Amiodarone in patients with recurrent sustained ventricular tachyarrhythmias: results of programmed electrical stimulation and long-term clinical outcome in chronic treatment

Thirty-three patients with clinically recurrent ventricular tachyarrhythmias were treated with amiodarone (200 to 600 mg/day) during a mean follow-up period of 23.7 months. Prior to amiodarone therapy, sustained ventricular tachycardia or ventricular fibrillation was initiated in all patients at control electrophysiologic study; patients failed a mean of 5.7 drugs, as assessed by programmed electrical stimulation. At electrophysiologic study after a loading phase (1000 mg/day for 10 days), 10 patients had no inducible ventricular tachycardia, nine patients had nonsustained ventricular tachycardia, 13 patients had persistent sustained ventricular tachycardia, and one patient had ventricular fibrillation. Patients were continued on amiodarone alone regardless of the findings at the electrophysiologic study, and during follow-up patients with no inducible sustained ventricular tachycardia or fibrillation on amiodarone had no recurrent arrhythmias or sudden death. Six of 14 patients (43%) with sustained ventricular tachyarrhythmias still inducible had recurrent ventricular tachycardia/fibrillation, and four of them died suddenly (29%). Programmed electrical stimulation predicts a good clinical long-term outcome during amiodarone therapy. Patients with persisting fast tachyarrhythmias (cycle length less than or equal to 300 msec) on amiodarone and a low ejection fraction (less than 35%) seem to have a higher incidence of sudden death. In these patients, therapeutic approaches such as antiarrhythmic surgery or implantation of antitachycardia devices should be considered.     

Electrophysiologic and antiarrhythmic efficacy of oral sotalol for sustained ventricular tachyarrhythmias: evaluation by programmed stimulation and ambulatory electrocardiogram

Programmed ventricular stimulation and ambulatory electrocardiography were performed both before and during oral sotalol therapy in 39 patients with ventricular tachyarrhythmia inducible by programmed stimulation (sustained ventricular tachycardia [n = 31], ventricular fibrillation [n = 3], nonsustained ventricular tachycardia [n = 5]). Oral sotalol was started at 80 mg twice daily and the dose thereafter was then gradually increased until a mean daily dose of 300 mg (range 160-480) was reached. In 12 of 34 patients with inducible sustained ventricular tachycardia or fibrillation the arrhythmia was suppressed; in 19 patients it was not and in 3 the spontaneous arrhythmia recurred. Reproducibly inducible nonsustained ventricular tachycardia was suppressed by sotalol in all five patients with this arrhythmia. Thus, a favorable electrophysiologic response was obtained in 17 (44%) of 39 patients. Arrhythmia suppression correlated with the type of arrhythmia (unsustained or sustained) induced during the control period (p less than 0.05), and nonresponders had a higher incidence of previously ineffective drug trials (p less than 0.05). In 22 patients treated long term with sotalol suppression of arrhythmia inducibility on programmed stimulation predicted freedom from recurrences (16 of 17), whereas continued inducibility indicated drug failure (5 of 5) (p less than 0.005). Serial ambulatory electrocardiograms performed in 37 of the 39 patients did not correlate with the results of electrophysiologic testing. For the patients on long-term treatment, invasive testing was superior to electrocardiographic monitoring in predicting outcome. These data indicate that in daily doses of 160 to 480 mg oral sotalol is a very useful agent in patients presenting with sustained ventricular tachycardia or fibrillation, and its efficacy is fairly well predicted by programmed stimulation.     

