05) and effective refractory period (306 +/- 67 to 338 +/- 38 ms, p less than 0.05).
Adult↗
The plasma catecholamine response to ventricular tachycardia induction and external countershock during electrophysiologic testing.
Adrenergic activation during electrophysiologic study could potentially alter the electrophysiologic properties of the arrhythmia substrate. However, the catecholamine response to ventricular tachycardia induction and termination during electrophysiologic testing has to date not been quantitated. Therefore, in 13 patients undergoing electrophysiologic study, arterial plasma norepinephrine and epinephrine were measured before, during and 1, 3, 5, 10 and 15 minutes after ventricular tachycardia induced by programmed stimulation and terminated by a single 100 J external countershock. Sinus rate and the effective refractory period at the right ventricular apex at a basic drive cycle length of 400 ms were measured after the countershock at the same time intervals used for the catecholamine measurements. The mean ventricular tachycardia cycle length (+/- SD) was 187 +/- 30 ms, and the mean duration of ventricular tachycardia was 18 +/- 4 seconds. Plasma norepinephrine and epinephrine increased, respectively, from a baseline of 286 +/- 141 and 119 +/- 40 pg/ml to 770 +/- 330 (169%) and 597 +/- 467 pg/ml (402%), (p less than 0.01) at 1 minute after the countershock. The mean plasma norepinephrine and epinephrine levels during ventricular tachycardia and at times greater than 1 minute after the shock did not differ significantly from baseline levels. Sinus rate increased from a baseline of 74 +/- 13 to 103 +/- 26/min (39%) at 1 minute after the shock (p less than 0.05) and then returned to baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Acute and chronic effects of amiodarone on ventricular refractoriness, intraventricular conduction and ventricular tachycardia induction.
In eight patients, the right ventricular effective refractory period, rate-dependent changes in intraventricular conduction (as reflected by QRS duration during ventricular paced cycle lengths of 600 to 250 ms) and results of programmed ventricular stimulation were determined in the control state, 5 minutes after the intravenous infusion of 10 mg/kg body weight of amiodarone and after 2 months of treatment with oral amiodarone. The right ventricular effective refractory period was 230 +/- 30 ms (mean +/- SD) in the control study, 248 +/- 27 ms after intravenous amiodarone (p less than 0.001) and 296 +/- 26 ms after oral amiodarone (p less than 0.001). In the control state, QRS duration was constant at all paced cycle lengths. Intravenous amiodarone resulted in a rate-dependent prolongation of QRS duration. This rate-dependent prolongation was markedly accentuated by oral amiodarone in six patients who had an elevated serum level of reverse triiodothyronine (T3) after 2 months of oral treatment, but it was not more pronounced than the effects of intravenous amiodarone in two patients with a normal reverse T3 serum level after oral therapy. Both intravenous and oral amiodarone either suppressed or modified the induction of ventricular tachycardia by programmed stimulation in some patients, but in a discordant fashion. The relative effects of intravenous and oral amiodarone on ventricular refractoriness and conduction and on ventricular tachycardia induction did not correlate with serum amiodarone levels. Chronic amiodarone therapy results in a marked prolongation in ventricular refractoriness compared with the relatively small but significant increase that occurs after intravenous amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
Comparative survival after permanent ventricular and dual chamber pacing for patients with chronic high degree atrioventricular block with and without preexistent congestive heart failure.
To determine whether survival after permanent ventricular demand (VVI) pacing differs from survival after permanent dual chamber (DVI or DDD) pacing in patients with chronic high degree atrioventricular (AV) block (Mobitz type II or trifascicular block), 132 patients who received a VVI pacemaker (Group 1) and 48 patients who received a DVI or DDD pacemaker (Group 2) were followed up for 1 to 5 years. There was no significant difference in sex distribution, mean age or incidence of coronary heart disease, hypertension, valvular heart disease, diabetes mellitus, stroke or renal failure between Groups 1 and 2. Overall, the predicted cumulative survival rate at 1, 3 and 5 years was 89, 76 and 73%, respectively, for Group 1 and 95, 82 and 70%, respectively, for Group 2. In patients with preexistent congestive heart failure, the predicted cumulative survival rate at 1, 3 and 5 years was 85, 66 and 47%, respectively, for Group 1 (n = 53) and 94, 81 and 69%, respectively, for Group 2 (n = 20). The 5 year predicted cumulative survival rate was significantly lower in Group 1 patients with preexistent congestive heart failure than in Group 2 patients with the same condition (p less than 0.02). There was no significant difference in 5 year cumulative survival rate between Groups 1 and 2 for patients without preexistent congestive heart failure. The results suggest that permanent dual chamber pacing enhances survival to a greater extent than does permanent ventricular demand pacing in patients with high degree AV block and preexistent congestive heart failure.
Age Factors↗
An analysis of post-pacing R-R intervals during atrial fibrillation.
