Search PubMed⌕ Search

Biomedical subjects

J Brugada

Publications and source records attributed to J Brugada.

At least 55 records · Page 3Linked to original sources
PubMed1999

Is inappropriate therapy a resolved issue with current implantable cardioverter defibrillators?

Patients with an implantable cardioverter defibrillator (ICD) can undergo inappropriate therapies if electrical activity not originating in the ventricle is wrongly recognized as ventricular by the device. Inappropriate therapy can be the result of detection of supraventricular tachycardias or over-sensing of other artifacts by the device. Enhanced detection criteria in third-generation ICD have been implemented to recognize fast supraventricular arrhythmias. Analysis of the use of these criteria in patients with an ICD has shown that arrhythmias detected in the ventricular tachycardia zone are frequently supraventricular (193 supraventricular of 690 tachycardia episodes in 23 of 59 patients). Use of sudden onset was very effective in detecting sinus tachycardia (65 of 67 episodes) and stability was very useful in detecting atrial fibrillation (31 of 32 episodes). However sensitivity in detecting ventricular tachycardia was only 90% (451 of 497 episodes). Application of the sustained, rate duration criteria allowed appropriate treatment of all ventricular tachycardia episodes, increasing sensitivity to 100%; however, specificity in appropriate nontreatment of supraventricular episodes decreased from 96% to 83%. Subsequent analysis of different algorithms showed that sudden onset > 9% and stability < 40 msec was the algorithm with the best specificity and sensitivity. Programming sudden onset and stability detection criteria with a sustained, rate duration safety net for triggering tachycardia therapy results in appropriate device management in most patients with supraventricular and relatively slow ventricular tachycardia.

Adult↗
PubMed1999

Use of the prophylactic implantable cardioverter defibrillator for patients with normal hearts.

About 10-20% of patients dying suddenly and unexpectedly do not have structural heart disease. The major causes of sudden death in this population are acute ischemia, the syndrome of right bundle branch block, and ST-elevation from V1 to V3, the long QT-syndrome, and the Wolff-Parkinson-While syndrome. In some patients, none of these syndromes can be recognized and ventricular fibrillation is classified as idiopathic. There are good preventive and therapeutic methods against acute ischemia and there are also curative treatments for the Wolff-Parkinson-White syndrome. Patients with idiopathic ventricular fibrillation cannot be recognized beforehand. However, there are electrocardiographic and genetic markers for the Brugada syndrome and the long QT syndrome. It is, therefore, justified to discuss the possible role of the prophylactic defibrillator to prevent sudden death in these 2 syndromes for which no effective treatment exists. Patients with Brugada syndrome have a high incidence of sudden death, and prophylactic defibrillators are indicated in patients with inducible arrhythmias at electrophysiologic study, irrespective of symptoms. On the contrary, the incidence of sudden death in the long QT syndrome is very low, making prophylactic defibrillator implantation not cost-effective.

Bundle-Branch Block↗
PubMed1999

[Analysis of local electrograms and characteristics of the ablation procedure in left-sided accessory pathways that required five or more pulses of radiofrequency].

INTRODUCTION AND OBJECTIVES: Radiofrequency ablation of left sided accessory pathways requires multiple pulses in some patients due to different factors such as inadequate mapping, inappropriate tissue electrode contact and particular anatomic factors. However these characteristics have not been specifically analyzed. METHODS: We have studied a prospective ablative series of 65 consecutive patients with left-sided pathways submitted to radiofrequency ablation by a simplified technique. In every application point, we analyzed the electrogram features, application point, impedance, potency and temperature. RESULTS: 52 patients (80%) required less than 5 radiofrequency pulses (group A) and 13 (20%) required > or = than 5 pulses (group B). The presence of a suggestive potential accessory pathway in local electrogram was similar in both groups and there were no differences in the local A-V or V-A intervals. However, in patients with pre-excitation the Delta-V interval was shorter in group A than in group B (8 ms vs 15 ms; p < 0.001). Furthermore, the impedance observed from the ablation point in group A was lower (108 +/- 12 vs 121 +/- 22 ohms; p < 0.001), and the maximum watts required to reach the predetermined temperature was higher in group A (42 +/- 16 vs 31 +/- 18 watts; p < 0.001). Final success of the procedure was 100%. CONCLUSIONS: Patients requiring more than 5 radiofrequency pulses had electrograms and tissue contact equal or better than those requiring less than 5 pulses. This suggests that difficulties encountered in some procedures can be due to anatomical factors rather than inaccurate mapping or insufficient tissue contact.

