[Old and new oral anticoagulants in the management of atrial fibrillation. Hungarian data]. / Régi és új orális antikoagulánsok hazai alkalmazása pitvarfibrillációban.

INTRODUCTION: Despite a progress in the management of patients with atrial fibrillation this arrhythmia is one of the major causes of stroke, heart failure, sudden death and cardiovascular morbidity. Oral anticoagulation with vitamin K antagonist or non-vitamin K antagonist markedly reduces stroke and mortality in atrial fibrillation patients. AIM: To estimate the real-life vitamin K antagonist and non-vitamin K antagonist oral anticoagulant treatment in past years in Hungary. METHOD: Analysis of the National Health Insurance Administation database for atrial fibrillation (BNO: I48) between 2010-2015. We assumed that AF patient would turn to health care provides at least once either as inpatients or outpatients in a 5-year period. The patient was accepted as adherent after 6 months therapy and at least 80% oral anticoagulant prescription. RESULTS: The prevalence of AF in Hungary is 3%. The mortality rate of AF 7%-10% per year. The adherence of the old oral anticoagulant treatment was 55%, but it was 69% among patient treated by "new" oral anticoagulant treatment. However, one third of the patients are not treated by effective old or new oral anticoagulant treatment. CONCLUSIONS: We need more effort to improve the effective and high adherence oral anticoagulant therapy in our country. Orv Hetil. 2017; 158(39): 1545-1549.

Modulation of conductive elements by Pitx2 and their impact on atrial arrhythmogenesis.

The development of the heart is a complex process during which different cell types progressively contribute to shape a four-chambered pumping organ. Over the last decades, our understanding of the specification and transcriptional regulation of cardiac development has been greatly augmented as has our understanding of the functional bases of cardiac electrophysiology during embryogenesis. The nascent heart gradually acquires distinct cellular and functional characteristics, such as the formation of contractile structures, the development of conductive capabilities, and soon thereafter the co-ordinated conduction of the electrical impulse, in order to fulfil its functional properties. Over the last decade, we have learnt about the consequences of impairing cardiac morphogenesis, which in many cases leads to congenital heart defects; however, we are not yet aware of the consequences of impairing electrical function during cardiogenesis. The most prevalent cardiac arrhythmia is atrial fibrillation (AF), although its genetic aetiology remains rather elusive. Recent genome-wide association studies have identified several genetic variants highly associated with AF. Among them are genetic variants located on chromosome 4q25 adjacent to PITX2, a transcription factor known to play a critical role in left-right asymmetry and cardiogenesis. Here, we review new insights into the cellular and molecular links between PITX2 and AF.

Developmental and genetic aspects of atrial fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia encountered in clinical practice. The abnormal rhythm is associated not only with a variety of symptoms, such as palpitations, dizziness, or shortness of breath, but also with increased risk of stroke, heart failure, and mortality. A genetic predisposition is suggested by the fact that the relative risk for the development of AF is estimated at 85% in individuals with at least one parent with a history of AF. Current therapeutic strategies include control of rate or rhythm with medication and catheter ablation procedures. Especially in the pathophysiology of paroxysmal AF, ectopic electrical activity originating in the myocardial sleeves surrounding the pulmonary veins is considered causal. In these cases, ablation is applied to isolate the pulmonary venous myocardium from the remainder of the left atrial myocardium. Other recent evidence has shown that genetic and developmental defects can be involved in the development of AF. In this review, it is our aim to discuss the possible underlying causes of AF from a combined genetic and cardiac developmental view.

Atrial electrical and structural abnormalities in an ovine model of chronic blood pressure elevation after prenatal corticosteroid exposure: implications for development of atrial fibrillation.

AIMS: Elevated blood pressure (EBP) is the most prevalent and potentially modifiable risk factor for AF, yet little is known of its atrial effects. We aimed to characterize the atrial electrical and structural changes in a chronic ovine model of EBP after prenatal corticosteroid exposure. METHODS AND RESULTS: Twelve sheep with chronically EBP (mean arterial pressure 94+/-3 mmHg) and six controls (71+/-4 mmHg, P<0.01) underwent acute open chest electrophysiologic and pathologic studies. We measured refractoriness at the atrial appendages at 3 cycle lengths (CL); conduction velocities at Bachmann's bundle, both atrial appendages and free walls at 4 CLs; conduction heterogeneity; atrial wavelength and AF duration. We performed light microscopy (LM) and electron microscopy (EM) and collagen and apoptosis studies. EBP was associated with widespread conduction abnormalities, shortening of atrial wavelength, and increased AF. There was no significant change in refractoriness. LM demonstrated atrial myocyte hypertrophy and myolysis in all EBP sheep and focal scarring in six. EM demonstrated mitochondrial and nuclear enlargement and increased collagen fibrils in EBP sheep, findings not present in any controls. Atrial collagen and apoptosis were increased in EBP animals. CONCLUSION: This study demonstrates that chronically, EBP is associated with significant atrial electrical and structural remodelling. These changes may explain the increased propensity to atrial arrhythmias observed with long-standing EBP.

[Fetal supraventricular tachycardia associated with anasarca: poor prognosis despite treatment. Apropos of two cases]. / Tachycardies supraventriculaires foetales avec anasarque: mauvais pronostic malgré le traitement. A propos de deux cas.

Two cases of foetal supraventricular tachycardia with hydrops with fatal outcomes illustrate the poor general prognosis of this condition. The absence of therapeutic consensus, of large series in the existing literature, does not prevent logical and reasonable management based on rhythmological, pharmacological and prognostic criteria. A combined approach associating antiarrhythmic therapy by the transplacental and intrafunicular approaches seems acceptable now that funicular puncture can be undertaken easily, and certain antiarrhythmic molecules suggest encouraging results. It is important to try to assess the haemodynamic tolerance by foetal Doppler echocardiography because the foetal prognosis depends on ischaemic cerebral lesions induced by anoxia, difficult to diagnose in utero: when observed, aggressive and occasionally dangerous therapies to foetus and mother may be justified in these extreme situations of foetoplacental hydrops.