Role of programmed ventricular stimulation in patients with idiopathic dilated cardiomyopathy and documented sustained ventricular tachyarrhythmias: inducibility and prognostic value in 102 patients

The role of programmed ventricular stimulation (PVS) in patientsat high risk of sudden death related to idiopathic dilated cardiomyopathy(DCM) is still controversial The possible reason is that moststudy series have been too small or that only a few patientshad documented sustained ventricular tachyarrhythmias. This study therefore, looked at PVS performed in 102 patientswith DCM and documented sustained ventricular tachycardia (VT;n=63) or ventricular fibrillation (VF; n=39). Sustained VT wasinduced in 27 of 63 patients (43%) with documented sustainedVT and in 14 of 39 patients (36%) with documented VF (ns). VFwas induced in nine patients (14%) with a history of sustainedVT and in seven (18%) with a history of VF (ns). At a mean follow-upof 32±15 months, sudden death occurred in 14 (14%) patients,a rate similar in both patients with documented VT and VF (ns).Incidence of sudden death at 36 months was 6% in patients withinducible sustained VT/VF compared to 29% in patients withoutinducible VT/VF (P<0·05) A favourable drug regimen(response to drug and no intolerable side effects) was obtainedby serial drug testing in 25 of all 102 patients (25%). A cardioverterdefibrillator (ICD) was implanted in 32 patients, in 63% ofwhom discharges were observed during 18±11 months offollow-up; only one patient (3%) died suddenly. Thus, in patients with DCM, there was no relationship betweendocumented and inducible ventricular tachzyarrhythmias, andinitiation of sustained VT or VF had little prognostic valuefor the prediction of subsequent sudden death. Wherever antiarrhythmic drug therapy was of limited value, implantationof an ICD may improve the prognosis of these high risk patients.     

Safety and efficacy of sotalol in patients with drug-refractory sustained ventricular tachyarrhythmias

The safety and efficacy of oral sotalol, an investigational beta-adrenergic blocker with class III antiarrhythmic drug properties, were examined in a multicenter study in 236 patients with sustained ventricular tachyarrhythmias. In 104 patients, the index arrhythmia was a cardiac arrest, and all patients had undergone at least 3 previous unsuccessful antiarrhythmic trials (mean = 5 per patient). In the 106 patients assessed by programmed electrical stimulation, sotalol completely suppressed induction of ventricular tachycardia (VT) in 33 (31%) and rendered VT slower (greater than 100 ms prolongation of cycle length) or more difficult to induce in 29 (27%). Using continuous 24-hour ambulatory monitoring methods, sotalol complete- and partial-response rates were 51 and 12%, respectively. Of the 236 acute-phase patients, 151 were discharged receiving long-term sotalol therapy. The median sotalol dose was 480 mg/day. At a mean follow-up of 346 +/- 92 days, 27 patients (18%) had recurrence of sustained arrhythmia; 9, sudden death; 11, sustained VT; 5, automatic defibrillator discharge; and 2, syncope. Adverse effects forced discontinuation of therapy in 10 patients (7%): 6 secondary to symptomatic bradyarrhythmia, 2 due to refractory heart failure, 1 due to torsades de pointes, and 1 from bronchospasm. Life-table analysis of sotalol's overall long-term efficacy at 6, 12 and 18 months were 80, 76 and 72%, respectively. Although mean follow-up was short (less than 1 year), neither acute-phase programmed stimulation nor 24-hour ambulatory monitoring responses were significantly predictive of subsequent arrhythmic outcome. Proarrhythmia was documented in 18 patients (7%), 17 during the acute phase and 1 during long-term follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiology and antiarrhythmic efficacy of intravenous pirmenol in patients with sustained ventricular tachyarrhythmias

We assessed the electrophysiologic effects and antiarrhythmic efficacy of intravenous pirmenol in 15 patients who had spontaneous and induced sustained ventricular tachyarrhythmias. At a plasma concentration of 2.29 +/- 0.75 micrograms/ml, pirmenol decreased sinus cycle length by 11 +/- 13%, increased QRS, QTc, and HV intervals by 14 +/- 12%, 13 +/- 12%, and 22 +/- 28%, respectively, and increased atrial and ventricular effective refractory periods (ERP) by 20 +/- 14% and 7 +/- 8%, respectively. There was a greater increase in QRS duration during ventricular tachycardia and ventricular pacing than during sinus rhythm (p less than 0.005). By electropharmacologic testing, pirmenol was judged effective in six patients (40%) and was proarrhythmic in one (6%). In the nine patients in whom pirmenol was judged ineffective, the cycle length of induced VT increased by 36 +/- 15% and the associated mean arterial pressure increased by 21 +/- 14 mm Hg. The only side effects were mild hypotension and mild nausea in one patient each. Intravenous pirmenol has type IA electrophysiologic effects. It can be administered safely to patients with sustained ventricular tachyarrhythmias and is as effective as approved antiarrhythmic drugs when assessed by electropharmacologic testing.     

