Reappraisal of criteria for assessing drug efficacy in patients with ventricular tachyarrhythmias: complete versus partial suppression of inducible arrhythmias

To test whether increased difficulty in inducing ventricular tachycardia during antiarrhythmic therapy can be considered a sufficient criterion for predicting long-term efficacy of such therapy in patients with ventricular tachyarrhythmias, 95 patients were studied with a graded stimulation protocol (single and double premature stimuli during sinus rhythm and ventricular drives of 120, 140, 160 and 180 beats/min). After a control study, the effects of oral antiarrhythmic drugs on the ability to induce ventricular tachycardia were assessed. The median number of drug trials was four per patient. After antiarrhythmic therapy, four subgroups of patients were identified. In 36 patients, there was no change in inducibility (group 1), whereas in 18 patients ventricular tachycardia was rendered more difficult to induce; that is, a sustained ventricular tachycardia was inducible at a basic drive at least 40 beats/min faster than during the control study (group 2). In 34 patients, ventricular tachycardia induction was suppressed (group 3) and in 7 patients with nonsustained ventricular tachycardia, only 3 to 5 repetitive ventricular responses were induced after treatment (group 4). During follow-up of 15.5 +/- 11.5 months, 10 patients of group 1 had a recurrence of ventricular tachycardia and 6 died suddenly, whereas in group 2 only 1 patient died suddenly and in group 3, 2 patients had a recurrence of ventricular tachycardia (group 1 versus 2 and 3, p less than 0.001, Mantel-Cox and Breslow; group 2 versus 3, no difference). Thus, increased difficulty in inducing ventricular tachycardia is a sufficient criterion for predicting long-term efficacy of an antiarrhythmic drug regimen.     

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Predictive value of electrophysiologic testing in the treatment of drug-refractory ventricular arrhythmias with amiodarone

The value of serial electrophysiologic testing in predictingthe outcome of patients receiving amiodarone is controversial.Thirty-six patients with drug-refractory sustained ventriculartachyarrhythmias underwent serial electrophysiologic drug testing.All patients had inducible sustained ventricular tachyarrhythmiasoff any antiarrhythmic medication. After an oral amiodaroneloading regimen there was no change in inducibility in 23 patients(group I), whereas ventricular tachycardia was made more difficultto induce in 5 patients, i.e. sustained ventricular tachycardiawas only inducible using a basic drive which was 40 bpm fasterthan during control (group II). In the remaining 8 patients,induction of ventricular tachycardia was suppressed (group III).During follow-up of II ± 12.3 months, 6 patients in groupI had a recurrence of ventricular tachycardia and 2 died suddenly,whereas the course of groups II and III patients was uneventful(P<0.03, Breslow; P<0.01, Mantel–Cox). The predictiveaccuracy of the response to serial electrophysiologic testingduring amiodarone therapy was 64%, the sensitivity was 46% andthe specificity 100%. Thus, serial electrophysiologic drug testingis useful in determinating prognosis and predicts the long-termresponse to amiodarone therapy in patients with ventriculartachyarrhythmias using a graded stimulation protocol.     

QT prolongation and the antiarrhythmic efficacy of amiodarone

Amiodarone is an antiarrhythmic agent known to cause prolongation of action potential duration which is reflected in the electrocardiogram as a prolongation of the QT interval. Prolongation of the QT interval in patients dying suddenly was compared with that in patients who remained alive to determine whether a difference existed between these two groups. The electrocardiogram and amiodarone levels were evaluated in 33 patients who presented with cardiac arrest and symptomatic ventricular tachycardia in whom no other antiarrhythmic agent was found effective in preventing induction of ventricular tachycardia during electrophysiologic studies. There were 30 men and 3 women (mean age 52 +/- 10 years). Twenty-three are alive after a mean follow-up period of 12 +/- 7 months. Ten died: six suddenly, three of non-cardiac causes and one of congestive heart failure. Using a two-way analysis of variance, the percent change in QT, QTc, JT and JTc intervals before and after amiodarone therapy was analyzed. Marked prolongation in the QT interval was present in patients who remained alive with amiodarone therapy. A significant difference in percent QT prolongation was seen between the latter patients and those who died suddenly (p less than 0.005). No difference was observed in the percent change in QRS interval between the two groups. The levels of amiodarone (2.5 versus 3.2 micrograms/ml) and its metabolite (desethylamiodarone) were not significantly different between the living patients and those who died suddenly. These findings suggest that a prolongation of the QT interval may be a marker for the therapeutic antiarrhythmic effect of amiodarone.     

