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      Valor del electrocardiograma en el diagnóstico y pronóstico del síndrome de Brugada

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          Abstract

          El electrocardiograma de 12 derivaciones asociado con las derivadas accesorias (precordiales derechas altas) es el método complementario con el cual se obtiene la mayor información diagnóstica y pronostica en pacientes portadores con síndrome de Brugada. Mediante este método sencillo, económico, reproducible y operador independiente, podemos estudiar las alteraciones tanto de la despolarización como de la repolarización ventricular. También permite el diagnóstico de las distintas arritmias supraventriculares que pueden acontecer así como caracterizar las diferentes taquicardias ventriculares. Por otro lado, el análisis vectocardiográfico con el método de Frank en pacientes con síndrome de Brugada, sugiere la dualidad de los mecanismos fisiopatológicos del patrón electrocardiográfico característico o tipo 1, demostrándose características distintivas y particulares, con respecto a individuos portadores de bloqueo de rama derecha. La compresión de todos estos mecanismos, pueden contribuir a orientar futuros esfuerzos terapéuticos que permitan controlar la disfunción de los canales asociados a esta rara y compleja canalopatía.

          Translated abstract

          Twelve-lead ECG associated to high right parasternal accessory leads is the resource that yields a greatest number of diagnostic and prognostic information in patients carriers of BrS. By this simple, cheap, reproducible, and operator-independent method, depolarization alterations can be studied as well as ventricular repolarization aspects. The method allows diagnosing frequent episodes of atrial fibrillation and other supraventricular arrhythmias, as well as characterizing the different ventricular tachyarrhythmias. The analysis of the Frank VCG (F-VCG) of patients with BrS suggests the duality of the underlying physiopathological mechanisms of the Brugada Type-1 ECG pattern. F-VCG of patients with Brugada type-1 ECG pattern has distinctive characteristics from the F-VCG of individuals with RBBB pattern. The understanding of these mechanisms may help to guide future therapeutic efforts to control the channels dysfunction associated with this intriguing channelopaty.

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          Most cited references129

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          Significance of a fragmented QRS complex versus a Q wave in patients with coronary artery disease.

          Q waves on a 12-lead ECG are markers of a prior myocardial infarction (MI). However, they may regress or even disappear over time, and there is no specific ECG sign of a non-Q-wave MI. Fragmented QRS complexes (fQRSs), which include various RSR' patterns, without a typical bundle-branch block are markers of altered ventricular depolarization owing to a prior myocardial scar. We postulated that the presence of an fQRS might improve the ability to detect a prior MI compared with Q waves alone by ECG. A cohort of 479 consecutive patients (mean+/-SD age, 58.2+/-13.2 years; 283 males) who were referred for nuclear stress tests was studied. The fQRS included various morphologies of the QRS ( 1 R' (fragmentation) in 2 contiguous leads, corresponding to a major coronary artery territory. The Q wave was present in 71 (14.8%) patients, an fQRS was present in 191 (34.9%) patients, and an fQRS and/or a Q wave was present in 203 (42.3%) patients. Sensitivity, specificity, and the negative predictive value for myocardial scar as detected by single photon emission computed tomography analysis were 36.3%, 99.2%, and 70.8%, respectively, for the Q wave alone; 85.6%, 89%, and 92.7%, respectively, for the fQRS; and 91.4%, 89%, and 94.2%, respectively, for the Q wave and/or fQRS. The fQRS on a 12-lead ECG is a marker of a prior MI, defined by regional perfusion abnormalities, which has a substantially higher sensitivity and negative predictive value compared with the Q wave.
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            Tpeak-Tend and Tpeak-Tend dispersion as risk factors for ventricular tachycardia/ventricular fibrillation in patients with the Brugada syndrome.

