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Atrial Remodeling (atrial + remodeling)

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Medical Sciences	100%

Selected Abstracts

Atrial Remodeling After Mitral Valve Surgery in Patients with Permanent Atrial Fibrillation

JOURNAL OF CARDIAC SURGERY, Issue 5 2004
Fernando Hornero M.D., Ph.D.
Mitral surgery allows an immediate surgical auricular remodeling and besides in those cases in which sinus rhythm is reached, it is followed by a late remodeling. The aim of this study is to investigate the process of postoperative auricular remodeling in patients with permanent atrial fibrillation undergoing mitral surgery. Methods: In a prospective randomized trial, 50 patients with permanent atrial fibrillation and dilated left atrium, submitted to surgical mitral repair, were divided into two groups: Group I contained 25 patients with left auricular reduction and mitral surgery, and Group II contained 25 patients with isolated valve surgery. Both groups were considered homogeneous in the preoperative assessment. Results: After a mean follow-up of 31 months, 46% of patients included in Group I versus 18% of patients included in Group II restarted sinus rhythm (p = 0.06). An auricular remodeling with size regression occurred in those patients who recovered from sinus rhythm, worthy of remark in Group II (,10.8% of left auricular volume reduction in Group I compared to ,21.5% in Group II; p < 0.05). A new atrial enlargement took place in those patients who remained with atrial fibrillation (+16.8% left auricular volume in Group I vs. +8.4% in Group II; p < 0.05). Conclusions: Mitral surgery produces an atrial postoperative volume that decrease especially when reduction techniques are employed. Late left atrial remodeling depended on the type of atrial rhythm and postoperative surgical volume. [source]

Is Atrial Remodeling a Viable Target for Prevention of Atrial Fibrillation Recurrence?

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2004
STANLEY NATTEL M.D.
[source]

Electrical Remodeling and Atrial Dilation During Atrial Tachycardia are Influenced by Ventricular Rate: Role of Developing Tachycardiomyopathy

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2001
BAS A. SCHOONDERWOERD M.D.
Atrial Remodeling in Tachycardiomyopathy. Introduction: Atrial fibrillation (AF) and congestive heart failure (CHF) are two clinical entities that often coincide. Our aim was to establish the influence of concomitant high ventricular rate and consequent development of CHF on electrical remodeling and dilation during atrial tachycardia. Methods and Results: A total of 14 goats was studied. Five goats were subjected to 3:1 AV pacing (A-paced group, atrial rate 240 beats/min, ventricular rate 80 beats/min). Nine goats were subjected to rapid 1:1 AV pacing (AV-paced group, atrial and ventricular rates 240 beats/min). During 4 weeks, right atrial (RA) and left ventricular (LV) diameters were measured during sinus rhythm. Atrial effective refractory periods (AERP) and inducibility of AF were assessed at three basic cycle lengths (BCL). After 4 weeks of rapid AV pacing, RA and LV diameters had increased to 151% and 113% of baseline, whereas after rapid atrial pacing alone, these parameters were unchanged. Right AERP (157 ± 10 msec vs 144 ± 16 msec at baseline with BCL of 400 msec in the A-paced and AV-paced group, respectively) initially decreased in both groups, reaching minimum values within 1 week. Subsequently, AERP partially recovered in AV-paced goats, whereas AERP remained short in A-paced goats (79 ± 7 msec vs 102 ± 12 msec after 4 weeks; P < 0.05). Left AERP demonstrated a similar time course. Inducibility of AF increased in both groups and reached a maximum during the first week in both groups, being 20% and 48% in the A-paced and AV-paced group, respectively. Conclusion: Nature and time course of atrial electrical remodeling and dilation during atrial tachycardia are influenced by concurrent high ventricular rate and consequent development of CHF. [source]

Reversal of Atrial Remodeling after Cardioversion of Persistent Atrial Fibrillation Measured with Magnetocardiography