The management and outcome of late post-infarct ventricular tachycardia presenting to a district general hospital.

A review was undertaken of late post-infarct ventricular tachycardia in a district hospital cardiac care unit in order to study the clinical course of a total population of such patients from initial presentation to ultimate outcome. Thirty-six patients with this diagnosis were identified over a 3 1/2-yr period. Twelve were treated by empirically chosen antiarrhythmic drugs. Twenty-four were referred for electrophysiologically guided treatment, of whom 16 were treated by antiarrhythmic drugs, 3 by anti-ischaemic measures alone, and 5 by non-pharmacological antiarrhythmic treatments (antiarrhythmic surgery, percutaneous ablation, defibrillator implantation, cardiac transplantation). Of those treated empirically, 4 died in hospital of their arrhythmia, 1 died suddenly at home, and 2 suffered non-fatal arrhythmia recurrences during mean follow-up of 20 months. There were no arrhythmic deaths in those whose treatment was guided by serial electrophysiology studies, although 4 patients died of cardiac failure or reinfarction, and 3 were hospitalised with a recurrence of ventricular tachycardia during mean follow-up of 16 months. Age, concomitant medical problems and the apparent response to initial antiarrhythmic therapy were the main factors influencing management decisions. The apparent superiority of more intensive management strategies based on electrophysiology studies must be interpreted in the context of the selection processes applied to the total population initially presenting.     

Exacerbation of ventricular arrhythmias during the postoperative period after implantation of an automatic defibrillator

The postoperative course of 68 consecutive patients treated with an implantable defibrillator during the period from 1982 through 1990 was studied. In 46 patients (group 1), no concomitant surgery was performed during the implantation. In 22 patients (group 2), concomitant surgery (coronary artery bypass [n = 12], valve replacement [n = 3] or arrhythmia surgery [n = 7]) was performed. All patients in group 1 were clinically stable before surgery, receiving an antiarrhythmic regimen chosen by serial drug testings. The same regimen was continued postoperatively. Eight of the 46 patients in group 1 whose condition had been stable in the hospital for 19 +/- 25 days preoperatively developed multiple episodes of sustained ventricular tachycardia 4 +/- 9 days after implantation while receiving the same antiarrhythmic regimen. Although the exacerbation was transient in some patients, six required different antiarrhythmic therapy and one eventually died. Two additional patients had frequent and prolonged episodes of nonsustained ventricular tachycardia that could trigger the defibrillator, requiring changes in the antiarrhythmic regimen. Another patient had progressive cardiac failure and died on day 5. A marked (sevenfold) increase in asymptomatic ventricular arrhythmias was noted in 42% of the remaining 35 patients. In group 2 (combined surgery), one patient developed refractory ventricular tachycardia 3 days postoperatively and died on that day. Three patients developed frequent nonsustained ventricular tachycardia postoperatively, requiring changes in the antiarrhythmic regimen. The overall surgical mortality rate was 4.4% (4.3% in group 1 and 4.5% in group 2) and was due to refractory ventricular tachycardia in two patients and cardiac failure in one.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic testing and follow-up of patients with aborted sudden death