Antiarrhythmic efficacy of solitary beta-adrenergic blockade for patients with sustained ventricular tachyarrhythmias

To assess the efficacy and predictability of solitary beta-adrenergic blocker (BB) therapy for ventricular tachyarrhythmia (VT), 30 patients (16 men and 14 women) with a mean age of 55 years, who initially had sustained ventricular tachycardia (70%) or ventricular fibrillation (30%), were studied. Results of baseline arrhythmia tests showed VT on ECG monitoring in 57% of the patients, during exercise in 50%, induced by programmed stimulation in 69%, increasing to 86% during isoproterenol. BB therapy prevented inducible VT during programmed stimulation in 37% of the patients, prevented VT on ECG monitoring in 54%, and prevented VT during exercise in 83%. Long-term BB therapy was given to 24 of 30 patients, whereas six other patients with hemodynamically unstable VT during BB therapy received other long-term treatment. During a mean follow-up of 824 days, 6 of 24 patients had recurrent VT. BB therapy was discontinued in two patients because of side effects. Long-term success was predicted by left ventricular ejection fraction greater than 45%, absence of coronary disease, and age less than 60 years (all p less than 0.02). Neither suppression of arrhythmia during exercise testing, nor results of programmed stimulation or ECG monitoring were predictive of outcome. Thus beta-adrenergic blockers can be effective as solitary antiarrhythmic therapy in selected patients with VT.     

Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group I), ventricular activation time averaged 115 +/- 2 ms, compared with 166 +/- 3 ms (p less than 0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 +/- 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 +/- 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p less than 0.001), but lower than that for group II (p less than 0.001). The incidence of delayed ventricular activation was 89% for group II, 26% for group III and 18% for group IV. Sustained VT was not inducible in group I patients, but was inducible in 78% of group II (p less than 0.001 vs group I) and 20% of group III (p less than 0.05 vs group I; p less than 0.001 vs group II) (group IV was not studied).(ABSTRACT TRUNCATED AT 250 WORDS)     

Amiodarone therapy for sustained ventricular tachycardia after myocardial infarction: long-term follow-up, risk assessment and predictive value of programmed ventricular stimulation

We determine the value of the programmed ventricular stimulation (PVS) and of clinical, angiographic and electrophysiologic variables in assessing the long-term risk of arrhythmia recurrence in a group of coronary artery diseased patients presenting with a first episode of monomorphic sustained ventricular tachycardia (VT) treated with amiodarone. Mortality and arrhythmia recurrence rates were retrospectively assessed in 55 consecutive patients with previous myocardial infarction presenting with a first VT episode. Results of left heart catheterization, echocardiography and time-domain signal-averaging were collected. Patients underwent PVS after amiodarone oral loading and were classified according to inducibility before being all discharged on amiodarone (200 mg daily). The mean follow-up was 42+/-31 months. Total and cardiac mortality rates were 29% (16 patients) and 23% (13 patients) respectively. Sudden death (SD) occurred in nine patients (16%). VT recurred in 13 patients (23%). Sustained monomorphic VT was inducible in 40 patients (72%) after amiodarone loading. Neither total mortality (10/40 vs. 6/15) nor cardiac mortality (3/40 vs. 1/15) were significantly different between inducible and non-inducible patients. Recurrent VT rate was 27% (11/40 patients) for the inducible group and 13% (2/15 patients) for the non-inducible group (NS). SD occurred in 6/40 inducible patients (15%) and in 2/15 non-inducible patients (13%) (NS). Arrhythmic events occurred in 42% (17/40) inducible patients vs. 26% (4/15) non-inducible patients (P=0.07). Parameters correlated with outcome were ejection fraction (EF) (5 SD/11 patients with EF <0.3 vs. 4/44 with EF >0.3, P=0.003), mitral insufficiency (MI) (4 SD/10 patients with MI vs. 4/44 patients without MI, P=0.004) and age (65+/-9 years for patients with VT recurrence vs. 58+/-9, P=0.02). Although the risk stratification can be improved, reliable and safe long-term prediction of recurrence of malignant ventricular arrhythmia in individual patients cannot be made. Consequently, the systematic implantation of a cardioverter-defibrillator in case of a first episode of sustained VT occurring in coronary artery disease patients should be further debated.     

