Feasibility and cost savings of outpatient electrophysiologic testing.

The feasibility of outpatient electrophysiologic testing was examined by reviewing 100 consecutive outpatient tests performed in 95 patients. Seventy-one of the patients (75%) had no underlying heart disease. The electrophysiologic tests were performed to evaluate supraventricular tachycardias (n = 47), nonsustained ventricular tachycardia (n = 20), unexplained syncope (n = 21), palpitation (n = 9) or intermittent heart block (n = 2). A mean of 2.8 +/- 0.5 6F electrode catheters were inserted through a femoral vein. An electrode catheter was inserted into a subclavian or internal jugular vein in 28 tests and a 5F cannula was inserted into a femoral artery to monitor the blood pressure in 20 tests. The results of 61 tests (61%) were abnormal. Patients were monitored for a mean of 3.8 +/- 1.2 h after the procedure and then discharged. No complications occurred. For cost analysis a subgroup of 60 of these patients was matched for age, gender, heart disease and indication for electrophysiologic testing with a group of 60 patients who underwent electrophysiologic testing as inpatients. Physicians' fees for the two groups were similar; however, the mean hospital charge was $5,845 +/- 3,763 for the inpatient group compared with only $2,120 +/- 1,244 for the outpatient group (p less than 0.001). Thus, outpatient electrophysiologic testing is feasible and safe and results in substantial cost savings in patients without life-threatening arrhythmias.

Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction.

Fifteen consecutive patients with drug-refractory, recurrent, sustained, monomorphic ventricular tachycardia and a history of remote myocardial infarction underwent catheter ablation of ventricular tachycardia. Shocks of 100 to 300 J were delivered to sites at which pacing during ventricular tachycardia resulted in concealed entrainment, in which the ventricular tachycardia accelerated to the pacing rate, there was a long stimulus to QRS interval and there was no change in the configuration of the QRS complex during pacing at several rates compared with the configuration during ventricular tachycardia, thus identifying a zone of slow conduction in the reentrant circuit. Concealed entrainment was demonstrated in nine (60%) of 15 patients, and the stimulus to QRS intervals were 90 to 400 ms. At sites of concealed entrainment, the endocardial activation time relative to the QRS complex during ventricular tachycardia ranged from -125 to +50 ms, the timing of the local electrogram relative to the QRS complex was the same during entrainment as during ventricular tachycardia and the pace map during sinus rhythm was discordant with that of the ventricular tachycardia in seven patients. In the six patients in whom a site of concealed entrainment could not be identified, the target site for ablation was selected on the basis of identification of an isolated mid-diastolic potential, activation mapping and pace mapping. The mean (+/- SD) cumulative number of joules delivered to the target site was 306 +/- 140. A successful long-term clinical outcome was achieved in 9 of the 15 patients (mean follow-up 20 +/- 7 months). The clinical success rate was the same whether the target site was selected on the basis of concealed entrainment (five of nine, 56%) or on the basis of the other mapping techniques (four of six, 67%). In conclusion, the responses to pacing suggest that sites at which there is concealed entrainment may be located within a zone of slow conduction in the ventricular tachycardia reentry circuit, although not necessarily in an area critical for the maintenance of reentry. The long-term clinical efficacy of catheter ablation targeted to sites of concealed entrainment is about 60%, similar to the results achieved when conventional mapping techniques are used.

Determinants of QRS alternans during narrow QRS tachycardia.