Adolescent↗
PubMed1999

Arrhythmia recurrence in patients with a healed myocardial infarction who received an implantable defibrillator: analysis according to the clinical presentation.

OBJECTIVES: The purpose of this study was to analyze the type of arrhythmia recurrence, based on stored electrograms, in patients with a healed myocardial infarction (MI) who received an implantable defibrillator. BACKGROUND: Previous studies suggest that patients presenting with cardiac arrest (CA) tend to recur as ventricular fibrillation (VF), whereas those suffering sustained monomorphic ventricular tachycardia (SMVT) tend to recur as SMVT. However, these data have not been confirmed in a homogeneous population of patients with MI. METHODS: A total of 88 patients was divided into three groups according to their clinical presentation: SMVT (n = 57), CA (n = 16) or syncope (n = 15). RESULTS: There were no significant differences in clinical characteristics among groups. In the electrophysiologic study SMVT was induced in 93%, 94% and 80% of patients, respectively (p = NS). During the follow-up period, 52% of patients presented a total of 671 episodes of ventricular arrhythmia treated by the defibrillator. All recurrences were as SMVT except for one VF. There were 610 episodes of SMVT treated with antitachycardia pacing, with an effectiveness of 96%. A total of 61 episodes was treated initially with cardioversion. No differences in the probability of recurrence were observed among groups, although the statistical power was low (50%). CONCLUSIONS: In patients with an old infarction and malignant ventricular arrhythmias, the majority of recurrences are due to SMVT independently of the clinical presentation (SMVT, CA or syncope) or the induced arrhythmia at the electrophysiologic study. The programming of an antitachycardia zone seems to be appropriate also for patients who present with CA or syncope.

Aged↗
PubMed1999

Genetics of cardiovascular disease with emphasis on atrial fibrillation.

Cardiology has embraced the techniques of molecular genetics later than other medical disciplines but is now completely submerged in the genetic mapping of cardiac diseases. The techniques of molecular biology, and in particular, their application to the genetics of inherited diseases, have brought the clinician and the scientist together in an unparalleled dependence. The chromosomal mapping of genes responsible for disease requires the identification of families with inherited diseases. This step involves the cooperation of the clinician. In order to continue improving our understanding of the molecular basis, it is imperative to raise the clinician awareness of the role of genetics in cardiac diseases. Arrhythmias can also have a familial origin and it is not generally appreciated that atrial fibrillation could be inherited. In the last two years, we have identified more than 100 families all over the world with individuals affected by the familial form of the disease. With the techniques of genetic mapping we have identified an area on chromosome 10 that carries a gene causing the disease in some of the families and there is ongoing research to identify the specific mutation. The clinician/scientist relationship has just started and the application of the discoveries in molecular genetics will probably have a direct role on how to approach medicine in the future, from prevention of diseases in patients carrying the susceptibility genes to gene therapy in those individuals with the disease.

Atrial Fibrillation↗
PubMed1999

The syndrome of right bundle branch block ST segment elevation in V1 to V3 and sudden death--the Brugada syndrome.

In 1992 a new syndrome was described consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and an electrocardiogram (ECG) characteristic of right bundle branch block with ST segment elevation in leads V1 to V3. The disease is genetically determined, with an autosomal dominant pattern of transmission. Three different mutations that affect the structure and function of the cardiac sodium channel gene SCN5A have been identified. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The incidence of the disease is difficult to estimate, but it causes 4 to 10 sudden deaths per 10000 inhabitants per year in areas like Thailand and Laos. In these countries, the disease represents the most frequent cause of death in young adults. Up to 50% of the yearly sudden deaths in patients with a structurally normal heart are caused by this syndrome. The diagnosis is easily made by means of the ECG. The presence of concealed and intermittent forms, however, make the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalizes the ECG, while intravenous ajmaline, flecainide or procainamide accentuate ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. Recent data suggest that loss of the action potential dome in the right ventricular epicardium but not the endocardium underlies ST segment elevation seen in the Brugada syndrome. Also, electrical heterogeneity within the right ventricular epicardium leads to the development of closely coupled extrasystoles via a phase 2 reentrant mechanism, which then precipitates ventricular tachycardia-ventricular fibrillation. Right ventricular epicardium is preferentially affected because of the predominance of transient outward current in this tissue. Antiarrhythmic drugs like amiodarone and beta-blockers do not prevent sudden death in symptomatic or asymptomatic individuals. Gene therapy may offer a cure in future years. Implantation of an automatic cardioverter-defibrillator is the only currently proven effective therapy.

