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.