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Biomedical subjects

Tamás Fazekas

Publications and source records attributed to Tamás Fazekas.

17 recordsLinked to original sources
PubMed2005

[Non-channel drugs to prevent atrial fibrillation].

Atrial fibrillation is the most prevalent sustained cardiac arrhythmia. To terminate or prevent atrial fibrillation, conventional "channel-blocking antiarrhythmics" are generally administered, which directly inhibit current flows through transmembrane sodium, calcium and/or potassium channels that give rise to the atrial action potential. However, prospective, randomized clinical trials have demonstrated that cardiomyocyte ion channel blocking antiarrhythmic drugs have limited long-term-efficacy for preventing recurrences of atrial fibrillation, their safety is far from ideal (because of the high incidence of proarrhythmic and extracardiac side-effects), and do not reduce mortality. Researchers during the last 10 years have revealed that the pathogenetic basis of the recurrence, persistence or permanence of atrial fibrillation is electrical and structural remodelling established by profound alterations in the electrophysiological, contractile and (ultra)structural properties of the myocardium (atrial remodelling). Accordingly, recent interest has shifted from ion channel blockers to the development of drugs that target underlying arrhythmogenic substrates by interference with receptors and specific signal transduction pathways involved in electrical and structural remodelling (non-channel drugs). They include antifibrotic angiotensin-converting enzyme inhibitors, angiotensin II AT1 receptor and aldosterone antagonists, beta-adrenergic blockers, anti-inflammatory statins and glucocorticoids, and a series of new atrioselective antifibrillatory agents that are currently undergoing clinical trials.

Adrenergic beta-Antagonists↗
PubMed2005

[Proarrhythmic (torsadogenic) effects of QT-prolonging non-antiarrhythmic drugs].

The authors review the rapidly expanding knowledge relating to the arrhythmogenic (torsadogenic) effects of non-antiarrhythmic drugs that lengthen ventricular repolarization (i.e. the duration of electrocardiographic QT interval). After outlining the ECG characteristics and electrophysiological mechanism of drug-induced long-QT syndrome and torsades de pointes ventricular tachycardia, they discuss the concept of repolarization reserve and its role in arrhythmogenesis. Information is provided on the cardiac ion channel background of the proarrhythmic action of QT-prolonging non-antiarrhythmic drugs. The authors present pharmacoepidemiological data on the clinical importance and incidence of this peculiar adverse drug reaction that can in certain cases cause sudden arrhythmic death. They draw attention to the predisposing factors of torsades de pointes ventricular tachycardia, and list those groups of drugs and individual agents that have QT-lengthening and torsadogenic side-effects.

Action Potentials↗
PubMed2004

[Pathophysiology and clinical management of atrial flatter].

The authors review the current knowledge relating to the pathophysiology and treatment of atrial flutter, the most common supraventricular macroreentrant tachycardia. After an account of the historical and epidemiological data, the atrial tachycardia classification system based on the up-to-date North American + European consensus is presented. The main electrophysiological and electrocardiographic features of right atrial isthmusdependent typical and reverse typical flutter are detailed, as are those of the nonisthmus dependent, atypical forms. The electrophysiological connection between the very frequently coexisting atrial flutter and atrial fibrillation, and also the transitional form (flitter), are discussed. Following the clinical presentation, an account is given of the drug and non-pharmacological therapeutic modalities. It is pointed out that the recently-developed drugs with Vaughan Williams class 3 antiarrhythmic action, which block potassium channels and prolong atrial refractory period, are now primarily used (e.g. ibutilide, dofetilide). Effective means of terminating atrial flutter include transthoracic direct-current cardioversion (pretreated with antiarrhythmic = hybrid therapy) and transoesophageal or intraatrial overdrive pacing. It is stressed that the efficiency of prevention of atrial flutter with the antiarrhythmic drugs currently used even today is poor. Accordingly, the optimum mode of treatment of atrial flutter, which is primarily a method of first choice in special cardiac centres, is curative radiofrequency catheter ablation.

Anti-Arrhythmia Agents↗
PubMed2003

[Non-pharmacologic treatment of atrial fibrillation].

