Recurrence of Atrial Fibrillation After Internal Cardioversion of Persistent Atrial Fibrillation Prognostic Importance of Electrophysiologic Parameters

Abstract

trial fibrillation (AF) is the most common cardiac arrhythmia, and its prevalence increases with age. 1 AF may cause symptoms of disability, increase the risk of thromboembolic events and is related to increased mortality. 2,3 The general treatment strategy for persistent AF (PAF) is the restoration and maintenance of sinus rhythm (SR). Whether this approach is superior to anticoagulation therapy and heart rate control remains controversial, 4,5 which increases the necessity to predict successful cardioversion and to maintain SR after successful cardioversion. Internal atrial cardioversion (IACV) is a useful technique for restoring SR in patients for whom external electrical cardioversion is unsuccessful or who have PAF of long duration; efficacy ranges from 70% to 90%. 6,7 Once cardioversion is successful, long-term maintenance of SR is the main treatment goal. Unfortunately, despite the use of antiarrhythmic drugs and serial cardioversions, the incidence of AF recurrence ranges from 40% to 50% in the first year. [8][9][10] It has been shown that recurrence of AF relates to atrial electrophysiologic properties. Recent animal studies have shown that AF results in a marked shortening of the atrial effective refractory period (ERP) or monophasic action potential (MAP) and loss of its physiological ability to adapt to rate. 11-13 These phenomena have been implicated in the self-perpetuation of AF or its early recurrence. Furthermore, the filtered P-wave duration (FPD), as a measure of the intra-atrial conduction time, has also been shown to be related to AF recurrence. 14-16 However, these data alone do not adequately clarify the relationship between atrial electrical remodeling and AF recurrence during short-and long-term follow-up (from 3 to 12 months of follow-up) in humans. Thus, we investigated the extent of atrial remodeling (atrial MAP duration (MAPD), its rate adaptation and FPD) and its relation to the recurrence of AF after cardioversion in patients with PAF. Methods PatientsConsecutive patients with sustained nonvalvular AF in whom the arrhythmia persisted for at least 2 months were considered for the study. The study protocol was approved by the institute's Committee of Human Subject Research. Signed written informed consent was obtained from all study patients before they underwent an IACV and electrophysiologic evaluation performed after antiarrhythmic drug washout period of at least 5 half-lives (37 men, 10 women, mean age 59.9±11.9 years). The patients were Background The purpose of this study was to determine whether the extent of atrial electrical remodeling affects the recurrence of atrial fibrillation (AF) after cardioversion of persistent AF (PAF). Methods and ResultsInternal atrial cardioversion was performed in 47 patients with PAF. The right atrial monophasic action potential duration (RA-MAPD) at pacing cycle lengths (PCLs) of 800-300 ms and P wave signal-averaged electrocardiogram were recorded after cardioversion. Bepridil (150-200 mg/day) and carvedilol (10 mg/day) were administered to a...

Electrophysiological Properties of the Atrium After Cardioversion of Chronic Atrial Fibrillation Relation to the Plasma Brain Natriuretic Peptide Level

“…24,25) In fact, BNP levels have previously been shown to increase in the presence of AF despite the absence of heart failure. [5][6][7][8] Lee, et al 7) concluded that BNP levels were found to be significantly correlated with the left atrial volume index and tissue Doppler-derived E/E' (as an indicator of diastolic function) in patients with lone AF after adjusting for clinical and echocardiographic variables. McCullough, et al 8) showed that elevated BNP levels in patients with AF reflect chronic changes in ventricular filling dynamics and wall tension, which are independent of ejection fraction.…”

“…[1][2][3][4] However, a recent study demonstrated that BNP levels were significantly elevated in outpatients with atrial fibrillation (AF) (median value, 131 pg/ mL) as compared to outpatients without AF (median value, 49 pg/mL; P < 0.001) despite a similar left ventricular ejection fraction (60% versus 60%, P = 0.85). [5][6][7][8] Although the pathophysiology of elevated BNP levels in AF patients has not been fully proven, this may be associated with a functional latent ventricular dysfunction such as an unfavorable hemodynamic profile or altered left ventricular filling pattern resulting from an atrial structural dysfunction. 7,8) However, the electrophysiologic consequences of the elevated BNP level in AF patients are not well known.…”

“…Verifying this relationship may reinforce the explanation for the mechanism of the elevated BNP level in AF patients or provide further insight into the electrophysiology of the human atria in AF. 5,[10][11][12][13][14][15][16][17][18][19][20][21] The present study, therefore, was designed to assess the relationship between the atrial action potential duration (APD), filtered P-wave duration (FPD) measured by the signal-averaged electrocardiogram, and plasma BNP levels in patients with chronic AF who had no history of a heart failure diagnosis or no symptoms suggestive of heart failure at the time of their recruitment.…”

Rate-Dependent Electrophysiologic Effects of the Class III Antiarrhythmic Drugs Nifekalant, Amiodarone, and Ibutilide on the Atrium in Patients With Persistent Atrial Fibrillation

“…10,[12][13][14] This AF-induced shortening of atrial action potential results from downregulation of a number of ionic currents (electrical remodeling). The L-type Ca 2+ (I ca, L ) current, the transient outward current (I to ), and the ultrarapid delayed rectifier current (I Kur ) are reduced after prolonged rapid atrial pacing or AF.…”

“…However, atrial MAPD and ERP in patients with persistent AF show rate-dependent shortening. [12][13][14]18) Therefore, some differences may exist in the electrophysiologic effects of various class III antiarrhythmic drugs on the remodeled atrium.…”