Malignant ventricular tachyarrhythmias in association with propafenone treatment

During treatment with the class Ic antiarrhythmic agent propafenone, the drug appeared to cause malignant ventricular tachyarrhythmias in five patients. Sudden cardiac death occurred in two of them. Three patients exhibited a transition from non-self-terminating ventricular tachycardia to ventricular fibrillation. In the other two patients electrocardiography during syncope revealed ventricular fibrillation. The observed malignant arrhythmias occurred within the first three days of treatment for chronic complex ventricular ectopic activity. Two of the five patients had markedly impaired left ventricular function. All patients received digoxin and low dose diuretic therapy. In contrast to drug induced arrhythmias encountered with other type I antiarrhythmic agents, the proarrhythmic effects of propafenone were not associated with marked QT prolongation. QRS duration was only slightly affected.     

Paired comparisons of efficacy of intravenous and oral procainamide in patients with inducible sustained ventricular tachyarrhythmias

Thirty-eight patients who had inducible sustained ventricular tachycardia during baseline programmed electrical stimulation underwent electrophysiologic testing after both intravenous and oral administration of procainamide. Each had presented clinically with documented sustained ventricular tachycardia or out of hospital cardiac arrest not associated with acute myocardial infarction. In 23 patients (61%) (Group I) the arrhythmia became noninducible during an intravenous infusion of procainamide. Oral procainamide was subsequently administered and retesting was carried out after dose titration to match plasma concentration at the end of the intravenous study. Among the 23 patients in Group I the mean (+/- SD) plasma procainamide level was 7.2 +/- 2.8 micrograms/ml after intravenous dosing and 7.9 +/- 2.5 micrograms/ml after oral dosing (p = 0.09). In 15 (65%) of the 23 patients, sustained ventricular arrhythmia was inducible on oral therapy with comparable plasma procainamide levels (intravenous = 6.3 +/- 2.1 micrograms/ml, oral = 7.5 +/- 2.1 micrograms/ml). The other eight patients (35%) had concordant responses to repeat testing with comparable intravenous (mean 9.0 +/- 3.3 micrograms/ml) and oral (8.8 +/- 3.1 micrograms/ml) plasma procainamide levels. In the additional 15 patients (Group II) sustained ventricular tachyarrhythmia remained inducible on intravenous procainamide therapy and the patients were retested on oral therapy with similar plasma concentration (p = 0.05). In seven patients (47%) sustained ventricular tachyarrhythmia was noninducible on treatment with oral procainamide (mean plasma level 7.6 +/- 2.7 micrograms/ml) after failure of intravenous procainamide (mean plasma level 10.3 +/- 2.3 micrograms/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

Bethanidine sulfate: efficacy in prevention of ventricular tachyarrhythmias during programmed stimulation. Report of a multicenter study of 56 patients