Clinical, electrophysiologic and follow-up data were analyzed for 108 patients with aborted sudden death. The mean follow-up interval was 2 years. All patients underwent baseline drug-free invasive electrophysiologic studies. Seventy-five patients (group I) had inducible ventricular arrhythmias (including nonsustained and sustained ventricular tachycardia and ventricular fibrillation) and 33 patients (group II) had no inducible arrhythmias. Noninducibility was not predictive of a favorable outcome, because the incidence of both sudden death and recurrent ventricular tachycardia was similar in the two groups. Treatment guided by electrophysiologic testing was used in 17 patients; in 13 (17%) in group I arrhythmias became noninducible, and in 4 (5%) sustained ventricular arrhythmias became nonsustained after administration of conventional drugs. There was a significantly higher incidence of sudden death and recurrent ventricular tachycardia in the 4 patients with inducible arrhythmias (n = 3, 75%) compared with the 13 patients whose arrhythmias were noninducible (n = 2, 15%) (p less than 0.05). For the group as a whole, 11% died suddenly and 15% had recurrence of ventricular tachycardia. Sixty-four patients were treated with amiodarone and, of these, four (6%) died suddenly during the follow-up period and nine (14%) had recurrent ventricular tachycardia. Ventricular arrhythmias could be induced in 69% of patients with aborted sudden death but inducibility could be suppressed in only 20% of them. The role of therapy guided by electrophysiologic testing could therefore not be fully assessed. The findings reveal a significant recurrence rate of symptomatic, potentially life-threatening ventricular arrhythmias in medically treated patients with aborted sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrophysiologic effects of bepridil in patients with refractory ventricular tachycardia assessed by programmed electrical stimulation

The effect of intravenous bepridil, a new calcium antagonist with class I and III properties, was tested in 21 patients with sustained ventricular tachyarrhythmias refractory to a mean of five antiarrhythmic agents as assessed by programmed right ventricular stimulation. At control electrophysiologic study without antiarrhythmic agents, sustained monomorphic ventricular tachycardia (VT) was initiated in 20 patients and ventricular fibrillation (VF) was initiated in one patient. After 3 mg/kg of bepridil was administered, VT was still inducible in 19 patients (3 patients had self-terminating VT); the other 2 patients had no inducible VT after bepridil. Bepridil prolonged significantly the QTc interval, the effective refractory period, and the cycle length of induced ventricular tachycardia. Two patients with no inducible VT after intravenous bepridil were placed on oral bepridil (300 mg/day). One patient died suddenly and one patient died of progressive heart failure. The results seem to indicate that the efficacy of bepridil in patients with refractory ventricular tachycardia is limited.     

Long-term survival of patients with malignant ventricular arrhythmia treated with antiarrhythmic drugs

The protective effect of antiarrhythmic agents for patients with malignant ventricular arrhythmia (defined as noninfarction ventricular fibrillation or sustained hemodynamically compromising ventricular tachycardia) remains uncertain. We have analyzed survival among 123 such patients (98 males, 25 females, average age 53.6 years) dependent on the abolition of antiarrhythmic drugs of salvos of ventricular tachycardia and R-on-T ventricular premature beats (Lown grades 4B and 5). Over an average follow-up of 29.6 months there were 35 deaths (11.2 percent annual mortality rate) of whom 23 patients succumbed suddenly (8.2 percent annual mortality rate). Among 98 patients in whom antiarrhythmic drugs abolished grades 4B and 5 ventricular premature beats, only 6 sudden deaths occurred for a 2.3 percent annual mortality rate. Of the 25 patients in whom advanced ventricular premature beats were not controlled, 17 died suddenly. Seventy-nine patients had left ventricular studies suitable for analysis. Among 44 patients with left ventricular dysfunction, control of ventricular premature beats was a critical element predicting survival. The annual sudden death rate for the 12 noncontrolled patients with left ventricular dysfunction was 41 percent contrasting with only 3.1 percent for the 32 patients with similar abnormalities in ventricular function in whom advanced ventricular premature beats were abolished. It is concluded that antiarrhythmic drugs can protect against the recurrence of life-threatening arrhythmias in patients who have manifest ventricular fibrillation or ventricular tachycardia and that abolition of certain advanced grades of ventricular premature beats provides an effective therapeutic objective.     