This study was designed to prospectively determine the incidence of QRS alternans during various types of narrow QRS tachycardia and to clarify the determinants of QRS alternans. An electrophysiologic study was performed in 28 consecutive patients with a narrow QRS tachycardia. Persistent QRS alternans was observed in 6 (43%) of 14 patients during orthodromic reciprocating tachycardia, 5 (71%) of 7 patients during atrial tachycardia and 3 (43%) of 7 patients during atrioventricular (AV) node reentrant tachycardia. Incremental atrial pacing during sinus rhythm resulted in QRS alternans in patients who had QRS alternans during tachycardia, unless the shortest pacing cycle length associated with 1:1 AV conduction exceeded the tachycardia cycle length. In patients without QRS alternans during narrow QRS tachycardia, incremental atrial pacing during sinus rhythm resulted in persistent QRS alternans in five patients in whom the shortest pacing cycle length associated with 1:1 AV conduction was 60 to 180 ms less than the tachycardia cycle length. In an additional 20 patients without a narrow QRS tachycardia, persistent QRS alternans was observed during incremental atrial pacing in 11 (55%) of the patients. In six of six patients who had QRS alternans during abrupt rapid atrial pacing, QRS alternans was not observed when the same pacing rates were achieved gradually. Among the patients with narrow QRS tachycardia, the mean tachycardia cycle length in those who had QRS alternans (mean +/- SD 288 +/- 44 ms) was significantly shorter than in those who did not (369 +/- 52 ms, p less than 0.001). The presence of QRS alternans was not related to the tachycardia mechanism, relative or functional refractory period of the His-Purkinje system (at a drive cycle length of 500 ms), age, presence of structural heart disease, direction of input into the AV node or concealed retrograde conduction in the His-Purkinje system. In conclusion, QRS alternans during narrow QRS tachycardias is a rate-related phenomenon that depends on an abrupt increase to a critical rate and is independent of the tachycardia mechanism.

Significance of ST segment depression during paroxysmal supraventricular tachycardia.

During paroxysmal supraventricular tachycardia, patients frequently experience chest pain and marked ST segment depression suggesting acute myocardial ischemia. The purpose of this study was to assess whether ST depression during supraventricular tachycardia is caused by myocardial ischemia as reflected by net myocardial lactate production. Twenty-five patients (14 men, 11 women) who had a history of paroxysmal supraventricular tachycardia and a mean age (+/- SD) of 38 +/- 14 years underwent electrophysiologic testing. Twenty-four of these patients had no evidence of coronary disease, whereas one patient had undergone previous coronary bypass surgery. Nineteen patients had orthodromic and six patients had atrioventricular node reentrant tachycardias. A 12 lead electrocardiogram and simultaneous femoral artery and coronary sinus blood samples for lactate determinations were obtained at baseline and at 5 and 10 min of supraventricular tachycardia. Mean baseline heart rate of 83 +/- 12 beats/min increased to 180 +/- 25 beats/min during supraventricular tachycardia. All patients had 1 to 8 mm of ST segment depression in 1 to 9 of the 12 leads. Chest pain occurred in 64% of patients during supraventricular tachycardia. Baseline myocardial lactate extraction was 28 +/- 13% with no significant change at 5 or 10 min of tachycardia. In contrast, in a comparison group of seven patients with known coronary artery disease, atrial pacing at 168 +/- 26 beats/min in five patients resulted in greater than or equal to 1 mm ST depression in 2 to 7 of the 12 leads and a change in lactate extraction from a baseline of 29 +/- 13% to -27 +/- 20% (p less than 0.05) indicating net myocardial lactate production.(ABSTRACT TRUNCATED AT 250 WORDS)

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).

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)

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)

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)

Antagonism of quinidine's electrophysiologic effects by epinephrine in patients with ventricular tachycardia.

The purpose of this study was to determine whether pharmacologically induced elevations in the plasma epinephrine concentration within reported physiologic limits alter the response to quinidine during electropharmacologic testing. Twenty-one patients with coronary artery disease and a history of unimorphic ventricular tachycardia were found to have inducible sustained unimorphic ventricular tachycardia that was suppressed by treatment with oral quinidine gluconate. Epinephrine was then infused at a rate of either 25 or 50 ng/kg per min and testing was repeated. These infusion rates of epinephrine were previously demonstrated to result in elevations of the plasma epinephrine concentration in the range of concentrations that occur during a variety of stresses. Quinidine significantly lengthened the ventricular refractory periods and the QRS duration at a ventricular pacing cycle length of 350 ms, which was used as an index of intraventricular conduction. Epinephrine partially or completely reversed the effects of quinidine on ventricular refractory periods, but had no effect on QRS duration. During electropharmacologic testing of quinidine, no ventricular tachycardia was inducible in 12 patients, and only nonsustained ventricular tachycardia, 8 to 48 beats in duration, was inducible in 9 patients. Retesting during infusion of epinephrine demonstrated inducible sustained unimorphic ventricular tachycardia in 2 of the 12 patients in whom quinidine had completely suppressed the induction of ventricular tachycardia and in 8 of the 9 patients in whom only nonsustained ventricular tachycardia had been inducible during testing of quinidine. In conclusion, physiologic elevations in the plasma epinephrine concentration may reverse quinidine-induced prolongation of ventricular refractoriness but not intraventricular conduction.(ABSTRACT TRUNCATED AT 250 WORDS)

Identification and catheter ablation of a zone of slow conduction in the reentrant circuit of ventricular tachycardia in humans.

