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Fotios Kardaras

Publications and source records attributed to Fotios Kardaras.

15 recordsLinked to original sources
PubMed2006

ST-segment elevation induced during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation.

We report two cases of transient coronary artery ischemia manifested as chest discomfort with ST-segment elevation in inferior leads during the transseptal procedure for radiofrequency catheter ablation of atrial fibrillation. This unexpected complication was resolved by intravenous administration of nitrates. All patients exhibited normal coronary arteries in angiography. A neurally mediated pathway activated by the mechanical effects of the transseptal puncture on the interatrial vagal network leading to coronary artery spasm may be considered as a possible explanation of this phenomenon. Coronary artery embolism following the transseptal procedure represents a different underlying mechanism.

Atrial Fibrillation↗
PubMed2006

Secondary prevention of sudden cardiac death in coronary artery spasm: is implantable cardioverter defibrillator always efficient?

Syncope and/or cardiac arrest in the setting of coronary artery spasm have been associated with atrioventricular block and asystole or ventricular tachyarrhythmias. Ventricular arrhythmias have been predominantly reported in cases of multivessel coronary artery spasm. The present report highlights the case of a young woman who suffered repeated episodes of multivessel coronary artery spasm in association with polymorphic ventricular tachycardia and cardiac arrest. The efficacy of implantable cardioverter defibrillator in secondary prevention of sudden cardiac death due to coronary artery spasm is discussed.

Adult↗
PubMed2006

Swimming-triggered aborted sudden cardiac death in a patient with Andersen-Tawil syndrome.

In this report we describe the case of a 42-year-old woman who experienced an episode of near drowning during recreational swimming. A diagnosis of Andersen-Tawil syndrome was made based on the patient's dysmorphic features, characteristic T-U-wave patterns and ventricular arrhythmias. To our knowledge, this is the first report of a swimming-triggered cardiac event in a patient with Andersen-Tawil syndrome.

Adult↗
PubMed2006

Open ended circulation pattern: a rare case of a protective coronary artery variation and review of the literature.

Persistent intercoronary communications, forming the so-called open ended coronary circulation pattern, are rare findings of coronary angiography. A case of intercoronary connection between the left anterior descending artery (LAD) and the right coronary artery (RCA), with an obstructive lesion, and no evidence of myocardial infarction is presented. This is an exceptional variant, only 20 cases of which were found in the literature. The potential protective role of this anomaly against occlusive coronary artery disease is discussed and similar reports are reviewed.

Aged↗
PubMed2006

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.

Adolescent↗
PubMed2005

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.

Bundle of His↗
PubMed2005

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.

Aged↗
PubMed2005

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.

Aged↗
PubMed2004

Facilitating internal cardioversion of chronic atrial fibrillation with ibutilide--predictors of atrial defibrillation-threshold decrease.

BACKGROUND: Internal atrial cardioversion has been successfully used in the treatment of atrial fibrillation. The object of this study was to depict the effect of ibutilide on sinus rhythm restoration and internal atrial defibrillation threshold in patients with chronic atrial fibrillation. MATERIAL/METHODS: Twenty-four patients (14 men and 10 women, mean age 63.16+/-8.55 years) with chronic atrial fibrillation were cardioverted using a single-lead system. The distal coil of the defibrillator catheter was placed in the coronary sinus and the proximal coil at the junction of the superior vena cava and the high right atrium. Synchronized biphasic shocks were applied using a step-up protocol from 1 to 30 joules until sinus rhythm was restored. In all patients with successful cardioversion, atrial fibrillation was reinduced and second cardioversion was attempted after intravenous administration of 1 mg ibutilide. RESULTS: Successful internal cardioversion was achieved in 22 (91.6%) and 23 (95.83%) patients before and after ibutilide administration, respectively. The amount of energy given was reduced from 13.89+/-11.44 to 8.28+/-9.64 joules (p=0.0001). Variables associated with the reduction of the defibrillation threshold after ibutilide administration were: duration of the last episode of atrial fibrillation (p=0.008), time since the first episode of atrial fibrillation (p=0.002), body mass index (p=0.01), ejection fraction (p=0.025), male gender (p=0.001), and diameter of the left atrium (p=0.028). CONCLUSIONS: Internal atrial defibrillation after ibutilide administration is a safe and effective method for sinus rhythm restoration, with concurrent significant reduction of the atrial defibrillation threshold.

Aged↗
PubMed2003

Studies on apoptosis and fibrosis in skeletal musculature: a comparison of heart failure patients with and without cardiac cachexia.

Apoptosis has been found in skeletal muscles of patients with chronic heart failure (CHF) and has been associated with exercise intolerance. In CHF, cachexia is characterized by neurohormonal activation and muscle wasting. Neurohormonal activation can lead to cell death and fibrosis. The purpose of the study was to determine the severity of apoptosis and fibrosis in skeletal muscles of patients with CHF and cachexia and its relationship to exercise intolerance in these patients. Skeletal muscle biopsies of 21 patients with CHF (eight with cachexia) and four healthy controls of similar age have been studied by in situ end labeling (ISEL) for apoptosis and by the Picrosirius Red technique for collagen. Apoptosis in skeletal muscles was detected by ISEL in 52% of the patients with CHF (11 out of 21) and in none of the controls. CHF patients with apoptosis-positive skeletal muscles had impaired exercise tolerance (peak oxygen consumption 11.4+/-5.7 vs. 16.91+/-6.6, P=0.029). Increased collagen was detected by Picrosirius Red in eight out of 21 patients with CHF and in none of the controls. Increased collagen (fibrosis) was detected in six out of eight patients with cachexia and in two out of 13 patients without cachexia (P=0.01). Peak oxygen consumption and apoptosis were similar in cachectic and non-cachectic patients. Thus, the skeletal musculature of patients with cardiac cachexia is characterised by the presence of fibrosis. Apoptosis was not found to be more frequent in cachectic CHF patients. Our data support the hypothesis that cachexia contributes by a different mechanism to skeletal muscle myopathy of CHF patients and different mechanisms are implicated in deterioration of exercise tolerance and progression to cardiac cachexia.

Aged↗
PubMed2003

Chemokines in cardiovascular remodeling: clinical and therapeutic implications.

Chemokines are newly discovered molecules that mediate the migration of leukocytes into inflammed tissues and control the inflammatory reactions in various immune-mediated diseases. Both in animal models and in human specimens, chemokine expression is associated with atherosclerotic lesion development and vascular remodeling and restenosis after angioplasty. Furthermore, recent studies have demonstrated that chemokines play an important role in the pathophysiology of acute coronary syndromes, post-infarction left ventricular remodeling and chronic heart failure. The capacity to control activation and movement of inflammatory cells suggests that chemokines and their receptors might provide novel targets for therapeutic intervention in a number of conditions characterized by chronic inflammation, including cardiovascular diseases. The present review summarizes current knowledge regarding the potential pathogenic role of chemokines in major cardiovascular disorders, as well as the modulation of the chemokine network as a novel, interesting therapeutic modality in this field.

Animals↗