The pre-FPD may strongly reflect atrial dysfunction, and thus may be useful for predicting a successful PVI. Shortening of the FPD after the PVI and similar FPD and BAT values suggest that the last component of the FPD represents the activation of the left PVs.

SummaryBrugada syndrome is an inherited disorder that predisposes some patients to sudden cardiac death. It is not well established which Brugada syndrome patients are at risk of life-threatening arrhythmias. We investigated whether standard 12-lead electrocardiograms (ECG) can identify such patients. The subjects were 35 men with Brugada syndrome (mean age, 50.1 ± 12.4 years). Documented ventricular fibrillation or aborted sudden cardiac arrests were judged to be related to the Brugada syndrome. Ten patients (mean age, 49.6 ± 14.9 years) were symptomatic, and 25 (mean age, 50.3 ± 11.5 years) were asymptomatic. We determined the PR interval, QRS duration, and QT interval from baseline 12-lead ECG leads II and V2 as well as the J point elevation amplitude of lead V2. The QRS interval was measured from QRS onset to the J point in leads II and V2. The only significant difference between the symptomatic and asymptomatic patients was the QRS duration measured from lead V2. The mean QRS interval was 129.0 ± 23.9 ms in symptomatic patients versus 108.3 ± 15.9 ms in asymptomatic patients (P = 0.012). A QRS interval in lead V2 ≥ 120 ms was found to be a possible predictor of a life-threatening ventricular arrhythmia and/or syncope (P = 0.012). Prolonged QRS duration as measured on a standard 12-lead ECG is associated with ventricular arrhythmia and could serve as a simple noninvasive marker of vulnerability to life-threatening cardiac events in patients with Brugada syndrome. (Int Heart J 2011; 52: 98-102) Key words: Brugada syndrome, Sudden death, Ventricular fibrillation, QRS width B rugada syndrome, which was introduced as a clinical entity in 1992, is a genetic disorder that increases the risk of sudden death secondary to ventricular tachycardia/fibrillation (VT/VF) in patients with structurally normal hearts.1,2) The syndrome is estimated to be responsible for 4% of all sudden deaths and at least 20% of sudden deaths in patients with structurally normal hearts.3) Inheritance of Brugada syndrome occurs via an autosomal dominant mode of transmission with variable penetrance involving several genes. SC-N5A, which codes subunit I Na of sodium channel α, is mutated in 20%-30% of Brugada syndrome patients. 4,5) Mutations in the GPD1L gene 6) and the CACNA1 and CACNB2 genes 7) have also been identified, but these gene variations are infrequent. The typical ST segment elevation in the precordial leads that characterizes Brugada syndrome electrocardiographically can be transitory, vary over time, or be modified by various factors such as vagal tonus, body temperature, and medications. 8,9) This elevation can have a saddleback appearance with a J wave amplitude of ≥ 2 mm and an elevation in the terminal portion of the ST segment of ≥ 1 mm, and then either a positive or biphasic T wave (type 2 electrocardiogram [ECG]) or can be characterized by either a saddleback or coved appearance with an ST segment elevation of < 1 mm (type 3 ECG).10)The vulnerability of individuals with the "Brugada sign" to sudden cardiac death or a life...

SummaryThe reported pathogenesis of Brugada syndrome is phase 2 reentry resulting from shortening of the epicardial action potential duration at the right ventricular outflow tract (RVOT). However, several studies have revealed a high incidence of ventricular late potentials and high rate of ventricular fibrillation (VF) induced by programmed ventricular stimulation (PVS). The aim of the present study was to evaluate the role of slow conduction at the RVOT for the initiation of VF by PVS and any underlying pathological conditions in Brugada syndrome. Endocardial mapping of the RVOT and endomyocardial biopsy of the right ventricle were performed in 25 patients with Brugada syndrome with inducible VF. Late potentials were positive in 11 of the 25 (44%) patients. Low-amplitude fragmented and delayed electrograms were recorded at the RVOT in 13 of 18 (72.2%) patients. Histologic examination of the biopsy samples revealed fatty tissue infiltration, interstitial fibrosis, lymphocyte infiltration, and/or myocyte disorganization in 13 patients. Slow conduction at the RVOT may contribute to the induction of VF by PVS in Brugada syndrome. Various pathomorphologic changes may contribute to slow conduction at the RVOT. (Int Heart J 2010; 51: 17-23)

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ypical atrial flutter (AFL), with both counterclockwise and clockwise rotation, results from a macroreentrant circuit in the right atrium (RA). [1][2][3][4][5] The tricuspid annulus forms the anterior boundary, and the crista terminalis (CT) has been suggested as the posterior boundary. [4][5][6][7][8][9] A linear lesion between the tricuspid annulus and inferior vena cava (IVC) terminates AFL and predicts long-lasting freedom from any clinical recurrence. [10][11][12][13] Transverse conduction block also has been documented along the CT, on the basis of recording double potentials (DPs) by conventional methods. [4][5][6][7][8][9] This is critical for the induction and maintenance of AFL, as it prevents the flutter wave from "short-circuiting" across the posterior RA. However, several recent studies have suggested that the CT may not be a consistent barrier to conduction in AFL; some studies showed the presence of a posteromedial functional block in the sinus venosa region, but not on the CT, using intracardiac echocardiography (ICE); [14][15][16] other studies showed double lines of block during AFL, with the first line located along the CT area and the second line located in the sinus venosa region. 17,18 The aim of this study was to delineate the posterior boundary in the RA and compare the block line in terms of functional and fixed components and the anatomical structures in patients with and without AFL using 2-and 3-dimensional (2D, 3D) ICE. Methods PatientsThe study group consisted of 50 symptomatic patients (34 men, 16 women, mean age 57.4±13.9 years, range 25-77 years) who were referred for catheter ablation. None had organic heart disease evaluated by the physical examination, 12-lead ECG, chest X-ray, echocardiography, and exercise test. These patients were divided into 2 groups: 34 with typical AFL and 16 control patients without AFL. The patients with AFL included 16 patients with inducible AFL during electrophysiologic study. The control patients consisted of 16 patients without a history of AFL and without inducible AFL. In all study patients, the administration of antiarrhythmic drugs was terminated for at least 5 half-lives before the ablation. Electrophysiologic StudyInformed consent to participate in the study was given by all patients, and the protocol was approved by the Investigational Review Board of the Nihon University School of Medicine. A 6F quadripolar steerable catheter with 2-4-