Clinical and electrophysiologic findings in patients with syncope following myocardial infarct

34 patients with syncope (median number of episodes 2) which remained unexplained after thorough medical and neurological evaluation underwent an intracardiac electrophysiological study with atrial and ventricular programmed stimulation. All patients had a history of well-documented myocardial infarction 24 months (median, 3-120) prior to the electrophysiological study. During programmed ventricular stimulation 6 patients had inducible ventricular fibrillation or flutter, and 10 patients had sustained ventricular tachycardia. In 14 patients non-sustained ventricular tachycardia was induced, whereas in only 4 patients 1 to 3 repetitive ventricular responses were induced. Therapy was instituted on the basis of electrophysiologic testing. During the follow-up of 8 months (median, 1-37) 27 patients had no recurrence of syncope. Syncope persisted and remained unexplained by the electrophysiological study in 3 patients. One patient had ventricular fibrillation and two died suddenly, two of these patients after having discontinued antiarrhythmic medication 2 weeks before. Another patient died of non-cardiac cause. It is concluded that 1) the results indicate a high ventricular vulnerability (88%) in patients with unexplained syncope after myocardial infarction, 2) the evaluation by electrophysiological studies may identify the potential mechanism for syncopes, 3) electrophysiological testing offers a rationale for specific prophylactic therapy.     

Usefulness of programmed stimulation in idiopathic dilated cardiomyopathy

The response to programmed electrical stimulation and the clinical outcome was determined in 47 patients with nonischemic dilated cardiomyopathy (DC). Thirteen patients (group 1) presented with sustained uniform ventricular tachycardia (VT), 14 (group 2) presented with cardiac arrest and 20 (group 3) presented with nonsustained VT. The mean ejection fraction of the study population was 28 +/- 9%. The response to programmed stimulation was related to arrhythmia presentation. In all patients in group 1 sustained, uniform VT was induced, compared with 1 patient in group 2 and 2 patients in group 3 (p less than 0.001). There were 14 sudden cardiac deaths and 1 cardiac arrest during a mean follow-up of 18 +/- 14 months. The only 4 patients who presented with sustained VT or a cardiac arrest in whom sustained arrhythmia induction was suppressed with antiarrhythmic therapy remain alive. Nine of the 23 patients (4 in group 2 and 5 in group 3) in whom no sustained ventricular arrhythmia was induced died suddenly, with 5 of the 9 receiving empiric antiarrhythmic therapy. Three other patients, who had a slower and hemodynamically tolerated VT at the time of arrhythmia induction, died suddenly. Thus, in patients with nonischemic DC, uniform, sustained VT is always and almost solely initiated in patients who present with this arrhythmia; although few patients presenting with sustained VT or cardiac arrest have inducibility of the arrhythmias suppressed with therapy, if it is suppressed the patient appears to have a good prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Improved survival with amiodarone in patients with hypertrophic cardiomyopathy and ventricular tachycardia.

The effect of amiodarone on survival was assessed in patients with hypertrophic cardiomyopathy and ventricular tachycardia in a drug trial with historical controls. During 1976 and 1977, 24 hour (seven) or 48 hour (79) electrocardiographic monitoring was performed in 86 consecutive patients; 24 had ventricular tachycardia and received conventional antiarrhythmic agents. Nineteen clinical, echocardiographic, and haemodynamic features were assessed. Seven patients died suddenly during follow up of three years; of these, five had continued to have ventricular tachycardia and two had no documented ventricular tachycardia. During 1978 and 1979, ventricular tachycardia was detected during 48 hour electrocardiographic monitoring in 21 of the next 82 consecutive patients with hypertrophic cardiomyopathy. They received amiodarone (150-400 mg/day, median 300); ventricular tachycardia was suppressed in all during repeat 48 hour electrocardiographic examination. Two patients died suddenly during a three year follow up, but neither belonged to the amiodarone treated group with ventricular tachycardia. The clinical and haemodynamic variables were similar in patients taking amiodarone and conventional agents. The fact that control of ventricular arrhythmia with amiodarone is significantly associated with improved survival suggests that amiodarone may prevent sudden death in patients with hypertrophic cardiomyopathy and ventricular tachycardia.     

