Sustained ventricular tachyarrhythmias during the early postinfarction period: electrophysiologic findings and prognosis for survival.

Forty patients with sustained tachycardia occurring 3 to 65 days after myocardial infarction underwent programmed ventricular stimulation within 3 months of the infarction. Patients were characterized clinically by a complicated initial 48 hours of hospitalization for their acute infarction (85% of study group). The development of bundle branch block in association with infarction occurred with an unusually high frequency (32%). Ventricular tachycardia similar in configuration to spontaneous arrhythmia was induced with programmed ventricular stimulation in 33 (83%) of the 40 patients. In 15 (45%) of these 33 patients, additional morphologically distinct ventricular tachycardia not seen clinically was initiated. The induction of ventricular tachycardia was not significantly related to the time after myocardial infarction at which spontaneous ventricular tachycardia was initially observed. Only 20 of the 40 patients are alive after a mean follow-up period of 20 +/- 15 months. Twelve of the 20 deaths were sudden cardiac deaths. Sixteen of the 33 patients with inducible ventricular tachycardia died; 8 of the 16 deaths were sudden. By comparison, four of the seven patients with no inducible ventricular tachycardia died (probability [p] = not significant), all suddenly. The mode of therapy did not influence subsequent survival. It appears that in patients with sustained ventricular tachycardia occurring more than 48 hours after a recent myocardial infarction, ventricular tachycardia similar to that clinically observed can usually be induced by programmed stimulation. In addition, multiple morphologically distinct ventricular tachycardias, some of which have not been previously observed, are frequently induced. Finally, the prognosis for survival is poor, regardless of inducibility or mode of therapy, and may in part be related to a changing arrhythmia substrate.

Usefulness of electrophysiologic study to determine the clinical tolerance of arrhythmia recurrences during amiodarone therapy.

The relation of clinical and electrophysiologic variables to outcome was evaluated in 121 patients treated with amiodarone for sustained ventricular tachyarrhythmias. Electrophysiologic study was performed in all patients a mean of 14 days after beginning amiodarone therapy. Forty-six patients who were given oral amiodarone therapy experienced arrhythmia recurrence. Multivariate analysis was performed using 16 clinical and electrophysiologic variables to determine which factors were associated with 1) arrhythmia recurrence and 2) a poorly tolerated arrhythmia recurrence (that is, cardiac arrest or sudden cardiac death) during oral amiodarone therapy. No variable predicted arrhythmia recurrence. Five variables correlated significantly with a poorly tolerated arrhythmia recurrence. Hemodynamic stability of the arrhythmia induced on electrophysiologic testing during amiodarone therapy had the best predictive value (p less than 0.001). Younger age, lower ejection fraction, a poorly tolerated rhythm at clinical presentation and absence of left ventricular aneurysm were also associated with a poorly tolerated arrhythmia recurrence. Only 3 of 57 patients who had a well tolerated arrhythmia induced on electrophysiologic testing during amiodarone therapy had recurrence of a poorly tolerated arrhythmia versus 19 of 47 who had hemodynamically unstable arrhythmias induced during amiodarone therapy (p less than 0.001). Thus, electrophysiologic testing during amiodarone therapy appears useful in identifying patients who are prone to have catastrophic arrhythmia recurrences and could allow for the institution of additional or alternative modes of therapy.

Spontaneous changes in ventricular tachycardia cycle length.

Understanding spontaneous fluctuations in ventricular tachycardia cycle length is required to develop algorithms for ventricular tachycardia detection and termination. Variations in cycle length, time to stable cycle length and the range of RR intervals during ventricular tachycardia were analyzed in 74 episodes of sustained monomorphic ventricular tachycardia induced in patients not taking antiarrhythmic medication. Linear regression demonstrated cycle length variability to decrease over time (41 +/- 24 to 17 +/- 19 ms, p less than 0.001). Slower ventricular tachycardia had more cycle length variability than faster ventricular tachycardia (p less than 0.001). Ventricular tachycardia that was initially more variable tended to remain more variable (p less than 0.001). Fifty-four percent of episodes stabilized within the first 15 beats, 75% by 30 beats and 93% by 50 beats. The number of beats to stable cycle length was independent of ventricular tachycardia rate. The average range in cycle length per episode was 127 +/- 72 ms; 12% of ventricular tachycardia episodes varied by less than 50 ms and 45% by less than 150 ms. The maximal range in RR intervals from a single episode of ventricular tachycardia was 290 ms. Therefore, ventricular tachycardia demonstrates a wide range of cycle lengths and has time-dependent changes in variability and stability. These cycle length changes should be considered in the algorithms for ventricular tachycardia detection and termination by automatic antitachycardia devices.