Bundle-Branch Block↗
PubMed1999

Dispersion-based reentry: mechanism of initiation of ventricular tachycardia in isolated rabbit hearts.

The aim of the study was to determine whether facilitation of reentry by potassium-channel openers is related to dispersion of refractoriness and/or modification of anisotropic properties of ventricular myocardium. The dispersion of ventricular effective refractory period (VERP), longitudinal and transverse ventricular conduction velocities (thetaL and thetaT, respectively), and wavelength [lambda = VERP x theta(L or T)] were studied in Langendorff-perfused left ventricular epicardium in 20 rabbits during infusion of incremental doses of levcromakalim or nicorandil. Dispersion of refractoriness was assessed using standard deviation of VERP mean (SD-VERP), dispersion index (DI; SD-VERP/mean VERP), and maximum dispersion (Dmax = VERPmax - VERPmin). Ventricular conduction velocities and anisotropic ratio were not modified, whatever the dose used. VERP and lambda were significantly shortened at high concentrations of levcromakalim and nicorandil. At these doses, SD-VERP, DI, and Dmax were increased significantly. Analysis of ventricular tachycardia induction, performed using a high-resolution ventricular mapping system, confirmed that heterogeneity and shortening of VERP were factors inducing functional conduction block. Our data suggest that, in rabbit left ventricular epicardium, functional conduction block facilitating the occurrence of reentry could be initiated by shortening and, especially, by dispersion of refractoriness during infusion of potassium-channel openers.

Animals↗
PubMed1999

[Brugada syndrome].

In 1992 we described a new syndrome consisting of syncopal episodes and/or sudden death in patients with a structurally normal heart and a characteristic electrocardiogram displaying a pattern resembling right bundle branch block with an ST segment elevation in leads V1 to V3. In 1998 it was described that the disease is genetically determined with an autosomal dominant pattern of transmission. Three different mutations have been identified. All three mutations affect the structure and the function of the sodium channel SCN5A. Two mutations result in total loss of function of the sodium channel. The other mutation results in acceleration of the recovery of the sodium channel from inactivation. The disease causes 4 to 10 sudden deaths per 10,000 inhabitants per year in areas like Thailand and Laos. Up to 50% of the yearly sudden deaths in patients with a normal heart might be caused by this syndrome. The diagnosis is easily made by means of the electrocardiogram (ECG). The presence of concealed and intermittent forms, however, makes the diagnosis difficult in some patients. The ECG can be modulated by changes in autonomic balance and the administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalises the ECG, while i.v. ajmaline, flecainide or procainamide accentuate the ST segment elevation and are capable of unmasking concealed and intermittent forms of the disease. The prognosis is poor for patients who do not receive an implantable cardioverter-defibrillator. Antiarrhythmic drugs like amiodarone or beta-blockers do not prevent sudden death in symptomatic or asymptomatic individuals.

Bundle-Branch Block↗
PubMed1999

[Arrhythmia recurrence in patients with an old myocardial infarct treated by implantable defibrillator: an analysis according to the initial clinical presentation].

