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Michalis Efremidis

Publications and source records attributed to Michalis Efremidis.

14 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

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↗
PubMed2006

QT interval prolongation associated with venlafaxine administration.

A significant number of non-antiarrhythmic drugs including psychotropic agents have been shown to prolong cardiac repolarization increasing the risk for torsade de pointes ventricular tachycardia. We briefly describe a 60-year-old woman who admitted to the hospital due to hypertension and mild dyspnea having a prolonged QT interval (QTc: 582 ms). The patient had a known history of depression treated with venlafaxine. The QT interval normalised a few days after cessation of the antidepressant agent. This is the first report of venlafaxine-induced QT interval prolongation.

Cyclohexanols↗
PubMed2006

Early repolarization syndrome: is it always benign?

Early repolarization syndrome is a well-recognized idiopathic electrocardiographic phenomenon characterized by prominent J wave and ST-segment elevation predominantly in left precordial leads. The syndrome shares remarkable cellular, ionic, and electrocardiographic similarities with the Brugada syndrome and idiopathic ventricular fibrillation (a variant of the Brugada syndrome with ST-segment elevation in inferior leads). Although early repolarization syndrome is considered a benign entity, its arrhythmogenic potential still remains unknown. We report the case of a 39-year-old male with a family history of sudden death and an electrocardiogram consistent with early repolarization syndrome. Diagnostic dilemmas are discussed.

Adult↗
PubMed2006

Pathophysiology and management of syncope in Kearns-Sayre syndrome.

A 20-year-old woman with known Kearns-Sayre syndrome was transferred to the emergency department due to syncopal episodes. The electrocardiogram on admission showed complete atrioventricular block. The diagnosis of mitochondrial encephalomyopathy was made when she was 14 years old. At the time of the initial diagnosis, she displayed a normal electrocardiogram pattern. At the age of 17, electrocardiogram recordings demonstrated right bundle branch block with left anterior fascicular block and a prolonged QTc interval of 485 milliseconds (Figure). She was taking coenzyme Q10, oral nicotinamide adenine dinucleotide (reduced), piribedil, amantadine, and primidone. Transthoracic echocardiography revealed normal wall motion of both ventricles and mitral valve prolapse without regurgitation. A permanent dual-chamber pacemaker was immediately implanted.

Adult↗
PubMed2005

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.

Cardiomyopathy, Hypertrophic↗
PubMed2005

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.

Adult↗
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↗
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↗
PubMed2002

Cardiotoxicity following different doses and schedules of 5-fluorouracil administration for malignancy -- a survey of 427 patients.

BACKGROUND: Although cardiotoxicity associated with 5-Fluorouracil (5-FU) administration is infrequent, there are case reports of acute coronary syndromes. We report on patients undergoing 5-FU chemotherapy who developed cardiac symptoms during its administration. MATERIAL/METHODS: In patients receiving 5-FU who experienced cardiac-related symptoms, ECG and serum cardiac enzyme determination were performed. If cardiotoxicity was detected, 5-FU infusion was interrupted, and the patients received sublingual nitrates and cardiac monitoring, while patients with more than 2-fold elevated enzyme levels were monitored in a coronary care unit for at least 72 hours. In cases of acute myocardial infarction, 5-FU was terminated. RESULTS: Of 427 patients entering the study, 17 (4%) developed clinical symptoms and ECG abnormalities indicating 5-FU cardiotoxicity. Patients with continuous infusion (c.i.) of 5-FU had a higher incidence of cardiotoxicity (12/197, 6%) than the remaining (5/235, 2.1%) (p=0.067), but more toxicity was encountered in patients with c.i. of 5-FU+LV for 24 hours for 5 days than in patients with the same regimen of 5-FU without LV (p<0.027) or patients with short 5-FU+LV administration (p=0.024). Seven of the 17 patients with 5-FU cardiotoxicity had an acute myocardial infarction, 4 developed ischemic changes, while 4 more patients had ECG abnormalities consistent with coronary vasospasm, of whom one subsequently died. CONCLUSIONS: The present study supports the toxic effect of 5-FU on myocardium, which is largely schedule-dependent. Considerable vigilance is required when using this drug, and its toxic effect on the coronary endothelium and myocardium merit further investigation.

Aged↗