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.