Subendocardial resection for refractory ventricular tachycardia: effects on ambulatory electrocardiogram, programmed stimulation and ejection fraction, and relation to outcome.

The inducibility of ventricular tachycardia by programmed stimulation was correlated with ventricular ectopic activity on ambulatory electrocardiogram, ejection fraction and clinical outcome in 36 patients after endocardial resection for medically refractory ventricular tachycardia. Ventricular tachycardia was noninducible postoperatively in 25 patients and was inducible in 11. After administration of antiarrhythmic drugs, ventricular tachycardia could no longer be induced in four patients and remained inducible in the other seven patients. All 36 patients had postoperative and 20 had preoperative ambulatory electrocardiograms obtained while they were not receiving drug therapy. Pre- and postoperative ambulatory electrocardiograms did not differ in mean hourly ventricular premature depolarization frequency, Lown arrhythmia grade or change in grade (pre- vs. postoperative). The majority of postoperative patients had repetitive forms of ventricular arrhythmia postoperatively and there was no difference between patients with inducible and noninducible ventricular tachycardia in regard to Holter monitoring characteristics. There was no significant difference in postoperative ejection fraction between patients with inducible and noninducible ventricular tachycardia postoperatively. Ventricular tachycardia has recurred in 2 of 29 patients who had no inducible tachycardia at the time of hospital discharge and were followed up for a mean of 1 year; it has recurred in one of seven patients in whom it was still inducible at the time of hospital discharge and who were followed up for a mean of 7 months.(ABSTRACT TRUNCATED AT 250 WORDS)

Limited role of intravenous propafenone hydrochloride in the treatment of sustained ventricular tachycardia: electrophysiologic effects and results of programmed ventricular stimulation.

The electrophysiologic effects and response to programmed ventricular stimulation of intravenous propafenone, an experimental antiarrhythmic agent, were studied in a group of 14 patients with both clinical and induced sustained ventricular tachycardia. Twelve of the 14 patients had not responded to conventional antiarrhythmic drug therapy. Propafenone had no significant effect on sinus cycle length (836 +/- 170 ms before and 750 +/- 124 ms after propafenone), P wave duration (108 +/- 24 ms before and 106 +/- 23 ms after propafenone) or PR interval (181 +/- 45 ms before and 194 +/- 53 ms after propafenone). QRS duration and ventricular effective refractory periods increased significantly (109 +/- 20 to 130 +/- 21 ms and 235 +/- 24 to 256 +/- 19 ms, respectively). Ventricular tachycardia remained inducible or occurred spontaneously in 13 of 14 patients after propafenone administration. Neither mode of initiation nor mode of termination of ventricular tachycardia was predictably altered. Additional forms of ventricular tachycardia were seen in six patients. Cycle length of ventricular tachycardia was 303 +/- 73 ms before and 346 +/- 143 ms after propafenone (p = NS). In conclusion, intravenous propafenone does not significantly affect sinus rate, intraatrial conduction or atrioventricular conduction. Ventricular refractoriness and intraventricular conduction are prolonged. The mode of initiation, mode of termination and ventricular tachycardia cycle length are not predictably altered, but ventricular tachycardia occasionally occurs spontaneously after propafenone. Intravenous propafenone rarely prevents induction of ventricular tachycardia in patients with sustained ventricular tachycardia refractory to conventional antiarrhythmic agents.

Predictors of the success or failure of medical therapy in patients with chronic recurrent sustained ventricular tachycardia: a discriminant analysis.

