Introduction
Atrial fibrillation (AF), being one of the most frequent types of
arrhythmia in clinical practice, affects the course of chronic heart
failure (CHF). Patients with both CHF and AF have poor prognosis,
including higher mortality regardless of the parameters of the LV
ejection fraction (LV EF) [1, 2]. The fact that AF often develops in
many patients with CHF is due to common risk factors and similar
pathophysiological mechanisms [3] including cardiac structural
remodeling, activation of neurohormonal mechanisms, and impairment of
the left ventricular function during ventricular flutter.
Drug and non-drug approaches to the management of patients are applied
today in order to reduce the frequency of atrial fibrillation or
to restore sinus rhythm [4]. However, there is a view that an
obvious beneficial effect of sinus rhythm maintenance with the use of
antiarrhythmic drugs is annihilated by unfavorable and often fatal
results, namely a 49% increase in mortality risk [5]. The non-drug
approach to managing patients with AF is radiofrequency ablation (RFA).
The sinus rhythm is successfully maintained in 20-80% of patients
within a year after RFA [6, 7]. Despite the development of the RFA
technique, the relapse of rhythm breakdown [8, 9] indicates the
necessity of detecting the mechanisms that promote the relapse.
An increased left atrial size is a well-established, independent
predictor of AF [10, 11]. Atrial remodeling is associated with
slower and more heterogeneous atrial conduction and increased PV firing.
Paroxysmal forms show a predominance of local triggers/drivers,
particularly from pulmonary veins (PVs) [12]. As AF becomes more
persistent and eventually permanent, reentry substrates (initially
functional and then structural) predominate. It is known that 90% of
paroxysmal AFs are driven by PV sources and respond well to PV-directed
ablation procedures; as AF progresses, atrial substrates become more
complicated and require more complex ablation procedures [4].
Research objective : The aim is to study the features of the
remodeling of the left atrium and pulmonary veins in CHF patients with
paroxysmal AF, with permanent AF, and without arrhythmia.
Materials and methods . The study retrospectively recruited 299
patients with chronic heart failure of the II-III New York Heart
Association (NYHA) functional classes and 132 practically healthy people
aged 35.08±1.80 (control group), examined in Klinika Uralskaya, LLC
(Ekaterinburg, Russia). Patients with CHF were divided into three
groups: group 1 (n=225) included patients with chronic heart failure
without atrial fibrillation; group 2 (n=38) consisted of patients having
chronic heart failure with paroxysmal atrial fibrillation; group 3
(n=36) was represented by patients having chronic heart failure with
permanent atrial fibrillation. Chronic heart failure was diagnosed in
accordance with the latest recommendations on CHF diagnostics [13].
Transthoracic echocardiography was recorded using a Philips HD-15 device
(USA) according to the standard protocol with the additional
determination of the maximum and minimum diameters of the visualized
pulmonary vein in order to diagnose pulmonary venous
hypertension [14]. The informed consent for research was obtained
from all the patients. All the patients gave a written consent for
participation in the study, which was approved by the local ethic
committee of the Institute of Medical Cell Technologies (Ekaterinburg,
Russia).
The investigation results were statistically processed according to the
Student’s criterion in connection with the normal data distribution with
the use of the Microsoft Excel spreadsheet program. Consistency with the
normal distribution was checked by the visualization method and the
Pearson test of fit. The differences were considered statistically
significant at p<0.05. The data is presented as M±m, where M
is the average of the measured values and m is the error.