Bursts of ventricular pacing at cycle lengths of 350-260 ms were introduced during atrial fibrillation in nine patients, and the post-pacing R-R intervals were compared to the R-R intervals of spontaneous QRS complexes. In eight of nine patients, the mean post-pacing R-R interval was 126-199 ms longer than the mean spontaneous R-R interval (p less than 0.005). Spontaneous runs of aberrantly conducted supraventricular complexes were recorded during atrial fibrillation in one patient. The mean R-R interval following the runs of aberrantly conducted supraventricular complexes was significantly longer than the mean R-R interval of spontaneous narrow QRS complexes (p less than 0.001), but not significantly different than the mean post-pacing R-R interval. The findings of this study suggest that the R-R interval that follows a wide-complex tachycardia during atrial fibrillation is unlikely to be of value in differentiating ventricular tachycardia from aberrantly conducted supraventricular complexes. Analysis of R-R intervals that follow bursts of ventricular pacing suggests that there is likely to be considerable overlap between the R-R intervals that follow runs of ventricular tachycardia and the spontaneous R-R intervals during atrial fibrillation. Furthermore, even when the post-tachycardia R-R interval clearly exceeds the longest spontaneous R-R interval during atrial fibrillation, this is still of little diagnostic value, because a long pause may occur after either a run of ventricular tachycardia or a run of aberrantly conducted QRS complexes of supraventricular origin.
Aged↗
Effects of incremental doses of procainamide on ventricular refractoriness, intraventricular conduction, and induction of ventricular tachycardia.
The short-term effects of incremental doses of procainamide (7.5, 15, 22.5, and 30 mg/kg) on right ventricular effective refractory period, intraventricular conduction, and induction of ventricular tachycardia were determined in 31 patients who had a history of sustained, unimorphic ventricular tachycardia. QRS duration during incremental ventricular pacing was used as an index of rate-dependent changes in intraventricular conduction. The mean plasma procainamide concentrations corresponding to the incremental doses were 5.5 +/- 1.2 (+/- SD), 9.0 +/- 1.6, 12.6 +/- 2.2, and 16.3 +/- 3.2 mg/liter. Each incremental dose of procainamide up to a dose of 30 mg/kg resulted in a significant increment in right ventricular effective refractory period and each dose up to 22.5 mg/kg potentiated a rate-dependent prolongation of QRS duration. After the 7.5 mg/kg dose of procainamide, induction of ventricular tachycardia was suppressed in eight of 31 patients. After higher doses of procainamide, induction of ventricular tachycardia was suppressed in two additional patients. In three of 10 patients in whom the induction of ventricular tachycardia was suppressed by 7.5, 15, or 22.5 mg/kg of procainamide, sustained unimorphic ventricular tachycardia was again inducible after a higher dose of procainamide. In three of 31 patients, only nonsustained ventricular tachycardia was inducible after a 7.5 to 22.5 mg/kg dose of procainamide; however, in two of these three patients, sustained ventricular tachycardia was again inducible after administration of a higher dose of procainamide. In conclusion, during electropharmacologic testing with procainamide, it is worthwhile to test a dose of 7.5 mg/kg, because this dose is often effective in patients who respond to this drug. However, the results of this study indicate that procainamide may be effective in suppressing the induction of sustained ventricular tachycardia at a relatively low plasma concentration, but not at a higher plasma concentration. Therefore, during long-term therapy with procainamide it may be important to avoid plasma procainamide concentrations not only lower, but also higher than the concentration that results in the suppression of induction of tachycardia.
Acecainide↗
A prevalent misconception regarding wide-complex tachycardias.
In response to a questionnaire, 59% of 196 physicians indicated that they were influenced by a patient's blood pressure and clinical status when attempting to distinguish ventricular tachycardia (VT) from paroxysmal supraventricular tachycardia with bundle-branch block. A sizable proportion of physicians are unaware that VT need not be associated with shock. More emphasis should be placed on making physicians aware that the differentiation of VT from paroxysmal supraventricular tachycardia should be based on electrocardiographic findings and not on the patient's blood pressure or clinical status.
Aged↗
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)
Adult↗
Clinical significance of ventricular fibrillation-flutter induced by ventricular programmed stimulation.
Two hundred twenty-four patients underwent ventricular programmed stimulation (VPS) without prior documentation of the clinical occurrence of sustained ventricular tachycardia (VT) or ventricular fibrillation-flutter (VF). Indications for VPS were: palpitations or nonsustained VT during ambulatory monitoring (85 patients), syncope or presyncope (137 patients), and a family history of sudden death (two patients). Sustained VF requiring transthoracic defibrillation was initiated by VPS in 18 patients (8.0%). Four patients were treated for inducible VF with antiarrhythmic agents directed by electropharmacologic testing; five patients were treated empirically; nine patients received no therapy. No patient has had a cardiac arrest or sudden death during a follow-up period 25.2 +/- 13.8 months (mean +/- standard deviation). VF was initiated by two ventricular extrastimuli in three patients and by three extrastimuli in 15 patients. The incidence of VF was similar in patients with and without previous symptoms (8.8% vs 6.9%) or heart disease (7.1% vs 9.6%). It was significantly higher when VPS at three ventricular sites with a current of 5 mA (pulse width 2 msec) was compared to programmed stimulation at two ventricular sites with a current twice diastolic threshold (pulse width 2 msec) (15.2% vs 3.0%, p less than 0.05). VF initiated by VPS in patients without prior VT or VF appears to be a nonspecific finding. Antiarrhythmic therapy for VF may not be necessary in these patients.
Adult↗