To identify predictors of the success or failure of medical therapy in chronic recurrent sustained ventricular tachycardia, univariate and multivariate statistical techniques were used to retrospectively analyze data in 84 patients with this arrhythmia. By univariate analysis, four factors were associated with successful medical treatment: age less than 45 years, ejection fraction greater than 50%, hypokinesia as the only contraction abnormality and the absence of organic heart disease. Four other findings, the induction of ventricular tachycardia with a single ventricular extrastimulus, an HV interval greater than 60 ms, the presence of a left ventricular aneurysm and Q waves on a baseline electrocardiogram, correlated with medical failure. However, none of these variables alone accurately predicted treatment results in more than 75% of cases. By discriminant analysis, a function incorporating eight variables was constructed which correctly classified 81% of patients. Moreover, three-quarters of the patients could be classified into groups with a high or low probability of success where accuracy increased to 90%. When the discriminant function was tested prospectively in 31 similar patients, 25 (81%) fell into the groups with a high or low probability of success. In the latter group, of 20 patients predicted to fail medical therapy, 19 (95%) did fail a complete trial of medical therapy. The overall accuracy remained a high 92%. In clinical application this function would allow patients with a high probability of responding to medical therapy to be selected for serial electrophysiologic drug testing. In patients with a low probability of responding to medical therapy, serial studies could be avoided and alternate forms of therapy explored.

Comparative electrophysiologic effects of intravenous and oral procainamide in patients with sustained ventricular arrhythmias.

Thirty-three patients with sustained ventricular arrhythmias underwent electrophysiologic testing after intravenous and again after oral procainamide administration. Two groups were identified: group 1 included 15 patients with concordant serum procainamide concentrations with less than a 3 micrograms/ml difference after intravenous (mean 8.6 +/- 2.7) and oral (mean 8.8 +/- 2.7) procainamide administration, with mean N-acetylprocainamide concentrations of 1.0 +/- 0.6 and 6.2 +/- 2.8 micrograms/ml, respectively. Group 2 included 18 patients with discordant serum procainamide concentrations after intravenous (mean 9.5 +/- 5.9 micrograms/ml) and oral (mean 14.1 +/- 5.2 micrograms/ml) procainamide, with mean N-acetylprocainamide concentrations of 0.9 +/- 0.5 and 10.7 +/- 5.7 micrograms/ml, respectively. In group 1, response to programmed stimulation was the same after intravenous and oral procainamide administration, with no inducible ventricular arrhythmia in 5 of 15 patients. In group 2, 3 of 18 patients had no inducible arrhythmia after intravenous compared with 7 of 18 patients after oral procainamide administration. There was a different response to programmed stimulation after oral compared with intravenous procainamide in 6 of 18 patients in group 2 but in none of 15 patients in group 1 (p = 0.02). The effective procainamide concentration was greater than the ineffective concentration in five of the six patients with a discordant response, and the effective route of administration was oral in five of the six patients. The change in ventricular refractoriness in group 1 was similar after intravenous (28 +/- 23 ms) and oral (29 +/- 19 ms) procainamide, whereas in group 2, refractoriness was increased more after oral (33 +/- 21 ms) than intravenous (20 +/- 17 ms) procainamide administration and paralleled the difference in procainamide concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Perceived and actual risks of driving in patients with arrhythmia control devices.

BACKGROUND: We surveyed patient attitudes about driving and about driving restrictions for patients with automatic defibrillators and pacemakers, and we assessed risk of arrhythmias occurring during driving. METHODS: One hundred two patients responded to a questionnaire (57 patients with defibrillators and 45 patients with pacemakers) about driving habits and opinions on restriction of patients who have devices and want to drive. In addition, the literature was reviewed for approximate incidences of sudden death and syncopal or nonsyncopal device therapy to estimate risk while driving of having a defibrillator discharge. RESULTS: Thirty-two patients with defibrillators (56%) and 28 patients with pacemakers (62%) currently drove an average of 196 and 161 km/wk, respectively. Most patients felt that driving was a right and 75% felt that restriction imposed a hardship on them. Respondents felt that common sense, limited distances, or physician input should set driving limitations. A minority felt that no restrictions should be placed on these drivers or that they should not drive at all. The risks of sudden death and syncopal and nonsyncopal defibrillator discharge were estimated at 0.0009%, 0.0011%, and 0.0015% per kilometer driven, respectively, based on weekly kilometers and published occurrences of these phenomena. CONCLUSIONS: Patients perceive that driving is their right and that there is a low risk of an arrhythmic event behind the wheel. The estimated risk and published accounts of sudden death support this. However, concurrent medical problems and stresses imposed by driving may increase risk. The physician must make reasonable recommendations to ensure patient and public safety, keeping in mind both state and federal driving regulations and reporting requirements.

Ventricular activation during ventricular endocardial pacing: I. Electrocardiographic patterns related to the site of pacing.

