%0 Journal Article
%T Recent Clinical and Experimental Advances in Atrial Fibrillation
%A Shigeru Miyagawa
%A Taichi Sakaguchi
%A Hiroyuki Nishi
%A Yasushi Yoshikawa
%A Satsuki Fukushima
%A Shunsuke Saito
%A Yoshiki Sawa
%J ISRN Cardiology
%D 2011
%R 10.5402/2011/958189
%X Atrial fibrillation (AF) is the most common arrhythmia in clinical settings (Fuster et al., 2001), and it is often associated with congestive heart diseases (Issac et al., 2007). Many studies in both laboratory and clinical settings have sought to analyze the mechanisms of AF, develop treatments based on these mechanisms, and examine atrial remodeling in chronic AF. The aim of this paper is to analyze recent findings regarding the atrial remodeling that occurs in AF. In particular, we will describe the electrical and structural changes that involve atrial myocytes and the extracellular matrix. We will also describe the general classification and basic pathophysiology of AF and its surgical treatments. 1. Classification of AF The joint American College of Cardiology/American Heart Association/European Society of Cardiology proposed a classification system for AF to simplify its heterogeneous clinical aspects and clarify its clinical states [1]. Patients are initially classified as having a ˇ°first detected episode of AF,ˇ± when AF is confirmed by clinicians. If a patient has two or more episodes, the AF is classified as recurrent. Recurrent AF is designated as paroxysmal or persistent. Paroxysmal AF is an episode that generally continues for 7 or fewer days and terminates on its own. Persistent AF usually continues for more than 7 days without self-terminating and requires clinicians to terminate it using pharmacological treatment or electrical cardioversion to restore the sinus rhythm. Permanent AF is a situation in which the sinus rhythm cannot be sustained after cardioversion, and further medical efforts are required to restore it. 2. Pathophysiology of AF 2.1. The Basic Mechanisms of AF Many researchers agree that inflammation [2], neurohormonal disorders [3], cardiovascular diseases such as valvular diseases [4], diabetes, hypertension, congestive heart failure, myocardial infarction [5], and genetic factors [6] are ˇ°modulating factorsˇ± that can induce AF. Classically, AF mechanisms are described by the concept of atrial ectopic foci [7], which fire spontaneously in the atrium, a single reentry circuit, or multiple reentry circuits [8, 9]. The surgical maze procedure is designed to block the multiple reentry circuits and create an isolated electrical lesion in the atrium [10]. Haissaguerre et al. reported that triggers located in the pulmonary veins initiate most cases of paroxysmal AF [7], while in some cases the trigger, such as a venous remnant in the left atrium (LA) and superior vena cavae, occurs outside the pulmonary vein. This finding supports
%U http://www.hindawi.com/journals/isrn.cardiology/2011/958189/