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J Brugada

Publications and source records attributed to J Brugada.

At least 19 recordsLinked to original sources

Outcomes after radiofrequency catheter ablation of atrial tachycardia.

The purpose of this study was to evaluate the efficacy, safety, and clinical benefit of radiofrequency catheter ablation (RFCA) in a large series of patients with atrial tachycardia (AT). The determinants of success or failure of RFCA in AT remain unclear. We evaluated the results of radiofrequency ablation in 73 women and 32 men (mean age 48 +/- 19 years) with AT. Mapping techniques were based on identification of the earliest endocardial atrial electrogram recorded during AT. AT originated from the right atrium in 91 patients and from the left atrium in 14. The cardiac ventricles were dilated in 12 patients. AT ablation was successful in 80 patients (77%) regardless of the site of origin. Age, gender, rate of tachycardia, temperature achieved during application, or presence of tachycardiomyopathy were not significant determinants of acute success by univariate analysis. There was a significantly higher acute success rate of ablation in patients with paroxysmal (88%, 45 of 51) and permanent (71%, 30 of 42) forms than in patients with repetitive forms of AT (41%, 5 of 12) (p <0.005). The mean local endocardial electrogram time (relative-to-surface P-wave onset) was -47 +/- 17 ms at successful ablation sites and -29 +/- 21 ms at unsuccessful sites (p <0.03). Ablation was unsuccessful in 25 cases. Thus, RFCA of AT can be performed with a high acute success rate. Patients with repetitive forms and those with multifocal origin had a lower acute success rate. The highest incidence of recurrences was found in anterior right atrial foci.

Adolescent↗

[Long-term efficacy of radiofrequency catheter ablation in atrial tachycardia].

INTRODUCTION AND OBJECTIVES: Radiofrequency ablation has shown to be an effective treatment for supraventricular tachycardias including flutter and atrial tachycardia, however the clinical information available on atrial tachycardia is limited. The aim of this study was to evaluate the immediate and long term effectiveness of radiofrequency ablation in patients with atrial tachycardia and to establish predictors of effectiveness and arrhythmia recurrence. METHODS: We analyzed a series of 126 procedures of atrial tachycardia ablation in 117 patients (69% women) with a mean age of 50 +/- 19 years. RESULTS: Ninety-one percent of the foci were located in the right atrium. A mean of 6 applications were necessary to achieve an efficacy of 74% during the first procedure with a total of 80%. The only predictor of ablation success was the number of foci being smaller in multifocal compared to unifocal (p < 0.01) whereas for recurrences a less premature electrogram at the application point (p = 0.02) was predictive of ablation success. Over a follow-up of 34 +/- 19 months 7.4% of patients had recurrent atrial tachycardia. The probability of recurrence at one year calculated by the Kaplan-Meier method was 12%. Seventy-one percent of the recurrences occurred during the first 3 months after ablation. CONCLUSIONS: Ablation is an effective, safe procedure for short and long term treatment of patients with atrial tachycardia. Effectiveness depends on the number of foci while the recurrence rate is related to the prematurity of atrial electrogram at the application point.

Adult↗

[Percutaneous pulmonary valvulotomy using radiofrequency in pulmonary atresia with intact interventricular septum].

Early pulmonary valvulotomy in patients with pulmonary atresia and intact interventricular septum allows the development and growth of the right ventricle and two-ventricle circulation. Percutaneous valvulotomy today is a valid alternative procedure to surgical valvulotomy. With the use of the radiofrequency 5F currently available for the treatment of arrythmias atretic pulmonary valve perforation and consecutive balloon dilation may be safely and effectively performed. We describe a case of perforation of a pulmonary valve by radiofrequency in a 15-day-old neonate with pulmonary valve atresia and intact ventricular septum.

Catheter Ablation↗

Coronary artery revascularization in patients with sustained ventricular arrhythmias in the chronic phase of a myocardial infarction: effects on the electrophysiologic substrate and outcome.