The QRS configuration produced by pacing at multiple left ventricular endocardial sites was evaluated in eight patients with (group 1) and six patients without (group 2) left ventricular wait motion abnormalities. Pacing was performed at a total of 122 sites, 4 to 13 sites in each patient. The QRS configuration resulting from apical pacing locations was compared with that at basal, septal to lateral and inferior to superior locations. Significant differences in QRS configuration during pacing from apical and basal locations were observed in electrocardiographic leads I, V1, V2 and V6 (probability [p] less than 0.01). Specifically, a QS pattern in leads I, V2 and V6 was more characteristic of an apical pacing location (p less than 0.001), and a monophasic R wave in leads V1 and V2 was more characteristic of a basal pacing location (p less than 0.01). Significant differences in leads V1 and V2 were observed when septal and lateral pacing sites were compared (p less than 0.001). A monophasic R wave in leads V1 and V2 was more characteristic of a lateral pacing location (p less than 0.01); a QS complex in lead V2 was more characteristic of a septal pacing location (p less than 0.001). Pacing at superior sites usually produced an inferior axis and vice versa (p less than 0.001). The electrocardiographic patterns produced by pacing at similar sites in patients in group 1 were less consistent than those in patients in group 2. The QRS complex during ventricular pacing was wider in patients in group 1 (159 +/- 30 ms) than in patients in group 2 (132 +/- 18 ms) (p less than 0.001). It is concluded that the QRS configuration recorded with 12 lead electrocardiography during endocardial pacing can help locate the region of the pacing site in patients with and without organic heart disease, although precise localization is not possible.

Improvement in early diastolic filling dynamics after aortic valve replacement.

With use of ultrafast computed tomography, 13 patients undergoing aortic valve replacement for aortic stenosis were prospectively followed to evaluate the relation between left ventricular mass and diastolic function. Studies were done before intervention, and then at 4 and 8 months later. Mass decreased from 161 +/- 11 g/m2 (+/- standard error of the mean) at baseline to 106 +/- 5 g/m2, and then to 97 +/- 7 g/m2 at 4 and 8 months, respectively, in 12 patients who demonstrated significant (greater than 20%) mass regression after operation. One patient failed to show significant changes in mass. Diastolic function, as defined by the peak filling rate of early diastole, improved (p less than 0.02) in the group with mass regression, from 2.11 +/- 0.17 s-1 at baseline to 2.12 +/- 0.23 s-1, and then to 2.62 +/- 0.26 s-1 at 4 and 8 months, respectively. Improvement in the time to peak filling rate was also noted. Heart rates were unchanged, whereas end-diastolic volumes decreased and ejection fractions increased slightly. Postoperative increase in peak filling rate correlated with regression of ventricular mass to within normal range (+/- 2 standard deviations) and attainment of New York Heart Association class I status by 8 months (p less than 0.02). Thus, improvement in diastolic function can be seen after aortic valve surgery and is associated with improved functional class. Diastolic function improves later than the regression in wall mass and may imply a delayed remodeling of the ventricle.

Oral amiodarone loading for the rapid treatment of frequent, refractory, sustained ventricular arrhythmias associated with coronary artery disease.

To evaluate the efficacy and safety of oral amiodarone in the treatment of recurrent, sustained, refractory ventricular arrhythmias, rapid high-dose oral loading was used to treat 12 critically ill patients with frequent, sometimes incessant, sustained ventricular arrhythmias refractory to 2 to 6 antiarrhythmic agents. Presenting arrhythmias included sustained monomorphic ventricular tachycardia and ventricular fibrillation associated with cardiac arrests in 6 patients. Patients experienced 2 to 10 episodes (mean 5 +/- 2) of sustained ventricular arrhythmias over a mean period of 6.2 +/- 5.0 days (range 1 to 14) before oral amiodarone was initiated at 1,200 to 1,400 mg/day. This included at least 1 to 4 episodes (mean 2.2 +/- 1.1) within 24 hours before amiodarone. One to 4 antiarrhythmic drugs were administered concurrently during amiodarone loading. Sustained ventricular arrhythmias no longer occurred after a mean of 5.2 days (range 1 to 22) with amiodarone. Arrhythmias were controlled in 4 patients within 24 hours, 5 patients within 48 hours, 7 patients within 4 days and 10 patients within 6 days. Patients experienced a mean of 0.6 +/- 0.8 episodes within 24 hours after amiodarone. Nine patients survived to hospital discharge. No patient had significant adverse effects during high-dose loading. In conclusion, high-dose oral amiodarone loading, when added to previously unsuccessful conventional antiarrhythmic therapy, is safe and often rapidly effective for at least short-term control of frequent, refractory, sustained ventricular arrhythmias.