Three patients who had incessant ventricular tachycardia and in whom a zone of slow conduction was identified are presented. Each patient's tachycardia was refractory to multiple antiarrhythmic drugs and was being treated with amiodarone at the time of the electrophysiologic study. The ventricular tachycardia cycle length was 500 to 580 ms. In Patients 1 and 2, a single site at the posterolateral wall or low septum in the left ventricle was identified at which overdrive pacing during ventricular tachycardia resulted in ventricular capture with a stimulus to QRS interval of 280 to 400 ms and with little or no change in the configuration of the QRS complexes during pacing as compared with during ventricular tachycardia. In Patient 3, the same phenomenon was observed at two areas in the left ventricle: at the inferior wall, overdrive pacing during ventricular tachycardia resulted in a stimulus to QRS interval of 440 to 470 ms, whereas at the posterolateral wall, the stimulus to QRS interval was 320 to 360 ms. Transcatheter shocks of 100 to 240 J delivered at the pacing sites have been successful in preventing recurrences of ventricular tachycardia over a follow-up period of 10 to 11 months. These observations may be explained by the pacing site being located within a reentrant circuit in a zone of slow conduction bounded by inexcitable tissue between the pacing site and the exit site of the reentrant circuit. In Patient 3, the variable stimulus to QRS intervals are explained by variable proximity of the pacing sites within the slow conduction zone to the exit site of the reentrant circuit.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

A prospective randomized comparison of direct current and radiofrequency ablation of the atrioventricular junction.

OBJECTIVES: The purpose of this study was to compare direct current and radiofrequency ablation of the atrioventricular (AV) junction in a prospective randomized fashion. BACKGROUND: Catheter ablation of the AV junction can be performed using either direct current shocks or radiofrequency energy. To date, these two techniques have never been compared prospectively or in a randomized study. METHODS: Forty patients with drug-refractory uncontrolled atrial fibrillation-flutter (38 patients) or inappropriate sinus tachycardia (2 patients) were randomly assigned to undergo direct current ablation (20 patients) using up to four shocks of 200 to 300 J or radiofrequency ablation (20 patients) using up to 15 applications of 16 to 25 W for 30 s. If complete AV block was not successfully induced, the ablation procedure was repeated using the alternate type of energy. A rate-responsive ventricular pacemaker was implanted in each patient. The intrinsic escape rhythm was evaluated 15 min, 2 days and 3, 6 and 12 months after ablation. RESULTS: Persistent complete AV block was successfully induced during the first ablation session in 13 (65%) of 20 patients randomly assigned to undergo direct current ablation, compared with 19 (95%) of 20 patients randomly assigned to undergo radiofrequency ablation (p < 0.05). Each patient whose first ablation attempt failed had a successful outcome with the alternate type of energy. The overall efficacy of radiofrequency ablation (26 [96%] of 27 patients) was significantly greater than that of direct current ablation (14 [67%] of 21 patients, p < 0.01). The duration of the direct current and radiofrequency ablation sessions did not differ significantly. The mean peak plasma creatine kinase MB fraction concentration was significantly higher after direct current ablation (58 +/- 29 IU/liter) than after radiofrequency ablation (2 +/- 2 IU/liter) (p < 0.001). An escape rhythm was present 15 min after ablation in an equal proportion of patients undergoing direct current and radiofrequency ablation (78% and 85%, respectively, p = 0.6). An escape rhythm was present in all patients 3, 6 and 12 months after ablation. The mean escape rhythm cycle length 15 min after direct current ablation (2,074 +/- 677 ms) was significantly longer than that 15 min after radiofrequency ablation (1,460 +/- 294 ms) (p < 0.05); however, the mean escape rhythm cycle lengths did not differ significantly at 2 days or 3, 6 or 12 months after ablation. Immediate arrhythmic complications did not occur after either procedure. One patient died suddenly 6.5 months after direct current ablation. CONCLUSIONS: Radiofrequency ablation of the AV junction is more efficacious and safer than direct current ablation and should be the preferred method for inducing complete AV block in patients who are appropriate candidates for ablation of AV conduction.