Improved survival with amiodarone in patients with hypertrophic cardiomyopathy and ventricular tachycardia

The effect of amiodarone on survival was assessed in patients with hypertrophic cardiomyopathy and ventricular tachycardia in a drug trial with historical controls. During 1976 and 1977, 24 hour (seven) or 48 hour (79) electrocardiographic monitoring was performed in 86 consecutive patients; 24 had ventricular tachycardia and received conventional antiarrhythmic agents. Nineteen clinical, echocardiographic, and haemodynamic features were assessed. Seven patients died suddenly during follow up of three years; of these, five had continued to have ventricular tachycardia and two had no documented ventricular tachycardia. During 1978 and 1979, ventricular tachycardia was detected during 48 hour electrocardiographic monitoring in 21 of the next 82 consecutive patients with hypertrophic cardiomyopathy. They received amiodarone (150-400 mg/day, median 300); ventricular tachycardia was suppressed in all during repeat 48 hour electrocardiographic examination. Two patients died suddenly during a three year follow up, but neither belonged to the amiodarone treated group with ventricular tachycardia. The clinical and haemodynamic variables were similar in patients taking amiodarone and conventional agents. The fact that control of ventricular arrhythmia with amiodarone is significantly associated with improved survival suggests that amiodarone may prevent sudden death in patients with hypertrophic cardiomyopathy and ventricular tachycardia.     

Prediction of sudden death and spontaneous ventricular tachycardia in survivors of complicated myocardial infarction: value of the response to programmed stimulation using a maximum of three ventricular extrastimuli

The prognostic significance of ventricular arrhythmias induced by programmed electrical stimulation was evaluated in 50 survivors of acute myocardial infarction complicated by a major new conduction disturbance (38 patients), congestive heart failure (33 patients) or sustained ventricular tachyarrhythmias (22 patients), alone or in combination. Programmed stimulation was performed in patients in stable condition 7 to 36 days (mean 16) after infarction using one to three extrastimuli at four times diastolic threshold at a maximum of two right ventricular sites. Two groups were identified by the response to programmed stimulation: 17 patients with sustained (greater than 15 seconds) or nonsustained (greater than 7 beats but less than or equal to 15 seconds) ventricular tachycardia (group I), and 33 patients with 0 to 7 intraventricular reentrant complexes in response to maximal stimulation efforts (group II). Group I patients had a higher incidence of anterior infarction than that of patients in group II (71 versus 42%), had lower left ventricular ejection fraction (mean 0.35 versus 0.48) and were more often treated with antiarrhythmic drugs (47 versus 18%, p less than 0.05). There were no significant differences between groups in the occurrence of congestive failure, new conduction disorders or sustained ventricular arrhythmias with infarction, or in the proportions treated with a beta-receptor blocking agent, coronary bypass grafting or a permanent pacemaker. Total cardiac mortality was 24% during a mean follow-up period of 23 months and did not differ between groups; however, the response to programmed stimulation identified a group at high risk of late sudden death or spontaneous ventricular tachycardia: 7 (41%) of 17 group I patients compared with 0 of 33 group II patients (p less than 0.001). The induction of sustained or nonsustained ventricular tachycardia identified all patients who died suddenly or had spontaneous tachycardia (sensitivity 100%), but triple extrastimuli were required to induce prognostically significant arrhythmias in five of these seven patients; the specificity of this protocol was only 57%. When the clinical variables of the group were evaluated individually, the response to programmed stimulation had a stronger association with occurrence of late sudden death than did any other factor (Fisher's exact test, p less than 0.001); however, a type II error could not be excluded.(ABSTRACT TRUNCATED AT 400 WORDS)     

Radiofrequency catheter ablation in recurrent ventricular tachycardia.