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2009
MIKA LEHTO M.D.
Background: Atrial fibrillation (AF) causes electrical, functional, and structural changes in the atria. We examined electrophysiologic remodeling caused by AF and its reversal noninvasively by applying a new atrial signal analysis based on magnetocardiography (MCG). Methods: In 26 patients with persistent AF, MCG, signal-averaged electrocardiography (SAECG), and echocardiography were performed immediately after electrical cardioversion (CV), and repeated after 1 month in 15 patients who remained in sinus rhythm (SR). Twenty-four matched subjects without history of AF served as controls. P-wave duration (Pd) and dispersion (standard deviation of Pd values in individual channels) and root mean square amplitudes of the P wave over the last 40 ms portions (RMS40) were determined. Results: In MCG Pd was longer (122.8 ± 18.2 ms vs 101.5 ± 14.6 ms, P < 0.01) and RMS40 was higher (60.4 ± 28.2 vs 46.9 ± 19.1 fT) in AF patients immediately after CV as compared to the controls. In SAECG Pd dispersion was increased in AF patients. Mitral A-wave velocity and left atrial (LA) contraction were decreased and LA diameter was increased (all P < 0.01). After 1 month, Pd in MCG still remained longer and LA diameter greater (both P < 0.05), while RMS40 in MCG, Pd dispersion in SAECG, mitral A-wave velocity, and LA contraction were recovered. Conclusions: Magnetocardiographically detected atrial electrophysiologic alterations in persistent AF diminish rapidly although incompletely during maintained SR after CV. This might be related to the known early high and late lower, but still existent tendency to AF relapses. [source]

Atrial Remodeling After Mitral Valve Surgery in Patients with Permanent Atrial Fibrillation

Bepridil Reverses Atrial Electrical Remodeling and L-Type Calcium Channel Downregulation in a Canine Model of Persistent Atrial Tachycardia

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2007
KUNIHIRO NISHIDA M.D.
Introduction: This study tested whether bepridil, a multichannel blocker, would reverse electrical remodeling induced by persistent atrial tachycardia. Methods and Results: Fourteen dogs were subjected to rapid atrial pacing at 400 bpm for 6 weeks after atrioventricular block was created to control the ventricular rate. During the study period, seven dogs were given placebo for 6 weeks (Control group), and seven were given placebo for 3 weeks, followed by 3 weeks of bepridil (10 mg/kg/day, Bepridil group). The atrial effective refractory period (ERP) and the inducibility and duration of atrial fibrillation (AF) were determined on a weekly basis. After 6 weeks, expression of L-type calcium channel ,1C messenger ribonucleic acid (mRNA) was quantified by real-time reverse transcription-polymerase chain reaction. In the Control group, ERP was shortened and the inducibility and duration of AF increased through the 6-week period. In the Bepridil group, the same changes occurred during the first 3 weeks, but were gradually reversed with bepridil. After 6 weeks, ERP was longer, AF inducibility was lower, and AF duration was shorter in Bepridil group than in the Control group. Expression of ,1C mRNA was decreased by 64% in the Control group (P < 0.05 vs sham), but in the Bepridil group, it was not different compared with the sham dogs. As a whole group of dogs, ERP was positively correlated with ,1C mRNA expression. Conclusion: Bepridil reverses the electrophysiological consequences of atrial remodeling to some extent and L-type calcium channel downregulation in a canine model of atrial tachycardia. [source]

Reverse Electrical Remodeling of the Atria Post Cardioversion in Patients Who Remain in Sinus Rhythm Assessed by Signal Averaging of the P-Wave

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2007
NAGIB CHALFOUN M.D.
Objectives: This study was designed to determine whether the signal-averaged electrocardiogram of the P-wave (SAPW) is an independent predictor of recurrence of atrial fibrillation (AF) post cardioversion (CV), and to assess atrial remodeling using SAPW. Background: There are limited electrophysiologic data to predict the recurrence of AF post-CV. The electrical remodeling that occurs post-CV is poorly understood. Methods: Sixty-four patients with persistent AF undergoing CV were prospectively enrolled. SAPW parameters were measured the day of CV and repeated at 1 month. These SAPW parameters were compared to other baseline indices for the recurrence of AF. Results: Sixty patients (94%) had successful CV. At 1 month, 22 (37%) maintained sinus rhythm (SR). The SAPW total duration decreased significantly in those who remained in SR (159 ms ± 19 to 146 ms ± 17; P < 0.0001). Only the duration of AF (46 ± 50 days vs 147 ± 227 days, P = 0.03) and the presence of left ventricular hypertrophy (LVH, 12% vs 65%, P = 0.0006) were significantly associated with recurrence of AF. Atrial size strongly correlated with the SAPW duration in patients who remained in SR (R2= 0.67, P = 0.003) but not in those who returned to AF (R2= 0.11, P = 0.65). Conclusions: Atrial electrical reverse remodeling occurs in patients with AF who maintain SR post-CV. This remodeling is likely inversely related to the duration of AF and LVH. SAPW duration does not predict recurrence of AF post-CV. [source]

