1 Introductıon
Atrial fibrillation (AF) is a supraventricular tachyarrhythmia resulting from the irregular activity of the atria and is characterized by the atrial mechanic functional loss [1]. The ventricular rate is variable and irregular depending on the conduction function of the atrioventricular node. On electrocardiogram, rapid, irregular, fibrillation waves of different shapes and sizes are seen instead of P waves [2].
In the developed countries, the prevalence of AF is estimated between 1.5-2% in the general population and the mean age of patients with this disease is steadily increasing. Today, the mean age of AF patients is between 75 and 85 years. This arrhythmia is associated with a five-fold increase in the risk of stroke, a three-fold increase in the incidence of congestive heart failure, and high mortality. Hospitalization is common among AF patients. This arrhythmia is an important cardiovascular problem in modern society and its medical, social and economical aspects will further worsen in the next decades [3]. AF usually starts as paroxysmal AF (PAF) and transforms into persistent AF [4]. The mechanism of PAF consists of initiating factors[5, 6].
Two main targets in AF treatment are protection against thromboembolic complications, and rate and/or rhythm control. Appropriate treatment methods to control the symptoms or prevent cardiomyopathy that may occur due to tachycardia are similar. The use of warfarin or new generation oral anticoagulants in eligible patients reduces the risk of stroke. Among two important studies comparing rhythm and rate control, in the randomized controlled AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) study no difference could be demonstrated between the two groups in terms of mortality and stroke from all causes [7]. In the RACE (Rate Control versus Electrical cardioversion for persistent atrial fibrillation) study, it was shown that rate control was not worse than rhythm control in the prevention of cardiovascular mortality and morbidity [8]. However, in the subgroup analysis of the RACE study, left ventricular function was shown to worsen less or even to improve in patients with heart failure and rhythm control with catheter ablation for AF [9, 10]. Long-term rhythm control can be achieved with antiarrhythmics or ablation. In a meta-analysis of studies investigating rhythm control in paroxysmal AF, ablation was shown to be superior over antiarrhythmics in ensuring and maintaining sinus rhythm [11, 12]. Ablation can be performed in patients who are symptomatic despite optimal medical therapy [13, 14].
Atrial fibrillation is thought to occur as a result of the combination of electrophysiological, metabolic, ischemic, hemodynamic, and genetic factors [15, 16]. Persistent AF causes electrical remodeling characterized by shortening of atrial refractoriness caused by changes in the expression of ion channels in the atria, contractile remodeling resulting in disruption of atrial contraction, and structural remodeling leading to changes in the cellular structure of atrial myocytes. All these changes affect each other, leading to continuity of the AF process [15]. While electrical activity foci in the pulmonary vein (PV) cause the development of AF, structural changes occurring in the left atrium due to chronic or recurrent AF cause remodeling lead to especially fibrosis and continuing rhythm disturbance [17, 18]. Atrial conduction time that can be easily measured simply by tissue Doppler echocardiography can give us an idea about the arrhythmogenic substrate changes that make AF sustained [19, 20].
The objective of this study was to evaluate the effect of PV electrical activity foci isolation treatment with RF ablation method on the left atrial arrhythmogenic substrate through tissue Doppler echocardiography and to investigate the structural remodeling process due to AF by the termination of electrical remodeling using RF ablation method.