OBJECTIVES: The objective of this study was to analyze the influence of coronary artery revascularization in patients with ventricular arrhythmias. BACKGROUND: Coronary artery revascularization is an effective treatment for myocardial ischemia; however, its effect on ventricular arrhythmias not related to an acute ischemic event has not been carefully studied. METHODS: Sixty-four patients (58 men, mean age 65 +/- 8 years old) with prior myocardial infarction, spontaneous ventricular arrhythmias not related to an acute ischemic event (55 ventricular tachycardia, 9 ventricular fibrillation) and coronary lesions requiring revascularization were studied prospectively. Electrophysiological study was performed before and after revascularization, and events during follow-up were analyzed. RESULTS: At initial study 61 patients were inducible into sustained ventricular arrhythmias. After revascularization, in 62 survivors, 52 out of 59 patients previously inducible were still inducible (group A), and 10 patients were noninducible (group B). No differences were found in clinical, hemodynamic, therapeutic and electrophysiological characteristics between both groups. During 32 +/- 26 months follow-up, 28/52 patients in group A (54%) and 4/10 patients in group B (40%) had arrhythmic events (p = 0.46). An ejection fraction <30% predicted recurrent arrhythmic events (p = 0.02), but not the presence of demonstrable ischemia before revascularization (p = 0.42), amiodarone (p = 0.69) or beta-adrenergic blocking agent therapy (p = 0.53). Total mortality was 10% in both groups. CONCLUSIONS: In patients with ventricular arrhythmias in the chronic phase of myocardial infarction, probability of recurrence is high despite coronary artery revascularization, but mortality is low if combined with appropriate antiarrhythmic therapy. Recurrences are related to the presence of a low ejection fraction but not to demonstrable ischemia before revascularization, amiodarone or beta-blocker therapy nor are they the results of electrophysiological testing after revascularization.

Aged↗

Prognostic value of electrophysiologic investigations in Brugada syndrome.

INTRODUCTION: The prognostic value of electrophysiologic investigations in individuals with Brugada syndrome is unclear. Previous studies failed to determine its value because of a limited number of patients or lack of events during follow-up. We present data on the prognostic value of electrophysiologic studies in the largest cohort ever collected of patients with Brugada syndrome. METHODS AND RESULTS: Two hundred fifty-two individuals with an ECG diagnostic of Brugada syndrome were studied electrophysiologically. The diagnosis was made because of a classic ECG with a coved-type ST segment elevation in precordial leads V1 to V3. Of the 252 individuals, 116 had previously developed spontaneous symptoms (syncope or aborted sudden cardiac death) and 136 were asymptomatic at the time of diagnosis. A sustained ventricular arrhythmia was induced in 130 patients (51%). Symptomatic patients were more frequently inducible (73%) than asymptomatic individuals (33%) (P = 0.0001). Fifty-two individuals (21%) developed an arrhythmic event during a mean follow-up of 34 +/- 40 months. Inducibility was a powerful predictor of arrhythmic events during follow-up both in symptomatic and asymptomatic individuals. Overall accuracy of programmed ventricular stimulation to predict outcome was 67%. Overall accuracy in asymptomatic individuals was 70.5%, with a 99% negative predictive value. Overall accuracy in symptomatic patients was 62%, with only a 4.5% false-negative rate. No significant differences were found in the duration of the H-V interval during sinus rhythm between symptomatic or asymptomatic individuals. However, the H-V interval was significantly longer in the asymptomatic individuals who became symptomatic during follow-up compared with those who did not develop symptoms (59 +/- 8 msec vs 48 +/- 11 msec, respectively; P = 0.04). CONCLUSION: Inducibility of sustained ventricular arrhythmias is a good predictor of outcome in Brugada syndrome. In asymptomatic individuals, a prolonged H-V interval during sinus rhythm is associated with a higher risk of developing arrhythmic events during follow-up. Symptomatic patients require protective treatment even when they are not inducible. Asymptomatic patients can be reassured if they are noninducible.

Adolescent↗

Clinical evaluation of defibrillation efficacy with a new single-capacitor biphasic waveform in patients undergoing implantation of an implantable cardioverter defibrillator.

AIMS: Improvements in the size and shape of implantable cardioverter defibrillators (ICDs) might be obtained by using one capacitor instead of the series connection of two capacitors traditionally used in ICDs. The aim of this study was to determine whether a biphasic waveform delivered from a single 336 microF capacitor had the same defibrillation efficacy as a standard biphasic waveform. METHODS AND RESULTS: Randomized, paired defibrillation threshold testing was acutely performed in 54 patients undergoing ICD implantation. A standard 140 microF 80% tilt biphasic waveform (two 280 microF capacitors connected in series) was compared with an experimental biphasic waveform delivered from a single 336 microF capacitor at either 60% tilt (33 patients) or 80% tilt (21 patients). All waveforms had a 60/40 phase1/phase2 duration ratio. Compared with the standard waveform, the 60% tilt experimental waveform had a lower delivered energy (6.7 +/- 2.8 vs 7.9 +/- 3.3 joules, P<0.02), lower peak voltage (218 +/- 43 vs 333 +/- 68 V, P<0.01), and a slightly longer pulse duration (13.4 +/- 1.4 vs 10.7 +/- 1.1 ms, P<0.01). Conversely, the 80% tilt experimental waveform had a higher delivered energy (9.1 +/- 3.5 vs 6.3 +/- 2.4 joules, P<0.01), a lower peak voltage (234 +/- 44 vs 302 +/- 51 V, P<0.01) and a much longer pulse duration (25.7 +/- 2.5 vs 1.13 +/- 1 ms, P<0.01). CONCLUSION: Waveforms delivered from a large capacitance are feasible but require a lower tilt. This technique may allow smaller, thinner ICDs without jeopardizing defibrillation success.

