Discussion.
The study of myocardial remodeling in the patients with chronic heart
failure without arrhythmia and those having paroxysmal or permanent
atrial fibrillation has shown structural changes in the heart, as
compared to the control group, in the form of the increased wall
thickness of both ventricles, increased myocardium mass index,
dilatation of both atria, the increased maximum and minimum diameters of
the left lower pulmonary vein, and elevated systolic pressure in the
pulmonary artery. The structural changes in the heart were the same in
each group regardless of the presence or absence of arrhythmia.
The study of myocardial remodeling in the patients with chronic heart
failure having atrial fibrillation has shown more evident structural
impairments of the heart walls and chambers as compared to those in the
patients without arrhythmia; this manifested itself in a more pronounced
dilatation of the left atrium, with a pulmonary vein flowing into it.
According to other researchers, PVs are critical in AF initiation and
maintenance [15].
The study of myocardial remodeling in the patients with chronic heart
failure having permanent atrial fibrillation has shown more evident
structural impairments of the heart chambers and hemodynamics as
compared to those in the patients having paroxysmal atrial fibrillation;
this manifested itself in a more pronounced dilatation of the left
atrium, with a pulmonary vein flowing into it, the value of the average
E/e’ ratio being higher. Besides, the CHF patients with permanent AF had
a dilatation of the right atrium with greater hypertrophy of the RV
inferolateral wall, together with increased systolic pressure in the
pulmonary artery and the RV systolic dysfunction estimated according to
TAPSE. Both the left atrium and the right atrium possess structural
features contributing to the pathogenesis of AF [16].
Thus, the CVD patients with CHF have left atrial dilatation with
dilatation of pulmonary veins as distinct from the control group.
Paroxysmal AF in the patients with CHF is likely to associate due to the
further myocardial remodeling of the atria in the form of an even
greater dilatation of the left atrium and pulmonary veins flowing into
it. The maximum atrial volumes and pulmonary vein diameters have been
detected in the patients having CHF and permanent AF.
Besides, the obtained results confirm that AF evolves from paroxysmal to
persistent and permanent forms through the influence of atrial
remodeling progression caused by arrhythmia [17, 18].
Remodeling-induced atrial dilatation promotes AF by increasing circuit
path space, so that larger reentry circuits can be supported and/or a
larger number of circuits can be maintained [17]. The study included
1,219 patients with paroxysmal AF. Progression of AF occurred in 178
(15%) patients.
Multivariate
analysis has shown that heart failure, age, previous
transient
ischemic attack or stroke,
chronic
obstructive pulmonary disease, and hypertension are the only
independent predictors of AF progression. The factors known to cause
atrial structural remodeling (age and underlying heart disease) are
independent predictors of AF progression. With consideration of the
nature of these factors and in view of the fact that they are associated
with future cardiovascular events, researchers conjecture that
structural rather than electrical remodeling of the
atria
is involved in AF progression [18]. Underlying diseases might cause
chronic stretch and atrial dilatation, which seem to be important
stimuli for chronic atrial structural remodeling (cellular hypertrophy,
fibroblast
proliferation, and tissue fibrosis), and this enables the maintenance of
AF [19].
Conclusion. Thus, more significant dilatation of the left
atrium with pulmonary veins flowing into it, with their increasing
dilatation in the association of paroxysmal AF and its transition into
permanent AF has been detected in patients with chronic heart failure
having atrial fibrillation.