INTRODUCTION AND OBJECTIVES: The importance of the clinical presentation in the frequency and type of recurrences of ventricular arrhythmias in patients that received an automatic implantable defibrillator is not well known. The purpose of this study was to analyze the frequency and type of recurrences in patients with an old myocardial infarction that received an automatic implantable defibrillator with electrogram recording. METHODS AND RESULTS: We analyzed 100 patients classified in 3 groups according to their clinical presentation: Sustained Monomorphic Ventricular Tachycardia (VT Group n = 65), Cardiac Arrest (CA Group = 19), and Syncope (Syncope Group n = 16). There were no significant differences in the clinical variables among the different groups, nor in the inducibility of arrhythmia at the electrophysiologic study. In a follow-up 27 +/- 14 months, 54% of patients presented at last one episode of sustained ventricular arrhythmia. All recurrences except one were as sustained monomorphic ventricular tachycardia (776 episodes). 81% of episodes of sustained monomorphic ventricular tachycardia (630) were treated with antitachycardia pacing with an effectiveness of 89%. There were no differences in the probability of arrhythmic recurrence among groups but death probability was higher in the ventricular fibrillation group at 36 follow-up months (38% vs 7% and 12% in the sustained monomorphic ventricular tachycardia and syncope groups respectively, p = 0.0113). CONCLUSIONS: In the patients with an old myocardial infarction and malignant ventricular arrhythmias, most of recurrences are due to sustained monomorphic ventricular tachycardia independently of the clinical presentation. The antitachycardia pacing is not only effective in patients with documented sustained monomorphic ventricular tachycardia but also in those that are presented as cardiac arrest or syncope.

Aged↗
PubMed1998

Genetic basis and molecular mechanism for idiopathic ventricular fibrillation.

Ventricular fibrillation causes more than 300,000 sudden deaths each year in the USA alone. In approximately 5-12% of these cases, there are no demonstrable cardiac or non-cardiac causes to account for the episode, which is therefore classified as idiopathic ventricular fibrillation (IVF). A distinct group of IVF patients has been found to present with a characteristic electrocardiographic pattern. Because of the small size of most pedigrees and the high incidence of sudden death, however, molecular genetic studies of IVF have not yet been done. Because IVF causes cardiac rhythm disturbance, we investigated whether malfunction of ion channels could cause the disorder by studying mutations in the cardiac sodium channel gene SCN5A. We have now identified a missense mutation, a splice-donor mutation, and a frameshift mutation in the coding region of SCN5A in three IVF families. We show that sodium channels with the missense mutation recover from inactivation more rapidly than normal and that the frameshift mutation causes the sodium channel to be non-functional. Our results indicate that mutations in cardiac ion-channel genes contribute to the risk of developing IVF.

Action Potentials↗
PubMed1998

Right bundle-branch block and ST-segment elevation in leads V1 through V3: a marker for sudden death in patients without demonstrable structural heart disease.

BACKGROUND: Five years ago, we described a specific ECG pattern of right bundle-branch block and ST-segment elevation in leads V1 through V3 associated with sudden death in patients without demonstrable structural heart disease. Information on long-term outcome has become available due to pooled data on a large cohort of patients with this syndrome who are followed at 33 centers worldwide. METHODS AND RESULTS: Data on 63 patients (57 men; mean age, 38+/-17 years) with the described ECG pattern were analyzed in terms of arrhythmic events and sudden death. Events were analyzed for patients with at least one episode of aborted sudden death or syncope of unknown origin before recognition of the syndrome (symptomatic patients, n=41) and for patients in whom the ECG pattern was recognized by chance or because of screening related to sudden death of a relative (asymptomatic patients, n=22). During a mean follow-up of 34+/-32 months, an arrhythmic event occurred in 14 symptomatic patients (34%) and 6 asymptomatic patients (27%). An automatic defibrillator was implanted in 35 patients, 15 received pharmacological therapy with beta-blockers and/or amiodarone, and 13 did not receive treatment The incidence of arrhythmic events was similar in all therapy groups (log-rank 0.86); however, total mortality was 0% in the implantable defibrillator group, 26% in the pharmacological group, and 31% in the no therapy group (log-rank 0.0005). All mortality was due to sudden death. CONCLUSIONS: Patients without demonstrable structural heart disease and an ECG pattern of right bundle-branch block and ST-segment elevation in leads V1 through V3 are at risk for sudden death. Amiodarone and/or beta-blockers do not protect them against sudden death, and an implantable defibrillator seems to be the present treatment of choice.

Adolescent↗
PubMed1998

[Long term follow-up in patients with the permanent form of junctional reciprocating tachycardia treated with radiofrequency ablation].

