Publications by authors named "Stavros P Kounas"

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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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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.

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