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Pedro Brugada

Publications and source records attributed to Pedro Brugada.

54 records · Page 3Linked to original sources
PubMed2003

"Double" potentials define linear lesion conduction block using a novel mapping/linear lesion ablation catheter.

INTRODUCTION: A novel mapping/ablation catheter using a coaxially ablation electrode (E) that is moveable between distal and proximal ring electrodes along its shaft was used to create a linear lesion over the cavotricuspid isthmus (CTI) and bidirectional block in 32 patients (21 men; age 38-79 years) undergoing ablation for counterclockwise atrial flutter. METHODS AND RESULTS: Two bipolar electrograms (E1 and E2) were recorded: between E and the distal ring electrode and between E and the proximal ring electrode. Interpole distance varied for both as the E traversed the slide shaft. Given the catheter's concept, these bipoles are orientated exactly along the line of lesion creation. Prior to ablation, unitary bipolar electrograms were recorded along the catheter slide shaft position. As the CTI lesion was created (E moved along the catheter slide shaft in 2-mm steps with radiofrequency energy delivered to achieve 65 degrees C for 60 sec at each), double potentials (DP) were observed. Interpotential distance became maximal with completion of the linear lesion and bidirectional block. DPs were noted in all these procedures. With pacing from the low septal right atrium at bidirectional block creation, interpotential timing was 140.9 +/- 15 msec and from the low right atrial free wall was 145.13 +/- 18 msec. In sinus rhythm, DP interpotential timing was less (35.13 +/- 9 msec) as activation fronts arrived from both septal and anterior atrial aspects. CONCLUSION: Bipolar recordings from the coaxially moveable electrode catheter provide unique electrogram data. DPs recorded during and after linear lesion creation can define conduction block across that lesion without the need for additional mapping catheters or complex mapping technology.

Adult↗
PubMed2003

Natural history of Brugada syndrome: the prognostic value of programmed electrical stimulation of the heart.

INTRODUCTION: The prognostic value of electrophysiologic studies in individuals with the syndrome of right bundle branch block and ST segment elevation in precordial leads V1 to V3 (Brugada syndrome) remains controversial. Our previous data from 252 individuals with the syndrome suggested that programmed ventricular stimulation had a good overall accuracy to predict events. However, studies from independent investigators questioned our results. We report here the largest population with Brugada syndrome ever studied by programmed electrical stimulation of the heart. METHODS AND RESULTS: Four hundred forty-three individuals with an ECG diagnostic of Brugada syndrome were studied by programmed electrical stimulation of the heart. The diagnosis was made because of the classic ECG showing a coved-type ST segment elevation in precordial leads V1 to V3. Of the 443 individuals, 180 had developed spontaneous symptoms (syncope or aborted sudden cardiac death) and 263 were asymptomatic at the time the diagnosis was made. The ventricular stimulation protocol included a minimum of two basic pacing cycle lengths with two ventricular premature beats from the right ventricular apex. A sustained ventricular arrhythmia was induced in 217 cases (49%). Symptomatic patients were more frequently inducible [126/180 (70%)] than asymptomatic individuals [91/263 (34%); P = 0.0001]. Males were more frequently inducible than females (54% vs 32%, P < 0.0001). Inducible individuals had a longer HV interval than noninducible patients (50 +/- 12 msec vs 46 +/- 10 msec, P < 0.002). HV interval and number of premature beats needed to induce VF were not related to outcome. Inducibility was statistically a powerful predictor of arrhythmic events during follow-up. Sixty of 217 inducible patients (28%) had spontaneous ventricular fibrillation compared with 5 of 221 noninducible patients (2%; P = 0.0001). CONCLUSION: Inducibility of sustained ventricular arrhythmias during programmed ventricular stimulation of the heart is a good predictor of outcome in Brugada syndrome.

Adolescent↗
PubMed2002

Genetic and biophysical basis of sudden unexplained nocturnal death syndrome (SUNDS), a disease allelic to Brugada syndrome.

Sudden unexplained nocturnal death syndrome (SUNDS), a disorder found in southeast Asia, is characterized by an abnormal electrocardiogram with ST-segment elevation in leads V1-V3 and sudden death due to ventricular fibrillation, identical to that seen in Brugada syndrome. We screened patients with SUNDS for mutations in SCN5A, the gene known to cause Brugada syndrome, as well as genes encoding ion channels associated with the long-QT syndrome. Ten families were enrolled, and screened for mutations using single-strand DNA conformation polymorphism analysis, denaturing high-performance liquid chromatography and DNA sequencing. Mutations were identified in SCN5A in three families. One mutation, R367H, lies in the first P segment of the pore-lining region between the DIS5 and DIS6 transmembrane segments of SCN5A. A second mutation, A735V, lies in the first transmembrane segment of domain II (DIIS1) close to the first extracellular loop between DIIS1 and DIIS2, whereas the third mutation, R1192Q, lies in domain III. Analysis of these mutations in Xenopus oocytes showed that the R367H mutant channel did not express any current and the likely effect of this mutation is to depress peak current due to the loss of one functional allele. The A735V mutant expressed currents with steady state activation voltage shifted to more positive potentials. The R1192Q mutation accelerated the inactivation of the sodium channel current. Both mutations resulted in reduced sodium channel current (I(Na)) at a time corresponding to the end of phase 1 of the action potential, as described previously in the Brugada syndrome. Based upon these observations we suggest that SUNDS and Brugada syndrome are phenotypically, genetically and functionally the same disorder.