Ventricular activation in normal sinus rhythm: abnormalities with recurrent sustained tachycardia and a history of myocardial infarction.

Left ventricular activation was studied in 21 patients: 7 with normal electrocardiograms (group I), 7 with prior transmural myocardial infarction (group II) and 7 with prior transmural myocardial infarction (MI) and recurrent sustained ventricular tachycardia (VT) (group III). Fragmented electrograms were defined as those less than 3 mV in amplitude and longer than 60 ms in duration. Such electrograms were found in no group I patients, 6 of 7 group II patients and all 7 group III patients. An average of 2 of the 12 sites mapped in each patient displayed fragmented electrograms in group II; an average of 6 of the 12 sites displayed fragmented electrograms in group III (p less than 0.01). Twelve of the 84 total sites mapped in group II displayed fragmented electrograms, whereas 39 of the 84 sites mapped in group III patients did (p less than 0.01). The longest fragmented electrogram found in the 6 group II patients in whom such electrograms were found was shorter in duration than the longest electrogram found in each of the 7 group III patients with fragmented electrograms (76 ms vs 135 ms, p less than 0.005). The duration of endocardial activation was longer in group II patients (79 +/- 7 ms) than in group I patients (39 +/- 4 ms, p less than 0.001). Duration of activation was also longer in group III patients (151 +/- 12 ms) than in either of the other groups (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Antiarrhythmic and pharmacokinetic evaluation of intravenous recainam in patients with frequent ventricular premature complexes and unsustained ventricular tachycardia.

The pharmacokinetics, antiarrhythmic activity and safety of intravenously administered recainam were evaluated in 15 men and 3 women. All patients had frequent (> 30/hour) ventricular premature complexes (VPCs) and unsustained ventricular tachycardia. Recainam was administered at a loading dose of 4.5 mg/kg/hour over 40 minutes, followed by a maintenance infusion of 0.9 mg/kg/hour for 23 hours and 20 minutes. Sixteen patients had satisfactory efficacy data. The mean frequency of total VPCs decreased by 92.6% and the mean frequency of runs decreased by 99.9% during the maintenance infusion. Suppressions of > or = 70% of total VPCs and > or = 90% of runs were maintained over the 23-hour, 20-minute maintenance infusion period in 16 of the 18 patients. During the maintenance infusion, hourly group plasma recainam concentrations ranged from mean +/- SD 2.6 +/- 0.7 to 3.4 +/- 0.9 micrograms/ml. Patients were observed for 24 hours after termination of the infusion. Periodic blood samples were obtained during and after termination of the infusion to determine recainam concentration. Urine specimens were collected over scheduled intervals to determine urinary excretion of recainam. A 2-compartment pharmacokinetic model was used to analyze the data. The following pharmacokinetic parameters were obtained: terminal elimination half-life, 5.0 +/- 0.8 hours; systemic clearance, 0.27 +/- 0.08 liter/hour/kg; and central and steady-state volume of distribution, 0.32 +/- 0.11 and 1.4 +/- 0.4 liter/kg, respectively. Adverse experiences were reported in 4 of the 18 patients, possibly drug-related in 2; none was considered severe or required discontinuation of recainam.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction.

The clinical, angiographic and demographic characteristics of 42 patients with low-grade (less than 50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p greater than 0.10) but were significantly older (52 +/- 12 vs 56 +/- 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (greater than 50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (greater than 50% diameter stenosis) residual vessel disease was 0.6 +/- 1.0 for group I and 1.9 +/- 0.9 for group II (p less than 0.001). In group I, average residual infarct lesion diameter stenosis was 36 +/- 7% in the right anterior oblique and 34 +/- 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 +/- 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Mexiletine for control of drug-resistant ventricular tachycardia: clinical and electrophysiologic results in 44 patients.