OBJECTIVES: This study sought to determine the long-term follow-up, safety and efficacy of radiofrequency catheter ablation in patients with the permanent form of junctional reciprocating tachycardia. We assessed the reversibility of tachycardia-related left ventricular dysfunction and we detailed the location and electrophysiologic characteristics of these atrioventricular decremental pathways. BACKGROUND: Permanent junctional reciprocating tachycardia is an infrequent form on reciprocating tachycardia, commonly incessant and usually drug-refractory. The electrocardiographic hallmarks include an RP interval > PR with inverted P waves in leads II, III, aVF and V3-V6. During tachycardia, retrograde ventriculo-atrial conduction occurs over an accessory pathway with decremental conduction properties, located predominantly in the posteroseptal zone. It is known that long lasting and incessant tachycardia may result in tachycardia-related severe ventricular dysfunction, the so called tachycardiomyopathy. PATIENTS AND METHODS: We included 24 patients (9 males, 15 females; mean age 42 +/- 22 years) with the diagnosis of permanent junctional reciprocating tachycardia at electrophysiologic study. Six patients had tachycardia-related left ventricular dysfunction. Radiofrequency energy was delivered at the site of earliest retrograde atrial activation during reciprocating tachycardia (n = 22) or ventricular pacing (n = 2). All patients were followed at the outpatient clinic and serial echocardiograms were performed in those who presented depressed left ventricular function. RESULTS: Radiofrequency catheter ablation was performed in 24 decremental accessory pathways. Earliest retrograde atrial activation was right posteroseptal in 22 patients (92%), right midseptal in 1 (4%) and right posterolateral in 1 (4%). Twenty-three accessory pathways were successfully ablated with a mean of 5 +/- 3 (median, 4) radiofrequency applications of a mean duration of 48 +/- 13 s. Only the midseptal accessory pathway could not be ablated. After a mean follow-up of 21 +/- 16 months (median, 15; range 2 to 64) 22 patients remain asymptomatic. There were recurrences in 4 patients after the initial successful ablation (three during the first month and one during the second month after the procedure), two were ablated in a second ablation procedure, one patient required a third procedure and one required a fourth. All patients with left ventricular dysfunction experienced an improvement after ablation. Mean preablation left ventricular ejection fraction in patients with tachycardiomyopathy was 28 +/- 6% (median, 27) and raised to 51 +/- 16% (median, 47) after ablation (p < 0.02). CONCLUSIONS: Our study supports the concept that radiofrequency catheter ablation is a safe and useful treatment for patients with permanent junctional reciprocating tachycardia. Radiofrequency current should be the treatment of choice in these patients because this arrhythmia is usually drug-refractory. The majority of accessory pathways with decremental conduction properties are localized in the posteroseptal zone. Cessation of the arrhythmia after successful ablation results in recovery of left ventricular dysfunction.

Adolescent↗
PubMed1998

[Hemodynamic deterioration in patients submitted to ablation of the atrioventricular node].

INTRODUCTION: Radiofrequency ablation of the atrioventricular conduction system has become an established therapy for patients with drug-refractory atrial fibrillation. We observed 14 patients with hemodynamic deterioration related to worsening of mitral regurgitation after the procedure. PATIENTS AND METHODS: We retrospectively evaluated 256 consecutive patients with drug-refractory atrial fibrillation referred for radiofrequency ablation of the AV node and implantation of a pacemaker. Because we found hemodynamic deterioration related to worsening mitral regurgitation, we compared the clinical history, electrophysiologic and echocardiographic data from the patients with hemodynamic deterioration and worsening mitral regurgitation (group A) with those without hemodynamic deterioration (group B). RESULTS: Fourteen out of 256 patients (group A) undergoing ablation of the atrioventricular conduction system deteriorated with acute pulmonary edema (3 patients) or congestive heart failure (11 patients) at a mean of 6 weeks after the ablation procedure. Four of these patients were referred for mitral valve surgery. The length of the procedure and the number of applications during ablation were similar in both groups. Compared with group B patients, group A patients had significantly higher left ventricular end-diastolic diameters (64 +/- 6 mm vs 56 +/- 9 mm; p < 0.05) at baseline despite similar left ventricular end-systolic diameters, fractional shortening and grade of mitral regurgitation (1.15 +/- 1.05 vs 1.11 +/- 0.97). Moreover, whereas no change was observed in left ventricular end-diastolic diameter, left ventricular end-systolic diameter, fractional shortening and grade of mitral regurgitation in group B patients after ablation, group A patients experienced a significant increase in left ventricular end-diastolic diameter (64 +/- 6 mm vs 72 +/- 9 mm; p < 0.01) and grade of mitral regurgitation (1.15 +/- 1.05 vs 2.90 +/- 1.15; p < 0.01). In patients operated on no ablation related structural damage to the mitral valve apparatus could be detected. The worsening of the mitral regurgitation was related to dilation of the mitral valve annulus. CONCLUSIONS: Hemodynamic deterioration together with progression of mitral regurgitation is a potential complication of ablation of the atrioventricular conduction system.

