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.