            Our objective in this study was to evaluate Tpeak-Tend interval (Tp-e) and other electrocardiographic parameters as risk factors for recurrence of life-threatening cardiac events in patients with the Brugada syndrome (BS). The Tp-e interval in the electrocardiogram (ECG) has been reported to predict life-threatening arrhythmias in the long QT syndrome. Twenty-nine patients with the ECG pattern of BS and 29 healthy age- and gender-matched controls were studied. The follow-up period was 42.65 +/- 24.42 months (range 11 to 108 months). Upon presentation, five patients had suffered aborted sudden death, five syncope, and two presyncope. Eleven patients with the ECG pattern of BS had a prolonged (>460 ms) QTc in V2 but usually not in inferior or left leads. No patient had abnormally prolonged QT dispersion. Programmed electrical stimulation induced ventricular tachycardia/fibrillation in 5 out of 26 patients. Inducibility did not predict recurrence of events. Cardioverter-defibrillators were implanted in 14 patients (all symptomatic and two asymptomatic). During follow-up, nine symptomatic patients experienced recurrences. Previous cardiac events and a QTc >460 ms in V2 were significant risk factors (p = 0.00002 and p = 0.03, respectively). Tp-e and Tp-e dispersion were significantly prolonged in patients with recurrences versus patients without events (104.4 and 35.6 ms vs. 87.4 and 23.2 ms; p = 0.006 and p = 0.03, respectively) or controls (90.7 and 17.9 ms; p = 0.02 and p = 0.001, respectively). Our study demonstrates significant correlation between previous events, QTc >460 ms in V2, Tp-e, and Tp-e dispersion and occurrence of life-threatening arrhythmic events, suggesting that these parameters may be useful in risk stratification of patients with the Brugada syndrome.
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              Right ventricular fibrosis and conduction delay in a patient with clinical signs of Brugada syndrome: a combined electrophysiological, genetic, histopathologic, and computational study.

              The mechanism of ECG changes and arrhythmogenesis in Brugada syndrome (BS) patients is unknown. A BS patient without clinically detected cardiac structural abnormalities underwent cardiac transplantation for intolerable numbers of implantable cardioverter/defibrillator discharges. The patient's explanted heart was studied electrophysiologically and histopathologically. Whole-cell currents were measured in HEK293 cells expressing wild-type or mutated sodium channels from the patient. The right ventricular outflow tract (RVOT) endocardium showed activation slowing and was the origin of ventricular fibrillation without a transmural repolarization gradient. Conduction restitution was abnormal in the RVOT but normal in the left ventricle. Right ventricular hypertrophy and fibrosis with epicardial fatty infiltration were present. HEK293 cells expressing a G1935S mutation in the gene encoding the cardiac sodium channel exhibited enhanced slow inactivation compared with wild-type channels. Computer simulations demonstrated that conduction slowing in the RVOT might have been the cause of the ECG changes. In this patient with BS, conduction slowing based on interstitial fibrosis, but not transmural repolarization differences, caused the ECG signs and was the origin of ventricular fibrillation.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                ruc
                Revista Uruguaya de Cardiología
                Rev.Urug.Cardiol.
                Sociedad Uruguaya de Cardiología (Montevideo )
                1688-0420
                September 2011
                : 26
                : 2
                : 122-140
                Affiliations
                [1 ] Fundação do ABC Brasil
                [2 ] Hospital Español de Mendoza Argentina
                [3 ] Queen's University Brasil
                Article
                S1688-04202011000200009
                acc62537-5273-4172-9de2-7b0b10af735d

                http://creativecommons.org/licenses/by/4.0/

                History
                Product

                SciELO Uruguay

                Self URI (journal page): http://www.scielo.edu.uy/scielo.php?script=sci_serial&pid=1688-0420&lng=en
                Categories
                CARDIAC & CARDIOVASCULAR SYSTEMS
                MEDICINE, GENERAL & INTERNAL
                SURGERY

                Surgery,Cardiovascular Medicine,Internal medicine
                ELECTROCARDIOGRAM,ELECTROCARDIOGRAMA,SíNDROME DE BRUGADA- diagnóstico,SíNDROME DE BRUGADA- pronóstico,BRUGADA SYNDROME- diagnosis,BRUGADA SYNDROME- prognosis

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