Introduction:
Atrial fibrillation is an arrhythmic consequence of multiple pathological processes leading to functional and structural changes in the atrial muscle [1, 2]. Among the major pathologies leading to this arrhythmia are hypertension, coronary artery disease and subsequent heart failure play the major role. Less frequently recently are acquired heart defects and hyperthyroidism, which also promotes atrial fibrillation [3, 4]. Despite treating both atria as a substrate of atrial fibrillation, it is clinically assumed that this arrhythmia occurs mainly due to left atrial pathologies - primarily due to the higher workload it needs to cope with as a consequence of the higher left ventricular resistance. These diseases cause changes in the structure of the atrial muscle through death and apoptosis of cardiomyocytes, contributing to stromal fibrosis. This affects generation of arrhythmia foci, local potential fragmentation and possible re-entry loops. However, the main consequence visible in echocardiography is the left atrial enlargement. This is also the result of an increase in left ventricular filling pressure as well as organic and functional mitral valve regurgitation.
Furthermore, atrial fibrillation is caused by other arrhythmias such as multiple atrial extrasystole, atrial focal tachycardia or atrial flutter [5, 6, 7]. Their constant duration or paroxysm lead to electrophysiological changes in the action potential, usually a shortening of the refractory period, the local intensity of which may be different. This is manifested by heterogeneity of the repolarization process. Repolarization disorders lead to functional conduction disturbances, which, superimposed on structural changes and conduction slowing associated with cardiomyocyte depletion, intensify the re-entry phenomenon and promote the maintenance and persistence of arrhythmias. The described pathologies have an impact on the electrocardiographic picture of the atrial muscle depolarization, depicted by the P wave of the electrocardiogram. With the duration and progression of functional and structural changes, the duration of the P wave prolongs, making it a risk factor for atrial fibrillation [8].
An interesting and clinically important issue is the positive relationship between atrial fibrillation paroxysm and the tendency of the arrhythmia to persist, which was reflected in the term “AF begets AF” created by Wijffels et al. [9]. Rapid atrial arrhythmias affect the functional changes in the process of atrial muscular repolarization and, above all, induce heterogeneity of refraction duration by the formation of local blocks and slow conduction zones [10]. In addition, atrial fibrillation episodes lead to left atrial enlargement, most likely due to an increase in filling pressure but also due to blood retention and functional mitral regurgitation. All the processes described cause that with time the paroxysmal AF becomes persistent, and finally the decision is made to leave the arrhythmia in a permanent form [4, 10, 11].
All the issues mentioned, indicate the necessity of complex systemic treatment and prevention of AF paroxysms. An important aspect is to reduce the duration of individual episodes using pharmacological or electrical conversion to sinus rhythm. Prolonged arrhythmia paroxysms lead to a deepening of functional and anatomical changes; hence it is likely that patients with persistent atrial fibrillation after sinus rhythm restoration have a longer duration of the P wave compared to patients with paroxysmal form of the arrhythmia.