Twelve cardiac electrophysiology centers conducted an open label prospective trial of bethanidine sulfate, an oral bretylium analog, for the prevention of ventricular tachyarrhythmias during programmed electrical stimulation. The study group included 56 patients (44 men, 12 women; mean age 60 years; 55 with structural heart disease). Sixteen patients had both ventricular tachycardia and fibrillation, 30 had ventricular tachycardia alone and 10 had ventricular fibrillation alone. Programmed stimulation on no antiarrhythmic drugs induced sustained ventricular tachycardia in 46 patients, nonsustained ventricular tachycardia in 4 patients and ventricular fibrillation in 6 patients. During programmed ventricular stimulation after 59 trials of 20 to 30 mg/kg body weight of oral bethanidine (acute dosing in 40 patients, and divided dosing over 24 hours in 19 patients), no ventricular tachyarrhythmias were inducible in 6 patients (11%), sustained ventricular tachycardia was converted to nonsustained ventricular tachycardia in 3 patients (5%), ventricular tachyarrhythmias remained inducible in 39 patients (70%) and spontaneous ventricular tachyarrhythmias occurred more frequently in 4 patients (7%). Side effects prevented repeat testing in four patients. The 10 patients presenting with only ventricular fibrillation appeared to have a higher response rate: no ventricular tachyarrhythmias were inducible in 2 patients and sustained ventricular tachycardia was converted to nonsustained ventricular tachycardia in 2 patients. Despite protriptyline administration in 54 of 59 bethanidine trials, symptomatic hypotension occurred in 30 trials (51%). In conclusion, the efficacy of bethanidine for preventing ventricular tachyarrhythmias as assessed by programmed stimulation is low. Patients presenting with only ventricular fibrillation may have a more favorable response to bethanidine sulfate. Symptomatic hypotension occurs frequently despite concomitant use of protriptyline.     

Usefulness of programmed stimulation in predicting efficacy of propafenone in long-term antiarrhythmic therapy for paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous (i.v.) and oral propafenone were evaluated in 14 patients with Wolff-Parkinson-White syndrome and in 10 patients with atrioventricular (AV) nodal reentrant tachycardia. The effective refractory periods of the right atrium and the AV node increased after both preparations. In patients with Wolff-Parkinson-White syndrome, i.v. propafenone blocked anterograde accessory pathway conduction in 2 patients and retrograde conduction in 1; during oral therapy, accessory pathway conduction block occurred in 2 additional patients. The mean cycle length of the supraventricular tachycardia (SVT) increased from 338 +/- 60 ms to 387 +/- 56 ms (p less than 0.05) after i.v. application, and from 336 +/- 65 ms to 367 +/- 65 ms (p less than 0.05) during oral propafenone. The shortest pacing interval maintaining a 1:1 AV conduction increased from 325 +/- 65 ms to 368 +/- 81 ms (p less than 0.05) after i.v. infusion, and from 333 +/- 57 ms to 369 +/- 75 ms (p less than 0.05) during oral therapy. There was no difference in the electrophysiologic effects between i.v. and oral propafenone. The induction of SVT was prevented by i.v. propafenone in 10 of 20 patients and in 4 additional patients with oral propafenone. During follow-up, 6 of 7 patients, whose SVT could not be initiated by electrophysiologic drug testing, remained free from recurrences, whereas 5 of 7 patients with inducible tachycardia had recurrences of SVT. Thus, in patients with SVT, propafenone prolonged accessory pathway and AV nodal conduction and had a beneficial effect on circus movement tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term reproducibility of responses to programmed cardiac stimulation in spontaneous ventricular tachyarrhythmias