The authors provide an update on non-pharmacological treatment of atrial fibrillation (AF). They emphasize that although antiarrhythmic drugs continue to be first-line therapy for the arrhythmia considered to be a cardiovascular epidemic, clinical research to develop non-pharmacological means of treatment has been unprecedentally intensified during the last decade. Electrical cardioversion is the most successful non-pharmacological method to restore sinus rhythm, also the efficacy and safety of AV node ablation for palliative ventricular rate-controll is established. "Hybrid" therapeutic procedures, involving combinations of pharmacological and non-pharmacological interventions have gained widespread use. Curative transcatheter ablation for arrhythmia prevention is to be considered in case of clinical suggestions that AF is initiated by a primary regular arrhythmia that is amenable to routine catheter ablation (secondary AF). Despite encouraging results, at this point in time, curative catheter ablation for primary AF may offer significant improvement or even cure only for a small subset of patients, mostly young individuals with normal heart, and paroxysmal AF with frequent, symptomatic episodes refractory to multiple antiarrhythmic drugs. These interventions are to be performed in the settings of a clinical research project in some institutions. Regarding pacemaker therapy in case of bradycardia indication, physiologic pacing (AAI or DDD) is associated with significantly lower incidence of atrial fibrillation than ventricular pacing. Large-scale randomized controlled trials are needed to assess the clinical value of specially designed implantable devices to prevent atrial fibrillation in patients with no conventional bradycardia indication. Also, technical optimization and proper clinical evaluation is needed for implantable atrioverters and implantable cardioverter defibrillators capable of atrial cardioversion therapy.

Atrial Fibrillation↗
PubMed2003

[Drug therapy of atrial fibrillation].

The authors summarize the up-to-date knowledge relating to the pharmacological treatment of atrial fibrillation. They emphasize that drug treatment continues to be in the forefront of the therapy of the arrhythmia, which can now be considered to constitute a cardiovascular epidemic. In the era following the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AF-FIRM) trial, the strategy of pharmacological treatment will certainly change: in place of "rhythm control", which in recent decades has been overforced in patients identical with the elderly, cardiac patients with an impaired left ventricular function who were enrolled into AFFIRM, there will be a more frequent use of ventricular "rate control". Naturally, this does not mean that, in certain patient groups, an effort should not be made to restore and maintain the sinus rhythm. In cases involving congestive heart failure and structural heart disease complicated by a depressed left ventricular systolic function, atrial fibrillation is currently treated with antiarrhythmic drugs possessing low proarrhythmic activity that prolong refractory period (Class 3), and with the even safer mortality-reducing beta-receptor blockers. The classical antiarrhythmic drugs (quinidine, procainamide, disopyramide) are being increasingly forced into the background, and the areas of indication of the novel Na(+)-channel blocker antiarrhythmics (propafenone, flecainide) have also narrowed: they are administered only in the event of atrial fibrillation in patients with a structurally intact heart or left ventricular hypertrophy. After a brief survey of the more important aspects of ventricular rate control, and of the drugs available, the research trends aimed at the progression of the pharmacological treatment of atrial fibrillation are outlined. The clinical introduction of procedures based on myocardial gene therapy is now a realistic therapeutic approach as concerns atrial fibrillation too.

Anti-Arrhythmia Agents↗
PubMed2003

[Torsades de pointes ventricular tachycardia induced by intravenous amiodarone].

The authors report on the case history of a 61 year old woman with hyperthyroidism induced atrial fibrillation, tachycardiomyopathy and congestive heart failure, in whom life threatening ventricular proarrhythmia (torsades de pointes) developed in response to intravenous amiodarone. The patient in a septic state was resuscitated because of ventricular fibrillation. The atrial fibrillation complicated by a high ventricular frequency was slowed down with intravenous amiodarone; additionally, the iodine-containing antiarrhythmic drug was expected to counter thyrotoxicosis. In response to amiodarone (2 x 300 mg), the sinus rhythm was restored, but the excessive post-cardioversion bradycardia led to the development of extreme QT interval prolongation and torsades de pointes ventricular tachycardias that often degenerated into ventricular fibrillation. In connection with this case, the authors survey those electropharmacological and pathophysiological factors which may have played a role in the emergence of ventricular proarrhythmia based on a lengthening of repolarization through the exhaustion of the repolarization reserve.

Amiodarone↗
PubMed2003

[Pathogenesis and clinical significance of atrial fibrillation].