Aged↗

Sudden death in high-risk family members: Brugada syndrome.

Brugada syndrome (an electrocardiographic pattern of right bundle branch block, ST segment elevation in leads V1 to V3, and sudden death) is genetically determined and caused by mutations in the cardiac ion channels. The mode of inheritance of the disease is autosomal dominant in half of familial forms. Sudden death may, however, occur from a variety of causes in relatives and patients with this syndrome. Twenty-five Flemish families with this syndrome with a total of 334 members were studied. Affected members were recognized by means of the typical electrocardiogram of the syndrome, either occurring spontaneously or after the intravenous administration of antiarrhythmic drugs. Sudden deaths in these families were classified as related or not to the syndrome by analysis of the data at the time of the event, mode of inheritance of the disease, and data provided by survivors. Of the 25 families with the syndrome, 18 were symptomatic (at least 1 sudden death related to the syndrome) and 7 were asymptomatic (no sudden deaths related to the syndrome). In total, there were 42 sudden cardiac deaths (12% incidence). Twenty-four sudden deaths were related to the syndrome and all happened in symptomatic families. Eighteen sudden deaths (43% of total sudden deaths) were not related to the syndrome (9 cases) or were of unclear cause (9 cases). Three of them occurred in 2 asymptomatic families and the remaining 15 in 5 symptomatic families. A total of 24 of the 50 affected members (47%) and 18 of the 284 unaffected members (6%) had aborted sudden death. This difference in the incidence of sudden death was statistically significant (p <0.0001). Patients with aborted sudden death caused by the syndrome were younger than patients with sudden death of other or unclear causes (38 +/- 4 years vs 59 +/- 3 years respectively; p = 0.0003). In families at high risk of sudden death because of genetically determined diseases, the main cause of sudden death remains the disease itself. However, almost half of sudden deaths are caused by unrelated diseases or from unclear causes. Accurate classification of the causes of sudden death is mandatory for appropriate analysis of the causes of death when designing preventive treatments.

Adolescent↗

Sodium channel blockers identify risk for sudden death in patients with ST-segment elevation and right bundle branch block but structurally normal hearts.

BACKGROUND: A mutation in the cardiac sodium channel gene (SCN5A) has been described in patients with the syndrome of right bundle branch block, ST-segment elevation in leads V1 to V3, and sudden death (Brugada syndrome). These electrocardiographic manifestations are transient in many patients with the syndrome. The present study examined arrhythmic risk in patients with overt and concealed forms of the disease and the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk. METHODS AND RESULTS: The effect of intravenous ajmaline (1 mg/kg), procainamide (10 mg/kg), or flecainide (2 mg/kg) on the ECG was studied in 34 patients with the syndrome and transient normalization of the ECG (group A), 11 members of 3 families in whom a SCN5A mutation was associated with the syndrome and 8 members in whom it was not (group B), and 53 control subjects (group C). Ajmaline, procainamide, or flecainide administration resulted in ST-segment elevation and right bundle branch block in all patients in group A and in all 11 patients with the mutation in group B. A similar pattern could not be elicited in the 8 patients in group B who lacked the mutation or in any person in group C. The follow-up period (37+/-33 months) revealed no differences in the incidence of arrhythmia between the 34 patients in whom the phenotypic manifestation of the syndrome was transient and the 24 patients in whom it was persistent (log-rank, 0.639). CONCLUSIONS: The data demonstrated a similar incidence of potentially lethal arrhythmias in patients displaying transient versus persistent ST-segment elevation and right bundle branch block, as well as the effectiveness of sodium channel blockers to unmask the syndrome and, thus, identify patients at risk.

Adult↗

The Brugada syndrome.

