Epsilon-like waves and ventricular conduction abnormalities in subjects with type 1 ECG pattern of Brugada syndrome.

BACKGROUND: Previous studies have demonstrated an overlap between the arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) and Brugada syndrome (BS). Conduction delay in the right ventricle has been demonstrated in both entities. OBJECTIVE: This study investigated specific ARVC/D electrocardiographic (ECG) markers in subjects with spontaneous or drug-induced type 1 ECG pattern of BS. METHODS: The study population consisted of 47 apparently healthy individuals (38 men, mean age 44.1 ± 13.3 years) with spontaneous (n = 17) or drug-induced (n = 30) type 1 ECG phenotype of BS. The clinical records of these individuals were retrospectively analyzed. RESULTS: Fifteen subjects (31.9%) were symptomatic, with a history of syncope. A family history of BS or sudden cardiac death was reported in 10 (21.3%) and 8 (17.0%) cases, respectively. Epsilon-like waves in leads V1-V3 were observed in 6 subjects (12.7%). Epsilon-like waves were seen in spontaneous type 1 ECGs in 2 cases and after sodium channel blocking test in 4 cases. In baseline ECGs, localized prolongation (>110 ms) of the QRS complex in leads V1-V3, QRS duration ratio in (V1+V2+V3)/(V4+V5+V6) ≥ 1.2, and prolonged S wave upstroke (>55 ms) in leads V1-V3 were seen in 48.8%, 29.8%, and 40.4% of subjects, respectively. Epsilon-like waves and delayed S wave upstroke were more commonly observed in subjects with family history of BS (P = .014 and P = .038, respectively). CONCLUSION: Specific ECG markers that reflect ventricular conduction delay in ARVC/D are commonly observed in subjects with spontaneous or drug-induced type 1 ECG pattern of BS as well. These depolarization abnormalities may be related to subtle underlying structural abnormalities.

Clinical characteristics of patients with drug-induced QT interval prolongation and torsade de pointes: identification of risk factors.

The present study aimed to investigate the causative medications and underlying risk factors that predispose to drug-induced QT interval prolongation. Twenty-one patients with drug-induced long QT (90% females, mean age 64.3 +/- 14.1 years) were included in the study. Transthoracic echocardiography as well as continuous or ambulatory 48-h electrocardiographic monitoring was carried out in all patients during their hospitalization. The mean corrected QT (QTc) interval was 542 +/- 56.8 ms. Known cardiac agents (mainly class III antiarrhythmics) were implicated in 13/21 (62%), antipsychotics in 8/21 (38%), and antibiotics in 5/21 patients (24%). Potential drug-interactions through inhibition of cytochrome P450 isoenzymes were considered responsible in 5/21 cases (24%). The underlying cardiovascular diseases included hypertension (57%) with left ventricular hypertrophy (29%), paroxysmal atrial tachyarrhytmias (48%), heart failure (14%), valvular heart disease (10%), and coronary artery disease (5%). Torsade de pointes (TdP) was recorded in 6/21 of patients, and cardiac arrest necessitating resuscitation occurred in five of them. A significant correlation was observed between administration of cardiac agents and TdP events (P < 0.05). TdP and cardiac arrest events were both associated with a QTc interval >510 ms (P < 0.05). Advanced age (>60 years), female gender, hypertension and paroxysmal atrial tachyarrhytmias were the most common identifiable pre-existing factors for drug-induced long QT in our patient cohort. Marked QTc interval prolongation should be considered of prognostic significance for TdP and cardiac arrest events.

Prevalence of Brugada sign in a Greek tertiary hospital population.

AIMS: The purpose of the present study was to determine for the first time the prevalence of Brugada-type electrocardiographic (ECG) pattern (Brugada sign) in unselected individuals served by an urban Greek tertiary hospital during a 4-year time period. METHODS AND RESULTS: Among 11,488 individuals (6640 males, 4848 females), 25 (23 males, 2 females, aged 36.8 +/- 19.2 years) were found to display the Brugada sign (0.22%). Two cases exhibited the diagnostic type 1 ECG pattern (0.02%) and 23 subjects fulfilled the ECG criteria for type 2 or 3 patterns (0.2%). The incidence of Brugada sign was higher among men (0.34%) than in women (0.04%). Structural heart disease was established in four cases (one of them exhibiting a type 1 ECG pattern). Twenty-one individuals (19 males, 2 females, aged 29.7 +/- 10.7 years) without structural heart disease displaying Brugada-type ECG features (4 cases with spontaneous or procainamide-induced type 1 ECG pattern) were subsequently selected and closely followed up for 24 +/- 12 months. No mortality or life-threatening ventricular arrhythmias were recorded during this period. CONCLUSION: The Brugada-type ECG pattern is infrequently seen in a Greek hospital-based population. All subjects with Brugada sign and structurally normal hearts displayed a benign clinical course without arrhythmic events during a relatively long follow-up period.

Enterovirus-induced fulminant myocarditis and hemophagocytic syndrome.

We report the case of a 17-year-old male who was admitted to the emergency department in cardiogenic shock and multiorgan failure due to fulminant myocarditis. The following days the patient developed anemia, thrombocytopenia, and hepatosplenomegaly. Bone marrow examination showed many mature histiocytes with active hemophagocytosis. Nested reverse transcriptase-PCR molecular analysis of blood samples and sequencing of the amplified alleles confirmed enteroviral infection. Our patient was treated with inotropic agents and immunoglobulin, and recovered completely. This is the first report that documents concomitant presentation of fulminant myocarditis and hemophagocytic syndrome due to enteroviral infection.

Hypertrophic cardiomyopathy in a patient with Crohn's disease: a case report.

Cardiac manifestations of Crohn's disease are rare; the most common is pericarditis. In the present report we briefly describe a 56-year-old man with Crohn's disease who presented to the emergency department due to paroxysmal atrial flutter. A transthoracic echocardiographic study revealed asymmetric left ventricular hypertrophy without outflow pressure gradient. Reviewing the literature, hypertrophic cardiomyopathy has not been previously described in patients with Crohn's disease.

Drug-induced QT interval prolongation after ciprofloxacin administration in a patient receiving olanzapine.

Several non-antiarrhythmic drugs including antibiotic and antipsychotic agents have been shown to prolong cardiac repolarization predisposing to torsade de pointes ventricular tachycardia. Blockade of the delayed rectifier (repolarising) potassium current and drug interactions with inhibitors of the CYP-mediated metabolism are the most common underlying mechanisms. In the present case report, an elderly woman receiving a long-term medication with azathioprine, olanzapine and valsartan developed a marked QT interval prolongation after intravenous administration of ciprofloxacin.

Exercise-induced second-degree atrioventricular block.

In this report we describe the case of a 56-year-old woman with normal 1:1 AV conduction at rest who developed 2:1 AV block during treadmill exercise testing. Electrophysiological study documented 2:1 AV block proximal to the His bundle with reappearance of 1:1 AV conduction at a higher pacing atrial rate. A gap phenomenon involving a proximal and distal part of the AV node may be a likely explanation of paradoxical AV conduction in our case.

QT interval prolongation and torsade de pointes associated with indapamide.

Direct blockade of the delayed rectifier repolarising potassium current is the major underlying mechanism of drug-induced QT interval prolongation. Indapamide is a well known blocker of the slow component of the delayed rectifier current leading to prolongation of cardiac repolarization. The case of an acquired long QT and torsade de pointes ventricular tachycardia in a woman with systemic lupus erythematosus and hypertension receiving prednisolone and indapamide, respectively, is described in the present report.

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.