New Causes and Predictors for the Development of Atrial Fibrillation and Its Complications

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia and its prevalence increases with aging of the population. It is reflected in the ECG recording by the replacement of regular P-waves by an undulating baseline and irregular ventricular complexes [2]. The uncoordinated atrial activity prevents effective atrial contraction, leading to clot formation. Atrial fibrillation contributes significantly to population morbidity and mortality, and presently available therapeutic approaches have major limitations, including limited efficacy and potentially serious side effects. It can be classified into one of the three following categories:

1. Paroxysmal: self-termination within 7 days
2. Persistent: requires termination by pharmacological or direct-current electric cardioversion
3. Permanent: restoration to sinus rhythm is impossible or inadvisable

It is believed that in many cases the natural history of AF involves evolution from paroxysmal to persistent to permanent forms through the influence of atrial remodeling caused by the arrhythmia itself and/or progression of underlying heart disease. As many underlying conditions contribute to the development and progression of AF, the full and exact mechanisms standing behind this common arrhythmia are not completely or sufficiently understood.

Thromboembolism is by far the most important complication of AF, and the most common factor in stroke in the elderly. The determinants of Virchow triad, including stasis, endothelial damage, and coagulation properties, are centrally involved in AF- related thrombus formation.

Hence, thorough searching for new possible causes or contributing factors for the developing and progression of AF and its most threatening complication, thromboembolism, is mandatory

The aim of the study is to look for new possible causes of atrial fibrillation and its complications.