Electrophysiologic effects of epinephrine in humans.

The electrophysiologic effects of circulating epinephrine in humans were examined in four study groups of 10 subjects each. In 10 subjects without structural heart disease (Group 1) and in 10 patients with coronary disease or dilated cardiomyopathy (Group 2) epinephrine infusion at 25 and 50 ng/kg body weight per min for 14 min resulted in an elevation of the plasma epinephrine concentration in the physiologic range. In both groups it produced a dose-dependent decrease in the effective refractory period of the atrium, atrioventricular (AV) node and ventricle and improvement in AV node conduction. Epinephrine facilitated the induction of sustained ventricular tachycardia in 3 of the 20 subjects. In Group 3, a beta-adrenergic blocking dose of propranolol was added to the infusion of 50 ng/kg per min of epinephrine. Propranolol not only reversed the effects of epinephrine, but also lengthened these variables compared with baseline values. In Group 4, propranolol was administered first, followed by 50 ng/kg per min of epinephrine. Propranolol alone slowed AV node conduction and mildly prolonged the refractory periods. In the presence of beta-blockade, epinephrine had no effect on AV node properties but resulted in a lengthening of the atrial and ventricular effective refractory periods. In conclusion, epinephrine in physiologic doses shortens the effective refractory period of the atrium, AV node and ventricle, improves AV node conduction and may facilitate the induction of sustained ventricular tachycardia. The overall electrophysiologic effects of epinephrine result from stimulation of beta-receptors. Stimulation of alpha-receptors by epinephrine has no effect on the AV node but prolongs the effective refractory period of the atrium and ventricle, partially offsetting the shortening of refractory periods mediated by beta-receptor stimulation.

Hemodynamic effects of nifedipine given alone and in combination with atenolol in patients with impaired left ventricular function.

The acute intravenous (IV) (0.1, 0.2 and 0.4 microgram/kg/min over 10 minutes each) and chronic oral (60 mg/day) administration of nifedipine was examined in 9 patients with significantly impaired left ventricular (LV) function (ejection fraction [EF] on radionuclide scanning was 0.20 to 0.40) who were already receiving beta-blocker therapy (greater than 25% reduction in peak exercise heart rate) with atenolol, 100 to 200 mg/day. The mean control LV end-diastolic pressure (EDP) at cardiac catheterization and EF for the group as a whole were 30 +/- 3 mm Hg (range 20 to 42) (mean +/- standard error of the mean) and 28.5 +/- 2.4%, respectively. Three of the 9 patients had hemodynamic deterioration and LV failure at some stage during the study, and their mean LVEDP and EF were 38 +/- 3 mm Hg (range 33 to 42) and 22.6 +/- 2.7%, respectively. In the 6 patients who tolerated the full treatment protocol, the mean LVEDP and EF were 26.5 +/- 2.0 mm Hg (range 20 to 35) and 31.5 +/- 2.8%, respectively. Seven patients received IV nifedipine, which had a negative inotropic action but did not precipitate cardiac decompensation. Chronic oral administration of nifedipine in combination with atenolol precipitated LV failure only in those with the lowest EF and highest LVEDP; usually LV failure was present with atenolol alone. Extensive infarction, frequently complicated by LV failure at the time, LVEDP greater than 32 mm Hg and control resting EF less than 30% were associated with LV failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of PY 108-068, a new calcium channel blocker, for angina pectoris.

