Antonios Sideris

QT Interval Prolongation and Torsades de Pointes Due to a Coadministration of Metronidazole and Amiodarone

This report documents the occurrence of torsades de pointes (TdP) caused by marked QT interval prolongation in the case of a 71‐year‐old woman receiving both metronidazole and amiodarone for the treatment of pseudomembranous colitis and paroxysmal atrial fibrillation. The case highlights a previously unknown drug interaction. The role of inhibition of cytochrome P‐450 CYP3A4 is discussed.

Prevalence of paroxysmal atrial fibrillation in Brugada syndrome: a case series and a review of the literature.

Objective The present study aimed at investigating the incidence of paroxysmal atrial fibrillation in 10 patients with spontaneous or induced type 1 electrocardiographic pattern of Brugada syndrome (three with syncopal episodes and seven asymptomatic). Both clinical entities are closely associated with changes in autonomic modulation and, particularly, with increased vagal tone. Methods Transthoracic echocardiography, exercise treadmill test and 24-h Holter recordings were performed to all patients. Results Episodes of atrial fibrillation were recorded in 2/10 patients (20%). These patients suffered from syncopal episodes, exhibited a positive electrophysiological study, and finally received an implantable cardioverter-defibrillator. Conclusions The present case series points out a high incidence of paroxysmal atrial fibrillation predominantly in symptomatic patients with type 1 electrocardiographic pattern of Brugada syndrome, indicating that the presence of atrial tachyarrhythmias may reflect an advanced stage of the disease. The prognostic significance of paroxysmal atrial fibrillation, particularly in asymptomatic patients with an electrocardiographic pattern consistent with Brugada syndrome requires further evaluation. Physicians should always be aware of Brugada syndrome in young patients with lone atrial fibrillation, especially in those with a history of syncope.

Brugada electrocardiographic pattern induced during febrile state with marked leukocytosis.

Several agents and conditions have been reported to unmask or accentuate the electrocardiographic pattern of Brugada syndrome including fever. At a molecular level, sodium channels have been showed to be temperature dependent. Herein, we describe a case of Brugada electrocardiographic pattern unmasked during febrile state and marked leukocytosis.

Effect of Atrial Pressure Increase on Effective Refractory Period and Vulnerability to Atrial Fibrillation in Patients with Lone Atrial Fibrillation

Background: There is evidence suggesting that atrial fibrillation (AF) may be induced by acute increase of atrial pressure. The aim of the present study was to investigate the effect of alterations in atrial pressure, induced by varying the atrioventricular (AV) interval, on atrial refractoriness, and on the frequency of induction of (AF), in patients with a history of lone atrial fibrillation (LAF).Methods and Results: Twenty-five patients were included in this study. The patients were divided in two groups: the LAF group, and the control group. None of the patients in either group had organic heart disease. Effective refractory period (ERP) and duration of atrial extrastimulus electrogram (A2) were measured at two right atrial sites (high lateral wall, atrial appendage) during AV pacing (cycle length: 500 msec) with different AV intervals. Peak, minimal and mean atrial pressure increased from 8.57 ± 2.37 to 18.14 ± 4.74 mm Hg, 2 ± 2.23 to 5.14 ± 2.60 mm Hg (p = 0.0001) and from 4.28 ± 1.6 mm Hg to 9.77 ± 2.9 mm Hg (p = 0.001), respectively during AV interval modification. During lateral and atrial appendage pacing, with a progressive decrease of AV interval to 160, 100, 80, 40, 0 msec, the ERP, the dispersion of ERP, functional refractory period (FRP), A2 and latency period (LP) did not change significantly, in both groups. The frequency of induction of AF was not statistically different in both lateral atrial wall and appendage, during pacing in different AV intervals.Conclusions: This study demonstrates that alterations in the intraatrial pressure does not have important effects on atrial refractoriness and does not increase vulnerability to AF in patients with a history of LAF.

Current Ablation Strategies for Persistent and Long-Standing Persistent Atrial Fibrillation

Atrial fibrillation (AF) is associated with an increased risk of cardiac and overall mortality. Restoration and maintenance of sinus rhythm is of paramount importance if it can be accomplished without the use of antiarrhythmic drugs. Catheter ablation has evolved into a well-established treatment option for patients with symptomatic, drug-refractory AF. Ablation strategies which target the pulmonary veins are the cornerstone of AF ablation procedures, irrespective of the AF type. Ablation strategies in the setting of persistent and long-standing persistent AF are more complex. Many centers follow a stepwise ablation approach including pulmonary vein antral isolation as the initial step, electrogram-based ablation at sites exhibiting complex fractionated atrial electrograms, and linear lesions. Up to now, no single strategy is uniformly effective in patients with persistent and long-standing persistent AF. The present study reviewed the efficacy of the current ablation strategies for persistent and long-standing persistent AF.