Alleles↗
PubMed2002

Long-term follow-up of individuals with the electrocardiographic pattern of right bundle-branch block and ST-segment elevation in precordial leads V1 to V3.

BACKGROUND: The electrocardiographic pattern of right bundle-branch block with ST-segment elevation in leads V1 to V3 is increasingly recognized among patients who have aborted sudden cardiac death, but also in asymptomatic individuals, raising questions about its prognostic significance. METHODS AND RESULTS: The clinical, electrophysiological, and follow-up data of 334 patients with the Brugada phenotype were analyzed. A total of 79 women and 255 men with a mean age at diagnosis of 42+/-16 years were studied. The abnormal ECG was recognized after a resuscitated cardiac arrest in 71 patients (group A), after a syncopal episode in 73 patients (group B), and in 190 asymptomatic individuals (group C). Sustained ventricular arrhythmias were inducible in 83%, 63%, and 33% of patients in group A, group B, and group C, respectively. During 54+/-54 and 26+/-36 months of follow-up, respectively, 62% of patients in group A and 19% of group B patients had a new arrhythmic event. Inducibility of ventricular arrhythmias was the only predictor of arrhythmia occurrence in both groups. During a mean follow-up of 27+/-29 months, 8% of group C individuals had a first arrhythmic event. In these individuals, inducibility of ventricular arrhythmias and a basal abnormal ECG were predictors of arrhythmia occurrence. CONCLUSIONS: An ECG showing right bundle-branch block and ST-segment elevation in the right precordial leads is a marker of malignant ventricular arrhythmias and sudden death. Recurrence of malignant arrhythmias is high after the occurrence of symptoms. Among asymptomatic individuals, those with a spontaneously abnormal ECG and inducible to ventricular arrhythmias have the poorer prognosis.

Adult↗
PubMed2002

[Genetics and arrhythmias].

In the last 50 years we have been very successful at prolonging survival and improving the quality of life of patients with cardiac disease. The innovations in technology and pharmacology, better preventive and diagnostic tools have provided tremendous breakthroughs. However, despite our best efforts, the majority of cardiac diseases are structural in origin and will progress to their ultimate outcome. Curative therapies are not available due in part to our poor understanding of the basic mechanisms responsible for these diseases. The new developments in molecular genetics and biology are likely to change the way we approach a cardiac patient in the future. The diseases are presently being deciphered at the most basic level, and the information obtained opens new possibilities not only for better therapeutic and diagnostic measures but also for prevention of the disease.

Arrhythmias, Cardiac↗
PubMed2002

Surgical treatment of tachyarrhythmias due to postinfarction left ventricular aneurysm with endoaneurysmorrhaphy and cryoablation.

OBJECTIVE: In this study, the efficacy of left ventricular (LV) endoaneurysmorrhaphy and cryoablation without intraoperative electrophysiologic mapping was evaluated in patients with postinfarction LV aneurysm and sustained ventricular tachycardia (VT). METHODS: A prospective study was performed on all patients operated with malignant VT in the presence of a resectable LV aneurysm between July 1990 and February 2001. RESULTS: The study included 31 patients, 20 men and 11 women, with a mean age of 65.5 years (47-84). Monomorphic, polymorphic VT or ventricular fibrillation was present in all patients prospectively, and VT was incessant in 11. Twenty-six patients had an anterior, four patients had an inferior and one patient a posterolateral myocardial wall infarction. All patients had a well-limited ventricular aneurysm. Ten patients had three, eight patients two and 13 patients had single vessel coronary artery disease. Mean preoperative ejection fraction was 34.8 +/- 14.5% (8-62) and mean end-diastolic volume index was 141.5 +/- 51.8 ml/m(2) (57-288). Six patients had mitral regurgitation grade III or IV. All patients underwent extensive cryoablation at the transition zone of scar and viable tissue and LV remodelling with prosthetic patch in 26 patients. Associated procedures were CABG in 19 patients (61%) and mitral valve reconstruction in six patients (19%). Postoperative electrophysiologic study (EPS) revealed freedom from VT induction in 25 patients and inducible VT in five patients. One patient had inducible polymorphic VT. Five patients received an implantable cardioverter defibrillator (ICD) and three patients had a permanent pacemaker implanted. After a mean follow-up of 30 +/- 27 months (6-132) there was one arrhythmia-related death. There was one early hospital readmission for clinical VT and no need for late ICD implantation. CONCLUSIONS: In patients suffering from ventricular arrhythmias in the presence of a complicated postinfarction LV aneurysm, combined 'blind' cryoablation and endoaneurysmorrhaphy offers excellent arrhythmia control and clinical and haemodynamic outcome.