Programmed electrical stimulation (PES) of the heart has been used to initiate and terminate ventricular tachyarrhythmias under controlled conditions in patients in whom these arrhythmias have occurred spontaneously. The long-term reproducibility of the response to programmed cardiac stimulation in patients with ventricular arrhythmias is unknown. Seventeen patients with previously documented spontaneously occurring ventricular tachyarrhythmias were evaluated: 5 with nonsustained ventricular tachycardia (VT), 10 with sustained VT and 2 with ventricular fibrillation. The underlying cardiac diagnosis was atherosclerotic coronary heart disease (CAD) in 11 patients, dilated cardiomyopathy in 2 patients, congenital heart disease in 1 patient and no structural heart disease in 3. All patients underwent PES in the absence of antiarrhythmic drug treatment, and patients with inducible VT underwent serial electrophysiologic-pharmacologic testing in an attempt to suppress the arrhythmia. All 17 patients were reexamined with PES at a mean of 18 months (range 2 to 42) after their initial electrophysiologic study, during which time none had a myocardial infarction or intervening cardiac surgery. Repeat electrophysiologic studies, performed in the absence of antiarrhythmic agents, were undertaken because of drug intolerance, availability of new drugs, recurrent arrhythmia or preoperative reevaluation. All 11 patients with CAD had inducible VT on both the first and second electrophysiologic evaluation. Of the 6 patients with no CAD, only 1 had inducible VT on both occasions. Thus, long-term reproducibility of PES-induced VT in patients with stable CAD appears to be high.     

Importance of programmed ventricular stimulation in patients with ventricular salvos

The yield of programmed ventricular stimulation in asymptomatic patients with documented ventricular salvoes is not definitely known. Therefore, we retrospectively evaluated the data of 57 patients in whom ventricular salvoes had been observed, either during resting ECG or 24-hour ECG monitoring, and who had been studied using programmed ventricular stimulation. Of these patients, 63% were male, with a mean age of 49 years. 28% had coronary artery disease, 21% dilated cardiomyopathy, 16% mitral valve prolapse, 9% hypertrophic cardiomyopathy, 9% valvular heart disease and 14% had no structural heart disease. Using a maximum of two premature ventricular extrastimuli during programmed ventricular stimulation, sustained ventricular tachycardia or ventricular fibrillation was induced in nine patients (16%). In 30 patients (53%) nonsustained ventricular tachycardia was induced (3-35 ventricular echo beats), in 18 patients only one to two ventricular echo beats could be induced. In 8/16 patients (50%) with coronary artery disease, sustained ventricular tachycardia/ventricular fibrillation could be induced. Mean left ventricular ejection fraction did not differ between patients with inducible sustained ventricular tachyarrhythmia and those with inducible non-sustained ventricular tachycardia or those with a normal result during programmed ventricular stimulation. 33 patients were treated with antiarrhythmic drugs; the efficacy of antiarrhythmic therapy was either controlled by "serial electrophysiologic testing" in four patients, or by repeated 24-hour long-term ECG in 29 patients. During a mean follow-up period of 31 +/- 24 months five patients died, two of them suddenly. None of the remaining patients had experienced a symptomatic sustained ventricular tachycardia or a syncope.(ABSTRACT TRUNCATED AT 250 WORDS)     

Value of post-operative programmed ventricular stimulation after map-guided surgery for ventricular tachyarrhythmias -- epicardial versus endocardial stimulation

To assess the efficacy of map-guided antitachycardia surgery,induction of ventricular tachycardia has mostly been performedusing endocardial stimulation. In addition, epicardial stimulationcan be done using temporary epicardial wires, thus not requiringpost-operative catheterization. However, the diagnostic valueof epicardial versus endocardial stimulation for the post-operativeevaluation of patients undergoing map-guided surgery for drug-refractoryventricular tachycardia is not known, especially with regardto the induction of non-clinical tachyarrhythmias. Therefore,we compared the results of epicardial and endocardial programmedventricular stimulation in 58 consecutive patients in whom pairsof steel wires were placed over the right ventricle during surgery.The stimulation protocol consisted of single and/or double prematurestimuli during sinus rhythm and paced ventricular drives of500, 430, 370 and 330 ms. Pre-operatively, all patients hadinducible monomorphic ventricular tachycardia by endocardialstimulation. Post-operatively, 36 patients were not inducibleby either epicardial or endocardial programmed ventricular stimulation,whereas epicardial and endocardial stimulation induced the clinicalventricular tachycardia in six patients and non-clinical ventriculartachycardia in three patients (45/58 patients, 77% concordant).However, in two patients the clinical ventricular tachycardiawas induced only by endocardial programmed ventricular stimulation.Non-clinical ventricular tachycardia was inducible in threepatients by epicardial stimulation only, and in eight patientsby endocardial stimulation only (13/58 patients, 23% discordant). Thus, in 77% of patients an identical result of programmed ventricularstimulation was obtained using epicardial and endocardial stimulation,whereas the results were discordant in 23%. Therefore, epicardialstimulation alone is not sufficient for the post-operative evaluationafter map-guided surgery.     