Long-term prognosis of asymptomatic individuals with spontaneous or drug-induced type 1 electrocardiographic phenotype of Brugada syndrome

BACKGROUND Risk stratification of asymptomatic individuals with type 1 electrocardiogram (ECG) phenotype of Brugada syndrome (BS) still remains controversial. This study investigated the long-term prognosis of asymptomatic subjects with spontaneous or drug-induced type 1 ECG pattern of BS. METHODS AND RESULTS Data from 33 apparently healthy individuals (30 males; age, 43.6 ± 13.4 years) with spontaneous (n = 12) or drug-induced (n = 21) type 1 ECG pattern of BS were retrospectively analyzed. Thirteen subjects (39.4%) displayed a positive family history of BS and/or sudden cardiac death. Electrophysiologic study was performed in 16 subjects, and programed right ventricular stimulation induced polymorphic ventricular tachycardia in 9 (56.3%) of them. A cardioverter defibrillator was implanted in 6 cases. During a mean follow-up period of 5.3 ± 2.8 years, all subjects remained asymptomatic. None of them had syncope or cardioverter defibrillator discharges due to ventricular arrhythmias. CONCLUSIONS Asymptomatic individuals with spontaneous or drug-induced type 1 ECG phenotype of BS display a benign clinical course during long-term follow-up.

QT Interval Prolongation and Torsades de Pointes in a Patient Receiving Zolpidem and Amiodarone

the fourth day, during ambulatory ECG Holter monitoring, she developed TdP ventricular tachycardia degenerated to ventricular fi brillation, that required defi brillation to restore sinus rhythm ( fi g. 1 ). A marked QTc interval prolongation (565 ms) was recorded before the episode ( fi g. 2 ). No evidence of ischemia was present at that time. Dear Sir, A growing number of non-antiarrhythmic agents have been shown to prolong cardiac repolarization predisposing to torsades de pointes (TdP) ventricular tachycardia [1] . Arrhythmogenicity can be facilitated in the presence of pre-existing risk factors that increase vulnerability to TdP such as female gender, congestive heart failure, bradycardia, subclinical long QT syndrome, ion-channel polymorphisms, electrolyte imbalance (hypokalemia, hypomagnesemia, hypocalcemia), digitalis therapy, hyperthermia, hypothyroidism and starvation [1, 2] . A 67-year-old woman with a history of prosthetic mitral valve and congestive heart failure (NYHA II) was admitted to the emergency department complaining of palpitations. She was on captopril, furosemide, and warfarin. Three weeks earlier, she was started on zolpidem for sleep disorders (insomnia). Baseline electrocardiogram (ECG) on admission showed sinus rhythm with left bundle branch block, premature ventricular complexes, and a QTc interval of 440 ms. Transthoracic echocardiography revealed global wall motion abnormalities of the left ventricle with an estimated ejection fraction of 45%. Ambulatory ECG Holter monitoring recorded multifocal premature ventricular complexes, couplets, and episodes of bigeminy and trigeminy. Intravenous loading with amiodarone was given as a 450-mg bolus followed by 900 mg daily. On Received: September 12, 2005 Accepted: October 4, 2005 Published online: January 31, 2006

Prognosis, risk stratification, and management of asymptomatic individuals with Brugada syndrome: A systematic review

Brugada syndrome (BrS) is a primary electrical disease associated with increased risk of sudden cardiac death due to polymorphic ventricular arrhythmias. The prognosis, risk stratification, and management of asymptomatic individuals remain the most controversial issues in BrS. Furthermore, the decision to manage asymptomatic patients with an implantable cardioverter‐defibrillator should be made after weighing the potential individual risk of future arrhythmic events against the risk of complications associated with the implant and follow‐up of patients living with such devices, and the accompanying impairment of the quality of life. Several clinical, electrocardiographic, and electrophysiological markers have been proposed for risk stratification of subjects with BrS phenotype, but the majority have not yet been tested in a prospective manner in asymptomatic individuals. Recent data suggest that current risk factors are insufficient and cannot accurately predict sudden cardiac death events in this setting. This systematic review aims to discuss contemporary data regarding prognosis, risk stratification, and management of asymptomatic individuals with diagnosis of Brugada electrocardiogram pattern and to delineate the therapeutic approach in such cases.

High risk electrocardiographic markers in Brugada syndrome

Several clinical, electrocardiographic (ECG) and electrophysiological markers have been proposed to provide optimal risk stratification in patients with Brugada syndrome (BrS). Of the different markers, only a spontaneous type 1 ECG pattern has clearly shown a sufficiently high predictive value. This review article highlights specific ECG markers based on depolarization and/or repolarization that have been associated with an increased risk of arrhythmic events in patients with BrS.

Right Ventricular Outflow Tract Electroanatomical Abnormalities Predict Ventricular Fibrillation Inducibility in Brugada Syndrome

Electroanatomical mapping has demonstrated abnormal bipolar electrograms at the anterior aspect of the right ventricular outflow tract (RVOT) epicardium along with histopathologic evidence of fibrosis in patients with Brugada syndrome (BrS).1,2 These epicardial abnormalities are believed to serve as the electric substrate for ventricular fibrillation (VF) initiation and maintenance in BrS.1,2 We have recently demonstrated that patients with BrS display wide areas of endocardial unipolar voltage abnormalities that possibly reflect epicardial structural abnormalities at the free wall of the RVOT.3 We hypothesized that electroanatomical abnormalities detected by high-density endocardial unipolar voltage mapping at the RVOT predict VF inducibility during programmed ventricular stimulation (PVS). The study population consisted of 17 asymptomatic probands (15 males, 37.3±10.8 years) with spontaneous type 1 BrS ECG pattern referred for risk stratification with PVS. A comprehensive evaluation including late gadolinium enhancement cardiac magnetic resonance imaging ruled out structural heart disease in all patients. The study was approved by the Hospital Ethics Committee and written informed consent was obtained from all patients. High-density electroanatomical mapping of the RVOT during sinus rhythm was performed as described previously (Methods in the Data Supplement).3 In brief, a minimum of 800 points were sampled to …