Catheter ablation by radiofrequency energy was carried out in 10 patients with one type of recurrent monomorphic sustained ventricular tachycardia resistant to medical antiarrhythmic management. Electrophysiological studies before ablation included activation and pace-mapping. In all patients, the origin of the tachycardia was localized in the left ventricle: in the septum in six, at the posterolateral wall in three and anterobasal in one. The earliest onset of endocardial activation preceding the QRS complex during ventricular tachycardia ranged between -45 and -90 ms. Transcatheter ablation was performed with a bipolar or quadripolar catheter using a radiofrequency generator (HAT 100, Osypka). No complications occurred during the ablation procedure. Thereafter, in all patients, the clinical tachycardia was no longer inducible by programmed stimulation. During a follow-up period of 22 to 32 months including eight patients, the tachycardia recurred in two; one of these patients subsequently died suddenly. A third patient had one episode of a new type of sustained ventricular tachycardia some hours after catheter ablation. In the remaining patients, there was no recurrence of symptomatic tachycardia under maintenance of the antiarrhythmic management which, prior to ablation had been ineffective. Thus, our preliminary results suggest that radiofrequency catheter ablation might be beneficial for these high risk patients.     

Amiloride. Antiarrhythmic and electrophysiologic actions in patients with inducible sustained ventricular tachycardia

This study assessed the antiarrhythmic activity of amiloride in 35 patients with inducible sustained ventricular tachycardia. Patients had failed to respond to 3.6 +/- 1.0 antiarrhythmic drugs. Ventricular tachycardia was reproducibly induced by programmed electrical stimulation in all patients at the baseline study. Amiloride was given at 10 and 20 mg/day p.o. on a twice-daily schedule that achieved serum concentrations of 21 +/- 17 and 36 +/- 18 ng/ml, respectively. The mean left ventricular ejection fraction was unchanged from 36 +/- 14% at baseline to 37 +/- 17% during amiloride treatment. Amiloride significantly increased serum potassium from 4.6 +/- 0.4 to 5.1 +/- 0.4 mM. Four patients failed amiloride therapy with spontaneous nonsustained ventricular tachycardia. The remaining 31 patients were assessed by repeat programmed stimulation. Six patients had complete antiarrhythmic response, and an additional six patients had less than 15 beats of ventricular tachycardia induced. Therefore, amiloride was an efficacious antiarrhythmic treatment in 12 of 35 (34%) patients. Amiloride concentrations were significantly higher (52 +/- 20 ng/ml) in patients that responded than in patients that did not respond (30 +/- 15 ng/ml). The only electrophysiologic measurement that changed significantly was the ventricular functional refractory period (from 269 +/- 24 to 283 +/- 25 msec, p less than 0.05). Amiloride also suppressed frequent, spontaneous ventricular premature beats in eight of 15 patients (53%). No somatic side effects occurred. Two of the five patients discharged on amiloride therapy developed asymptomatic nonsustained ventricular tachycardia, and this prompted a change in antiarrhythmic therapy. Both died suddenly of arrhythmia during substitute empiric antiarrhythmic drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical characteristics and long-term follow-up in 119 survivors of cardiac arrest: relation to inducibility at electrophysiologic testing

Electrophysiologic studies were performed in 119 survivors of cardiac arrest. Sustained ventricular arrhythmias were initiated by programmed ventricular stimulation in 72 patients (61%). Coronary artery disease patients with induced sustained ventricular arrhythmias had a higher incidence of prior myocardial infarction (95 versus 72%) and ventricular aneurysm (59 versus 28%) and a lower ejection fraction (37 versus 50%) than those with no inducible sustained ventricular arrhythmias. Of the 72 patients with inducible ventricular arrhythmias, 11 (15%) died suddenly during a mean follow-up of 18 months (range 15 days to 58 months). In this group, 6 of 41 patients (15%) discharged on a successful antiarrhythmic regimen and 5 of 27 patients (19%) discharged on an unsuccessful regimen or without a predischarge study have died suddenly. Of these 27 patients, 1 of 12 patients treated with amiodarone and 4 of 15 (27%) with conventional antiarrhythmic therapy died suddenly. The remaining 4 patients died of nonarrhythmic causes in the postoperative period. Of 47 patients without inducible sustained ventricular arrhythmias, 15 (32%) died suddenly at a mean follow-up of 20 months, 10 (34%) with and 15 (28%) without empiric therapy. It is concluded that sustained ventricular arrhythmias can be initiated in most patients resuscitated from cardiac arrest. Patients with inducible arrhythmias have greater left ventricular dysfunction than those without inducible arrhythmias. Medical or surgical therapy that prevented the induction of sustained ventricular arrhythmias was predictive of a successful outcome in 85% of the patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Long-term reproducibility and significance of provokable ventricular arrhythmias after myocardial infarction