Isoproterenol reversal of antiarrhythmic effects in patients with inducible sustained ventricular tachyarrhythmias

Seventeen patients (16 men and 1 woman) were challenged with isoproterenol after their initially inducible sustained ventricular tachyarrhythmia (monomorphic tachycardia in 14 patients and fibrillation in 3) was completely suppressed by class I antiarrhythmic drugs. Coronary artery disease was documented in 11 patients, dilated cardiomyopathy in 2 and no structural heart disease in the remaining 4 patients. The initial presentation was aborted sudden cardiac death (five patients), syncope (eight patients) and symptomatic nonsustained ventricular tachycardia (four patients). The antiarrhythmic drug that rendered the initial ventricular tachyarrhythmias noninducible was class IA in 11 cases, class IC in 5 and combined class IA and IB in 1. The original ventricular tachyarrhythmia became reinducible in 10 patients (group A) and remained noninducible in 7 patients (group B) after isoproterenol infusion at a rate necessary to achieve a 20% increase in heart rate. Despite the results of isoproterenol challenge, all patients were maintained on their electrophysiologically guided antiarrhythmic regimen. During a mean follow-up period of 13 +/- 9 months, 3 of the 10 patients in group A experienced clinical recurrence of tachyarrhythmia; no recurrence was noted in group B. In conclusion, reinducibility of ventricular tachyarrhythmia after beta-adrenergic stimulation seems to identify a subgroup of patients at high risk of subsequent arrhythmic events. Beta-adrenergic blockade or surgical therapy may be indicated in some patients with a positive isoproterenol challenge.     

Predictors of inducible sustained ventricular tachyarrhythmias in patients with coronary artery disease

To determine predictors of inducible sustained ventricular tachycardia or fibrillation by programmed electrical stimulation in patients with coronary artery disease and ventricular tachyarrhythmias, 14 clinical and angiographic variables were analyzed in 60 consecutive patients. All patients had angiographically documented coronary artery disease and symptomatic ventricular arrhythmias (sustained ventricular tachycardia in 21, ventricular fibrillation in 21 and nonsustained ventricular tachycardia in 18). Baseline programmed electrical stimulation while the patient was not taking antiarrhythmic drugs was performed with use of single, double and triple extrastimuli and burst pacing from two right ventricular sites. The variables analyzed were presenting arrhythmia; presence, frequency and complexity of ventricular ectopic activity on baseline 24 h electrocardiographic (Holter) monitoring; greater than or equal to 70% narrowing in either the left anterior descending, proximal left anterior descending, right coronary or circumflex coronary artery (independently assessed); single, double or triple vessel coronary disease; anterior, apical or inferior wall motion abnormalities; segmental dyskinesia and ejection fraction. Thirty-seven patients (62%) had inducible sustained ventricular tachycardia (rate greater than 100 beats/min, duration greater than 30 s or requiring cardioversion) and two patients (3%) had ventricular fibrillation induced. Eleven patients (18%) had nonsustained ventricular tachycardia (duration greater than or equal to 3 beats, less than 30 s) induced and 10 patients (17%) had no inducible arrhythmia (duration less than 3 beats). Multivariate stepwise logistic regression analysis identified three independent variables predictive of inducible sustained ventricular arrhythmias: sustained ventricular tachycardia as the presenting arrhythmia (p = 0.004), proximal left anterior descending artery lesion (p = 0.002) and anterior wall motion abnormality (p = 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)