The antiarrhythmic efficacy of mexiletine was evaluated in 44 patients with drug-resistant ventricular tachyarrhythmias. In 33 of these patients, the efficacy of mexiletine was assessed on the basis of the results of programmed ventricular stimulation. Mexiletine did not alter the ventricular effective refractory period, the Q-Tc interval, or the methods of tachyarrhythmia induction and termination during programmed stimulation. The mean cycle length of ventricular tachycardia (VT) increased from 270 +/- 49 to 313 +/- 80 ms in 21 patients in whom VT remained inducible on mexiletine alone (p less than 0.002). Overall, VT remained inducible with methods similar to control (no drugs) inductions in 25 patients receiving mexiletine alone or in combination with a type I agent. VT induction was prevented in only 8 patients, 3 on mexiletine alone and 5 receiving mexiletine combined with another drug. Mexiletine alone (in 2 patients) or with another agent (in 3) suppressed clinical recurrence of VT in an additional 5 of 11 patients who did not undergo electrophysiologic study. These 13 patients were discharged on mexiletine alone (5 patients) or in combination with other drugs (8 patients), and remained arrhythmia-free over a mean follow-up period of 7.7 +/- 4.1 months. Adverse effects occurred in 27 of 44 patients (61%) and were gastrointestinal in 17 and/or neurologic in 22. The drug was discontinued because of adverse effects in 6 patients (14%). Thus, mexiletine has limited efficacy when used alone, but when combined with other drugs it may be useful in up to 30% of patients with drug-resistant ventricular arrhythmias. Adverse effects are relatively common.

Electrophysiologic studies in nonsustained ventricular tachycardia: relation to underlying heart disease.

Electrophysiologic studies were performed in 83 patients with spontaneous episodes of nonsustained ventricular tachycardia (VT). The clinical arrhythmia was reproduced in 63% (in 42 patients by programmed stimulation and in 10 by isoproterenol infusion). In 15 patients sustained VT could be reproducibly induced by programmed stimulation. Inducibility was related to the associated heart diseases: programmed stimulation induced VT in 25 of 33 patients (75%) with coronary disease, 6 of 18 patients (33%) with cardiomyopathy (dilated in 16, hypertrophic nonobstructive in 2), in 4 of 8 patients (50%) with mitral valve prolapse and in 7 of 24 patients (29%) without structural heart disease. Isoproterenol infusion induced VT in no other patient with coronary artery disease, 1 other patient with mitral valve prolapse, 3 patients with cardiomyopathy, and in 6 of 24 patients without structural heart disease. Sustained VT was induced only in patients with structural heart disease, and correlated with the presence of left ventricular aneurysms: Sustained VT was induced in 9 of 13 patients with left ventricular aneurysms. The study demonstrates that electrophysiologic techniques can reproduce episodes of nonsustained VT in most patients with spontaneous arrhythmias. Some patients who demonstrate only nonsustained VT spontaneously have inducible, sustained VT, most often in the setting of coronary artery disease and left ventricular aneurysms.

Disopyramide: evaluation of electrophysiologic effects and clinical efficacy in patients with sustained ventricular tachycardia or ventricular fibrillation.

The efficacy of disopyramide in the management of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was evaluated in 50 patients by programmed ventricular stimulation: 38 patients had coronary artery disease (16 with left ventricular aneurysm), 8 had other cardiac diseases, and 4 had no apparent heart disease. Disopyramide was administered orally for 72 hours (dosage 400 to 1,600 mg/day), resulting in a plasma level of 3.6 +/- 1.2 micrograms/ml (mean +/- standard deviation [SD]). Disopyramide prevented induction of sustained ventricular tachyarrhythmias in 17 patients (34%) and failed to prevent induction in 33 patients (66%). Plasma levels were not significantly different regardless of response to disopyramide. The VT cycle length in patients responding to disopyramide was shorter than in nonresponding patients (225 +/- 51 ms versus 281 +/- 70 ms, p = 0.005). Disopyramide increased VT cycle length in those patients in whom it was ineffective (failed to prevent induction) from 281 +/- 70 ms to 347 +/- 64 ms (p less than 0.001). Ventricular refractory periods, QRS, and QTc durations significantly increased after disopyramide administration. Of the 17 patients in whom tachyarrhythmias were noninducible on disopyramide, 11 were discharged on disopyramide and followed up for 19 +/- 9 months; 9 of them remained free of VT. Heart failure developed in 2 of these patients. One other patient in whom disopyramide was ineffective had irreversible heart failure and died. It is concluded that disopyramide (1) prevents induction of ventricular tachyarrhythmias in one third of patients studied and remains clinically effective in approximately 80%, (2) is more frequently effective in rapid tachycardias, (3) prolongs the VT cycle length when ineffective, and (4) may produce marked hemodynamic embarrassment in patients with significant left ventricular dysfunction.