The Brugada syndrome is a hereditary disease causing sudden cardiac death in apparently healthy individuals with a structurally normal heart. The disease is caused by mutations in the cardiac sodium channel gene SCN5A. Patients with this disease have a peculiar electrocardiogram with elevation of the ST segment in leads V1 to V3, an electrocardiogram that every doctor should recognize. There exist variants of the electrocardiogram with minimal ST segment elevation and even concealed forms that can only be unmasked by the administration of class I antiarrhythmic drugs. When left untreated or when treated with all known antiarrhythmic drugs, patients with Brugada syndrome have a high mortality (approximately 10% per year). The only effective treatment to prevent sudden death is the implantable defibrillator.

Anti-Arrhythmia Agents↗

[Sudden death (VI). The Brugada syndrome and right myocardiopathies as a cause of sudden death. The differences and similarities].

In 1992 we described a new syndrome characterized by syncopal or sudden death episodes in patients with a structurally normal heart and a characteristic electrocardiogram 9 showing a pattern of right bundle branch block and ST segment elevation in right precordial leads V1 to V3. The disease is genetically determined with and autosomic dominant pattern of transmission. Until now three mutations and one polymorphism in the sodium cardiac channel gene have been identified in two families and one sporadic patient. As in many other genetically determined diseases, the disease is heterogeneous, caused by more than one gene. The syndrome has been identified in almost all countries in the world. Its incidence is difficult to evaluate, but it seems to be responsible for 4 to 10 sudden deaths per year per 10,000 inhabitants in areas like Laos or Thailand, and it represents the most frequent cause of death in young male adults in these countries. Up to 50% of all sudden deaths in patients with structurally normal heart are caused by the disease. The diagnosis can be easily made thanks to the characteristic electrocardiographic pattern. In some patients, the presence of concealed and intermittent forms might make the diagnosis more difficult. The electrocardiogram can be modulated by autonomic changes and administration of antiarrhythmic drugs. Beta-adrenergic stimulation normalizes the electrocardiogram, whereas ajmaline, flecainide or procainamide administration increase ST segment elevation. These drugs allow the unmasking of concealed or intermittent forms of the disease. Prognosis of patients with the syndrome is poor without an implantable defibrillator and antiarrhythmic drugs like amiodarone or betablockers do not protect against sudden death. The poor prognosis is similar in patients with a history of aborted sudden death or syncope and in asymptomatic patients in whom the abnormal electrocardiogram characteristic of the syndrome, was identified during a routine examination.

Arrhythmogenic Right Ventricular Dysplasia↗

[Prospective and comparative study of pacemaker implants carried out at the electrophysiology laboratory and the operating room].

INTRODUCTION AND OBJECTIVES: Permanent pacemaker implantation is done by different physicians with either a surgical or clinical training. Our objective was to evaluate if there were significant differences in the implantation parameters and in the complication rate among implantations performed by cardiologists in the electrophysiologic laboratory and cardiological surgeons in the operating room. MATERIAL AND METHODS: We prospectively collected those patients' data who received a first pacemaker implantation by cardiovascular surgeons and electrophysiologists during the year 1998. Data collected included demographic information, indication for pacing, surgical time, complications during procedure, stimulation and sensing thresholds as well as type of pacing. RESULTS: We first-implanted 216 pacemakers in a one year period, 101 by cardiovascular surgeons and 115 by electrophysiologists. 56% were male patients. Average age in the surgery group was 74.2 +/- 9 years and 72.09 +/- 12 in the electrophysiology group (p = NS). Main diagnoses were as follows: complete heart block in 32.9% patients, complete heart block 2. degrees 16.4%, sinus node dysfunction 12.2%, AV node ablation 12.2% and others. The complications rate for surgery group was 4% and 1.7% for electrophysiologists (p = NS). Electrophysiologists placed more bicameral devices. No clinically significant differences were found among other implant parameters. CONCLUSIONS: Pacemaker implant by cardiologists in an electrophysiologists laboratory is a safe procedure that does not have more complications when compared to the same procedure done in the operating room by surgeons. This allows hospital resource optimization and reduction of hospital stay length.

Aged↗

[Familial sick sinus syndrome associated to strabismus and persistent left superior vena cava].

We report a family in which the mother and her three sons suffered sick sinus syndrome and strabismus. Two members had a persistent left superior vena cava with drainage into coronary sinus. The illness in all members of this family was oligosymptomatic, and well tolerated with mild symptoms like dizziness, fatigue and exercise dyspnea associated with nodal rhythm. Three of them, had episodes of paroxysmal atrial fibrillation. All patients remain asymptomatic after pacemaker implantation.

Adult↗