The authors review the current knowledge relating to the epidemiology, classification and pathogenesis of atrial fibrillation, and then discuss those cardiac electrophysiological changes that play roles in the initiation and/or maintenance of atrial fibrillation. They draw attention to the fact that atrial fibrillation is the most common cardiac arrhythmia in humans, its prevalence increasing continuously with the increase in average lifespan of the population. Atrial fibrillation doubles all-cause mortality, it gives rise to considerable haemodynamic alterations and clinical symptoms, and it is responsible for almost half of the cases of hospitalizations attributable to arrhythmia. Because of the great pathogenetic variety, the most important diagnostic task is to establish the nature of the underlying disease, the arrhythmia substrate, and the predisposing and triggering factors; this permits selection of the therapeutic procedure that is optimum for the given patient. The results of the most recent prospective randomized clinical trials indicate that, in certain groups of patients, it will no longer be absolutely necessary in the future to strive to restore and maintain sinus rhythm: effective oral anticoagulant treatment in combination with pharmacological ventricular rate control ensures the same survival chances and the same quality of life for the patient as those achieved in earlier years with the preferred sinus rhythm-preserving treatment strategy based on pharmacological and/or electrical cardioversions and prophylactic antiarrhythmic drug therapy.

Atrial Fibrillation↗
PubMed2003

[The clinic for internal medicine at Szeged headed by István Rusznyák].

István Rusznyák was one of the most remarkable members of the internist school of Baron Sándor Korányi, whose functional understanding of body processes made his school famous. Rusznyák started his career at Szeged where he much improved the university internist teaching hospital, originally opened in December 1928, which beside healing was a base of medical research and tuition alike. Rusznyák led the Clinique as a director until World War Two. In developing of the Clinique it was not only Rusznyák's medical expertise and efficiency in organisation which helped but also his wide ranger of personal contacts. In spite of the later he was, nevertheless, deported. After the war he was appointed the post of director of the 1st Clinique of Internal Medicine of the Budapest University. His reputation during his years at Budapest, alike in Szeged made him a well known internist and an effective director. Among his friends he could count the best Hungarian medical experts. The article also touches the rather negative role Rusznyák played for the Stalinist regime in Hungary.

History, 20th Century↗
PubMed2002

[Wenckebach AV block, as part of vasovagal syncope].

Vasovagal syncope or common faint is the most frequent form of syncopes. With regard to the different involvement of the efferent mechanisms, several forms of the neurally mediated syncope syndromes are recognized. The authors present a case of mixed type vasovagal syncope, diagnosed by tilt table testing. The efferent mechanisms of syncope included Wenckebach type atrioventricular block due to increased vagal tone, and sympathetic withdrawal, reflected by sudden drop in the blood pressure. The significance and interrelationship of these factors are discussed.

Blood Pressure↗
PubMed2002

[History of atrial fibrillation].

The authors review the history of atrial fibrillation, the most frequent clinically observed cardiac arrhythmia. A French "clinicopathologist", Jean Baptist de Sénac (1693-1770), was the first who assumed a correlation between "rebellious palpitation" and a stenosis of the mitral valve. From an analysis of simultaneously recorded arterial and venous pressure curves, the Scottish Sir James Mackenzie (1853-1925) demonstrated that a praesystolic a wave can not be seen on the jugular phlebogram during "pulsus irregularis perpetuus". The first human ECG depicting atrial fibrillation was published by Willem Einthoven (1860-1927) in 1906. The proof of a direct connection between absolute arrhythmia and auricular fibrillation was established by two Viennese physicians, Rothberger and Winterberg. The major discoveries relating to the pathomechanism and the clinical features of atrial fibrillation in the 20th century stemmed from the scientific activities of Karel Frederik Wenckebach, Sir Thomas Lewis, Gordon Moe and Maurits Allessie.

Atrial Fibrillation↗
PubMed2002

[Clinical proarrhythmias induced by anti-arrhythmic drugs, non-cardiovascular agents and implantable cardioverter-defibrillators].

The authors survey the electrophysiological mechanisms and clinical spectrum of the aggravation of cardiac arrhythmias provoked by antiarrhythmic drugs, non-cardiovascular agents and implantable cardioverter-defibrillators. The main aspects of the recognition, the differential diagnostics and the therapy are discussed. It is demonstrated that prevention of drug-induced arrhythmogenesis necessitates a fundamental understanding of the risk factors of proarrhythmias and of the clinical pharmacological properties of the drugs that are intended to be used, including proarrhythmic drug interactions. A systematic account is presented of those drugs prescribed in non-arrhythmic diseases which may lead to out-of-hospital cardiac arrest. The proarrhythmias that may be observed in recipients of implantable cardioverter-defibrillators are discussed, as are the undesirable interactions between these devices and antiarrhythmic drugs in such patients.

Anti-Arrhythmia Agents↗