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

The ability of programmed ventricular stimulation to identify risk of sudden death after acute myocardial infarction (MI) was compared with 24-hour electrocardiographic assessment of ventricular ectopic activity and determination of left ventricular (LV) dysfunction. Forty-six patients underwent programmed stimulation 8 to 60 days (mean 22) after documented MI. Programmed stimulation consisted of single and double extrastimuli from the right ventricular apex at 2 times diastolic threshold during ventricular pacing and normal sinus rhythm. Of the 46 patients, 44 underwent electrocardiographic monitoring at least 6 days after MI. In 43 of the 46 patients, LV ejection fraction (EF) and the presence of LV aneurysm were determined. In response to programmed ventricular stimulation, 5 patients had sustained ventricular tachycardia (VT), 5 had nonsustained VT (greater than or equal to 4 beats), 13 had intraventricular reentrant repetitive responses, and 23 had either bundle branch reentrant repetitive responses or no extra responses to programmed ventricular stimulation (negative study). During a mean follow-up of 18 months, 10 patients died, 6 suddenly. One of the 10 patients with sustained or nonsustained VT died suddenly, compared with 3 of 13 patients with intraventricular reentrant responses and 2 of 23 patients with a negative study (difference not significant). Of 25 patients with Grade 0 to 2 ventricular ectopic activity, 3 died suddenly after MI, compared with 3 of 19 patients with Grade 3 or 4 activity (difference not significant). By comparison, the frequency of sudden death was greater in patients with an LVEF of less than 40% (5 of 16 versus 1 of 27 patients) or an LV aneurysm (5 of 13 versus 1 of 30 patients).(ABSTRACT TRUNCATED AT 250 WORDS)

Role of catheter mapping in the preoperative evaluation of ventricular tachycardia.

Although surgery is an accepted mode of therapy for refractory ventricular tachycardia, routine aneurysmectomy has yielded unpredictable results. This is believed to have occurred because there was no documentation that the arrhythmia actually arose from resected aneurysmal tissue. Catheter endocardial mapping has been used to localize preoperatively the area of origin of the arrhythmia. This technique has established that the arrhythmias arise near the endocardium at the borders of the aneurysm or infarction, or both. These regions, particularly when they occur in the interventricular septum, are not resected by standard aneurysmectomy. Intraoperative endocardial and epicardial mapping have validated the accuracy of this technique. We believe that catheter mapping should be performed before surgery for the following reasons: (1) In some patients ventricular tachycardia is not inducible in the operating room (for example, automatic ventricular tachycardia can be mapped in the catheterization laboratory); (2) in some patients not all morphologic forms of tachycardia can be induced or mapped intraoperatively because of failure of inducibility, time constraints or degeneration of the arrhythmia to ventricular fibrillation; and (3) intraoperative endocardial mapping occasionally cannot be performed because of lack of technical skills, physical factors such as mural thrombosis, or the inability to induce ventricular tachycardia after aneurysmectomy. Other methods currently being evaluated to localize the origin of ventricular tachycardia that do not require induction of arrhythmia are analysis of ventricular electrograms during sinus rhythm and pacemapping.

Termination of ventricular tachycardia. Evaluation of a new pacing method.

Ventricular extrastimuli or rapid ventricular pacing used to terminate ventricular tachycardia (VT) may be ineffective or may accelerate VT. Therefore, a new method to facilitate termination of VT and decrease the incidence of acceleration was evaluated. The new method utilized rapid ventricular pacing at cycle length 10 to 100 ms shorter than VT cycle length with the introduction of 1 or 2 ventricular extrastimuli. The efficacy of this combination method in terminating VT was assessed in 25 patients in whom ventricular extrastimuli and rapid ventricular pacing at cycle lengths and coupling intervals comparable with those used in the new method were unsuccessful. This combination method successfully terminated VT in 21 of 25 patients with cycle lengths of 230 to 400 ms. VT was terminated in 6 of 8 patients receiving drugs in whom VT could not be terminated by 1 to 2 ventricular extrastimuli or rapid ventricular pacing; in 6 of 8 patients unresponsive to ventricular extrastimuli and in whom rapid ventricular pacing produced acceleration of VT; and in 9 of 9 patients in whom antiarrhythmic agents made VT unresponsive to ventricular extrastimuli or rapid ventricular pacing. A combination of rapid pacing and extrastimuli can terminate VT unresponsive to ventricular extrastimuli or rapid ventricular pacing alone and may avoid acceleration of VT using rapid ventricular pacing at very short cycle lengths for termination.