Adult↗
PubMed1998

[Long-term follow up of patients with nodal reentry tachycardia who had undergone radiofrequency ablation].

INTRODUCTION: The aim of this study was to assess the long term results (minimum of 3 years) of radiofrequency catheter ablation in patients with common (slow-fast) atrioventricular nodal reentrant tachycardia. PATIENTS AND METHODS: Sixty consecutive patients (mean age 56 +/- 16 years, range 14 to 83, 16 men and 44 women) underwent slow pathway (n = 51, Group A) or fast pathway (n = 9, Group B) radiofrequency catheter ablation between January 1992 and March 1994. All patients were followed at 1, 3, 6 and 12 months after ablation with serial examinations and electrocardiograms and the last follow-up was made on April 1997. RESULTS: During a mean follow-up period of 48 +/- 7 months (range 38 to 63) all evaluated patients remained asymptomatic. Eight recurrences were observed at a mean of 1 +/- 2 months (range, 0.5 to 7) after a successful ablation procedure. A second procedure was effective in eliminating the dual atrioventricular nodal pathway in each of them. In Group A patients, the pre-ablation PR interval, at 12 months after ablation and at last follow-up were 122 +/- 11, 124 +/- 13 and 124 +/- 15 ms, respectively. In Group B patients, the pre-ablation PR interval, at 12 months after ablation and at last follow-up were 130 +/- 24, 200 +/- 12, 200 +/- 24 ms, respectively. No significant atrioventricular conduction disturbances in any patient were observed. One patient developed a new onset left bundle branch block and 4 patients died of noncardiac causes. CONCLUSIONS: In patients with atrioventricular nodal reentrant tachycardia, radiofrequency catheter ablation is a safe and effective therapy, with substantial good results that persist during long term follow-up, with a low recurrence rate and without complications during short and long term outcome.

Adolescent↗
PubMed1998

[Patients with structural heart disease, syncope of unknown etiology and inducible ventricular arrhythmias treated with implantable defibrillators].

OBJECTIVES: This study evaluates the hypothesis that in patients with syncope of unknown origin and heart anomalies, inducible ventricular arrhythmias are specific arrhythmias and therefore should be treated as such. BACKGROUND: Although syncope is a frequent clinical entity, the evaluation and treatment of patients with syncope without a clear etiology still remains undefined. Many patients with syncope of undetermined origin undergo invasive electrophysiologic evaluation. Abnormalities of the sinus node, prolongation of conduction times or inducible arrhythmias found during these evaluations are usually assumed to be the cause of syncope, and are consequently treated. However, whether tachyarrhythmias are truly the cause of syncope, and whether treatment of these tachyarrhythmias can prevent recurrent syncope and arrhythmic death, is unknown. PATIENTS AND METHODS: An electrophysiological study was performed on 160 patients with structural heart disease and syncope of unknown origin. In 23 out of the 160 patients (16%), programmed electrical stimulation induced sustained ventricular arrhythmias. In 18 out of the 23 patients an automatic defibrillator was implanted and they form the study group. RESULTS: In these 18 patients, programmed ventricular stimulation induced sustained monomorphic ventricular tachycardia in 12, sustained polymorphic ventricular tachycardia in 2 and ventricular fibrillation in 4. During a mean follow-up of 14 months, 9 patients received 81 appropriate therapies from the device (53 because of ventricular tachycardia and 23 because of ventricular fibrillation). The probability of appropriate therapy was 100% at 1 year follow-up. There were no episodes of sudden death and 1 patient died of congestive heart failure. CONCLUSIONS: In patients with syncope of undetermined origin, heart disease and inducible ventricular tachyarrhythmias treated with a implantable cardioverter defibrillator, there is a high incidence of appropriate therapies. Our results support the practice of using implantable cardioverter defibrillators in patients with syncope of unknown origin, heart disease and inducible ventricular arrhythmias.

Adolescent↗