Aged↗
PubMed2002

Novel mutations in domain I of SCN5A cause Brugada syndrome.

Brugada syndrome, an autosomal dominantly inherited form of ventricular fibrillation characterized by ST-segment elevation in leads V1-V3 and right bundle-branch block on surface electrocardiogram, is caused by mutations in the cardiac sodium channel gene SCN5A. Patients with Brugada syndrome were studied using single-strand conformation polymorphism analysis, denaturing high-performance liquid chromatography, and DNA sequencing of SCN5A. Mutations were identified in SCN5A in two families and one sporadic case. In one family, a missense mutation leading to a glycine to valine substitution (G351V) in the pore region between the DIS5 and DIS6 transmembrane segments was detected. Biophysical analysis demonstrated that this mutation caused significant current reduction. In the other family, a 20-bp deletion of the exon 5 splice acceptor site was identified; as exon 5 encodes part of the intracellular loop between DIS2 and DIS3, this portion of the channel is disrupted. In the sporadic patient, a missense mutation resulting in the substitution of lysine by glutamic acid (K126E) in the intracellular loop at the boundary with DIS1 was identified. These three new SCN5A mutations in Brugada syndrome patients are all located within domain I of SCN5A, a region not previously considered important in the development of ventricular arrhythmias.

Animals↗
PubMed2002

Left ventricular dysfunction is associated with prolonged average ventricular fibrillation cycle length in patients with implantable cardioverter defibrillators.

OBJECTIVES: In cellular studies, ventricular refractoriness (ERP) is prolonged in heart failure (CHF), but clinical evidence is lacking. The average ventricular fibrillation cycle length (VFCL) has been shown to correlate with local ERP. We hypothesized that the VFCL increases with left ventricular (LV) dysfunction. Therefore, we evaluated intracardiac VFCL recorded by implantable defibrillators (ICD) in patients with and without LV dysfunction. METHODS: We analyzed intracardiac VFCL recorded by sensing leads of Ventak MINI (Guidant) ICD in 49 patients (35 men; age 54 +/- 13 years; 25 (51%) with coronary artery disease; mean LV ejection fraction (EF) 41 +/- 17%, range 76-10) from the European Ventak MINI Investigator Group. No patients were receiving antiarrhythmic drugs, including beta-blockers. Mean and median VFCL were obtained at predischarge testing during first charge time (4.5 +/- 2.7 s, range 1.4-11). RESULTS: Mean median VFCL was 186 +/- 21ms (range 150-230 ms). Patients with LVEF >/= 50% (n = 14) had shorter median VFCL than patients with LVEF < 50% (n = 35), (171 +/- 14 vs. 191 +/- 20 ms; p = 0.002). Median VFCL correlated with LVEF (r = -0.41; p = 0.003) and age (r = 0.28, p = 0.04), but was not significantly associated with charge time and defibrillation threshold at implant. Similar results occurred with mean VFCL. In multiple linear regression and correlation models, only LVEF% was a significant predictor (p < 0.05 for all models) of median VFCL. CONCLUSIONS: LV dysfunction prolongs averaged VFCL in patients at risk for malignant ventricular arrhythmias who have implantable cardioverter defibrillators. This phenomenon might be related to alterations in the ventricular refractory period.

Analysis of Variance↗
PubMed2002

Combined atrial fibrillation and mitral valve surgery using radiofrequency technology.

Recently, intraoperative radiofrequency ablation of the left atrium combined with mitral valve surgery has become widely used. In our center, 30 patients underwent this combined procedure; median sternotomy was used in 16 patients, and port access was used in 14 patients. At hospital discharge, 18 patients (60%) were no longer in atrial fibrillation, and at 6 months, 19 patients (65%) remained in sinus rhythm. All sinus rhythm patients had a well-defined transmitral A wave detectable by echocardiography. One patient sustained a major stroke. Two patients required pacemaker implantation. Such encouraging preliminary results have triggered worldwide interest in the percutaneous and surgical treatment of atrial fibrillation. However, the excellent long-term results with the classic Cox-Maze III operation have not yet been achieved with these newer approaches. Further basic and clinical research is required before a predictable simple and safe technique can be introduced as a new standard for the surgical treatment of atrial fibrillation in patients with or without structural heart disease.

Atrial Fibrillation↗