The long-term reproducibility and significance of inducible ventricular arrhythmias were assessed in 21 survivors of a myocardial infarction. Programmed ventricular stimulation performed a mean of 12 +/- 2 days (range 8 to 18) after infarction provoked ventricular fibrillation in 2 patients, sustained monomorphic ventricular tachycardia in 8 and nonsustained ventricular tachycardia in 11. Patients were restudied using the same protocol a mean of 8 +/- 2 months (range 4 to 11) after infarction. All patients underwent programmed ventricular stimulation studies in the absence of antiarrhythmic drug treatment. Ventricular tachyarrhythmias could be reinitiated in 16 patients (76%): ventricular fibrillation in 2, sustained ventricular tachycardia in 5 (monomorphic in 4) and nonsustained ventricular tachycardia in 9. A preponderance of inferior infarction was observed among patients with reinducible tachycardias (9 of 16 patients versus 0 of 5 with noninducible tachycardias) (p less than 0.05). No significant difference existed between patients with and without reinducible arrhythmias with respect to severity of coronary artery disease, degree of left ventricular dysfunction, occurrence of ventricular fibrillation in the acute phase of infarction and ventricular arrhythmias detected by 24 hour ambulatory electrocardiographic (Holter) monitoring. There was no significant difference between patients with and without a positive late study in stimulation thresholds, ventricular refractory periods, time interval between initial and repeat testing and use of beta-adrenergic blocking agents. During a mean follow-up period of 17 months (range 10 to 23) one patient with inducible sustained monomorphic ventricular tachycardia at both studies died suddenly. The remaining patients have survived follow-up without experiencing an arrhythmic event.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Determinants of prognosis in ventricular tachyarrhythmia patients without induced sustained arrhythmias

We studied 59 patients with sustained ventricular tachycardia (VT) or ventricular fibrillation in whom programmed stimulation induced 15 or fewer repetitive ventricular complexes. During follow-up of 2.2 +/- 1.5 years, 13 patients had an arrhythmia recurrence and seven died suddenly. At 1, 2, and 3 years, the actuarial incidence of arrhythmia recurrence was 15 +/- 5%, 17 +/- 5%, and 23 +/- 6%, and that of sudden death was 6 +/- 4%, 15 +/- 6%, and 21 +/- 8%. Prior myocardial infarction (MI) was the only independent predictor of arrhythmia recurrence (p less than 0.02) and sudden death (p = 0.05): at 2 years, 36 +/- 12% of 18 patients with MI and 8 +/- 4% of 41 patients without MI had arrhythmia recurrence, and 24 +/- 12% with MI and 3 +/- 3% without MI died suddenly. None of the nine patients with greater than or equal to 70% coronary stenosis but no MI had arrhythmia recurrence after anti-ischemic therapy. Possible arrhythmia-precipitating conditions were present during all arrhythmias in 14 patients, but did not predict freedom from arrhythmia recurrence (p = 0.52) or sudden death (p = 0.81). The maximum number of induced ventricular complexes did not predict arrhythmia recurrence or sudden death: for patients with 0 to 2, 3 to 5, and 6 to 15 induced complexes, the 2-year incidence of arrhythmia recurrence was 16 +/- 7%, 15 +/- 10%, and 18 +/- 10%; for sudden death, it was 9 +/- 6%, 0 +/- 0%, and 14 +/- 9%. In this group of patients, prior MI predicted arrhythmia recurrence and sudden death.(ABSTRACT TRUNCATED AT 250 WORDS)