The efficacy of PY 108-068 (75 and 150 mg/day), a new dihydropyridine calcium antagonist, was compared with placebo for treatment of chronic stable angina. Twelve patients were studied in a placebo-controlled, double-blind, randomized, crossover trial of 2 weeks each. Antianginal efficacy was assessed by the number of episodes of angina and nitroglycerin tablets consumed during each 2-week period, as well as the number of episodes of ischemia during 48-hour ambulatory monitoring and the area and severity of ST-segment depression during 16-point precordial exercise mapping. Nitroglycerin consumption (mean +/- standard error of the mean) decreased from 6.1 +/- 2.9 with placebo to 1.8 +/- 1.5 with 75 mg/day of PY 108-068 (p less than or equal to 0.03) and to 3.6 +/- 2.3 with 150 mg/day of PY 108-068 (p less than or equal to 0.01 vs placebo, difference not significant vs 75 mg/day of PY 108-068), whereas episodes of angina were reduced significantly only by the high dose (p less than or equal to 0.03) (11.1 +/- 3.9 with placebo, 6.3 +/- 2.4 with 75 mg/day of PY 108-068 and 8.1 +/- 3.4 with 150 mg/day of PY 108-068). The low dose alone significantly reduced ST-segment depression during exercise testing (p less than or equal to 0.03) (29.6 +/- 3.6 with placebo, 23.1 +/- 5.6 with 75 mg/day of PY 108-068 and 24.4 +/- 5.0 with 150 mg/day of PY 108-068), whereas neither dose significantly altered the number of episodes of ischemia during ambulatory monitoring.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Acute changes in pacing threshold and R- or P-wave amplitude during permanent pacemaker implantation.

This study examines the changes in pacing threshold and R- or P-wave amplitude during the first 30 minutes after implantation of tined and screw-in leads. The leads examined were those of 1 manufacturer (Medtronic) and consisted of 3 ventricular pacing leads (model numbers 6957 unipolar screw-in [11 patients], 6961 unipolar tined [12 patients] and 6962 bipolar tined [7 patients]) and 1 atrial lead (model number 6957J unipolar screw-in [10 patients]). After optimal lead position was obtained fluoroscopically in the right ventricular apex or right atrium, the pacing threshold and R- or P-wave amplitudes were measured at 5-minute intervals for 30 minutes. The acute ventricular pacing threshold with the screw-in lead was significantly higher than with the tined lead (0.84 +/- 0.17 vs 0.58 +/- 0.15 volts; p less than 0.001). There was a significant (p less than 0.001) acute decrease in the ventricular pacing threshold with both lead types, with the maximum decrease occurring 5 minutes after lead implantation. There was a significant acute increase in R-wave size with the ventricular screw-in lead that peaked 20 minutes after lead implantation (11.9 +/- 3.0 to 14.7 +/- 4.1 mV; p less than 0.001). The atrial screw-in lead behaved in a manner identical to its counterpart in the ventricle. In conclusion, there are acute changes in the pacing threshold and R- or P-wave amplitude obtained with tined and screw-in pacing leads.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Value of programmed ventricular stimulation in presumed carotid sinus syndrome.

This study determines the results of programmed stimulation in patients with syncope or near-syncope presumed to have the carotid sinus syndrome based on the finding of carotid sinus hypersensitivity and the absence of any other apparent cause for syncope or near-syncope after clinical evaluation. Fourteen patients had coronary artery disease, 1 had dilated cardiomyopathy and 18 patients did not have structural heart disease. Programmed simulation was performed at 2 basic drive cycle lengths and 2 right ventricular sites with 1 to 3 extrastimuli. Sustained unimorphic ventricular tachycardia (VT) was induced in 5 of 15 patients who had structural heart disease, and in none of the 18 patients who did not (p less than 0.05). Polymorphic VT or ventricular fibrillation (VF) was induced in 5 of 15 patients (33%) who had structural heart disease, and in 5 of 18 patients (27%) who did not (p greater than 0.05). Patients who had inducible unimorphic VT were treated with antiarrhythmic drugs that suppressed the induction of VT, and 4 of 5 patients also received a pacemaker; no patient had a recurrence of syncope during follow-up. Patients who had inducible polymorphic VT and VF (n = 10) or no inducible VT (n = 18) received treatment directed at only carotid sinus syndrome. Two patients with inducible VT or VF and 1 patient without inducible VT had recurrent syncope during follow-up, but none had cardiac arrest or died suddenly.(ABSTRACT TRUNCATED AT 250 WORDS)

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.