We evaluated two patients without previous episodes of syncope who showed characteristic ECG changes similar to Brugada syndrome following administration of Class IC drugs, flecainide and pilsicainide, but not following Class IA drugs. Patient 1 had frequent episodes of paroxysmal atrial fibrillation resistant to Class IA drugs. After treatment with flecainide, the ECG showed a marked ST elevation in leads V2 and V3, and the coved-type configuration of ST segment in lead V2. A signal-averaged ECG showed late potentials that became more prominent after flecainide. Pilsicainide, a Class IC drug, induced the same ST segment elevation as flecainide, but procainamide did not. Patient 2 also had frequent episodes of paroxysmal atrial fibrillation. Pilsicainide changed atrial fibrillation to atrial flutter with 2:1 ventricular response, and the ECG showed right bundle branch block and a marked coved-type ST elevation in leads V1 and V2. After termination of atrial flutter, ST segment elevation in leads V1 and V2 continued. In this patient, procainamide and quinidine did not induce this type of ECG change. In conclusion, strong Na channel blocking drugs induce ST segment elevation similar to Brugada syndrome even in patients without any history of syncope or ventricular fibrillation.

No abstract

Enalapril suppressed atrial pacing-induced AF with tachycardia-mediated cardiomyopathy by suppressing interstitial fibrosis, connexin43 over-expression and conduction delay.

The effects of a new benzopyran derivative, NIP-142, on atrial fibrillation (AF) and flutter (AFL) and on electrophysiological variables were studied in the dog. NIP-142 (3mg/kg) was administered intravenously to pentobarbital-anesthetized beagles during vagally-induced AF and during AFL induced after placement of an intercaval crush. Isolated canine atrial tissues were studied using standard microelectrode technique. NIP-142 terminated AF in 5 of 6 dogs after an increase in fibrillation cycle length (CL) and prevented reinitiation of AF in all 6 dogs. NIP-142 terminated AFL in all 6 dogs without any appreciable change in flutter CL, and prevented reinitiation of AFL in all 6 dogs. NIP-142 prolonged atrial effective refractory periods (11+/-5%, 3+/-3%, 12+/-3%, and 10+/-5% from the baseline value at basic CLs of 150, 200, 300, and 350ms, respectively) without changes in intraatrial conduction time. The prolongation of the atrial effective refractory period was greater in the presence of vagal stimulation. NIP-142 decreased action potential phase-1 notch and increased phase-2 plateau height without making any changes in the action potential duration, although it did reverse carbachol-induced shortening of the action potential duration. In conclusion, NIP-142 is effective in treating AFL and vagally-induced AF by prolonging atrial refractoriness.

rugada syndrome (BS), a distinct subtype of idiopathic ventricular fibrillation (VF), is characterized by a distinctive ST segment elevation in the right precordial leads. [1][2][3] The mechanism responsible for this ST segment elevation and genesis of VF is still under investigation. Several possible mechanisms have been proposed for the ST segment elevation in BS. Among them are conduction delay, accentuation of the action potential notch and loss of the action potential dome in the right ventricular outflow epicardium. 3,4 In BS, unlike other diseases, VF and sudden death mainly occur in the resting state, predominantly during sleep. 5,6 The typical ECG changes are variable over time and are modulated by exercise or pharmacological interventions that interact with autonomic nervous activities. 5,[7][8][9] We recently reported an inadequate prolongation of the QT interval (short QT interval) at longer RR intervals 10 and an augmentation of the ST elevation through vagal activity in patients with BS. 11 The nighttime onset of VF episodes may be related to both a shorter QT interval and an enhanced ST elevation during bradycardia at night. This could be because of a slow recovery from the inactivation of prominent Ito. 12 However, it is still unclear how the RR intervals affect the ECG changes in BS and whether rate dependent changes in the ECG would be different between symptomatic and asymptomatic patients. The present study was therefore designed to examine the effects of the RR intervals on ECG changes during an electrophysiologic study (EPS) in both symptomatic and asymptomatic patients. Methods Study PopulationTwenty-one consecutive male patients with BS were studied: 9 were symptomatic with either documented VF or episodes of unexplained syncope, and the other 12 were asymptomatic without either spontaneous VF or inducible VF during the EPS. The study protocol was approved by the institutional review board and written informed consent was given by all patients before participation. We diagnosed BS in accordance with recently established ECG criteria. 3 Patients with coved-type ST elevation accompanied by Jwave amplitude ≥2 mm in one of the leads V1-3 were included. 3 For patients with saddle-back-type ST elevation (type 2 or 3), coved-type ST elevation ≥2 mm induced by pilsicainide, a class Ic antiarrhythmic drug, was required. 3 In all patients, physical examination, chest X-ray, 2-dimensional-echocardiography, exercise test and thallium or 99m Tc-tetrofosmin myocardial single photon emission computed tomography failed to disclose apparent evidence of organic heart disease. Patients with diabetes mellitus, long QT syndrome or electrolyte abnormality and patients taking any drugs were excluded from the present study. EPS and Analysis of ECGsEPS was performed in all 21 patients after all antiarrhythmic drugs had been discontinued for at least 5 halflives of the drug. A steerable 6F octapolar catheter with Background In patients with Brugada syndrome (BS), ventricular fibrillation (VF) occurs mainly during ...