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.