Evaluation of Atrial Thrombus Formation and Atrial Appendage Function in Patients with Pacemaker by Transesophageal Echocardiography

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2006
ABOLFATH ALIZADEH M.D.
Background: Physiologic pacing is claimed to be superior to ventricular pacing in as much as it entails lower risk of atrial fibrillation, stroke, and atrial remodeling. There are few data on the relation between atrioventricular (AV) synchrony and atrial clot formation. Utilizing transesophageal echocardiography (TEE), this study sought to evaluate the effect of AV synchrony loss on left atrial physiology, atrial stasis, and clot formation. Methods: We conducted a cross-sectional study on patients with both AV and ventricular pacing with left ventricular ejection fraction (LVEF) >30%. TEE enabled us to explore atrial and pacing leads thrombi and measure left atrial appendage (LAA) flow velocity Results: A total 72 patients (mean age, 65 ± 11.7) were enrolled in the study. The pacing mode was VVI in 53% and AV sequential in 47% of patients. LVEF (mean ± SD; %) was 53.3 ± 6.2% in ventricular pacing mode and 52.2 ± 6.6 in physiologic pacing mode. Thrombus formation on pacing lead (<10 mm in 97% of patients) was observed in 32% of all the patients (23% in patients with AV sequential pacing mode and 39% with VVI mode). Left atrial appendage flow velocity (LAA-FV) was significantly higher among the patients with AV sequential pacing mode (49.44 ± 18 cm/s vs 40.94 ± 19.4 cm/s, P value = 0.02). LAA-FV >40 cm/s was detected in 60% of the patients, 60% of whom were in physiologic mode. Left atrial size was significantly larger among the patients with VVI pacing mode (42.3 ± 2.3 mm vs 37.79 ± 4.5 mm, P = 0.001). Multivariate analysis showed no relation between LAA-FV and age, hypertension, diabetes mellitus, left atrial size, and left ventricular function. Only one patient had right atrial clot. There was no thrombus in the ventricles and atrial appendage. Conclusion: Long-term loss of AV synchrony induced by VVI pacing is associated with the impairment of LAA contraction. Thrombus formation in the LAA is not increased by VVI pacing in patients with relatively good left ventricular (LV) function and sinus rhythm. [source]

Electrophysiological Remodeling in Human Atrial Fibrillation

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 7p2 2003
DAVID R. VAN WAGONER
Atrial fibrillation (AF) is a progressive disease characterized by cumulative electrophysiological and structural remodeling of the atria. Cellular electrophysiological studies have revealed marked reductions in the densities of the L-type voltage-gated Ca2+ current, ICa,L, the transient outward K+ current, ITO, and the ultra-rapid delayed rectifier K+ current, IKur, in atrial myocytes from patients in persistent or permanent AF. The density of the muscarinic K+ current (IKACh) is also reduced, however the inward rectifier K+ current (IK1) density is increased. The net shortening or lengthening of the action potential is dependent on the balance between changes in inward and outward currents. The prominent reduction in ICa,L appears to be sufficient to explain the observed decreases in action potential duration and effective refractory period that are characteristic of the fibrillating atria. Earlier studies have shown that calcium overload and perturbations in calcium handling play prominent roles in AF induced atrial remodeling. More recently, we have shown that AF is associated with evidence of oxidative injury to atrial tissue, and suggested that oxidative stress may directly contribute to the pathophysiology of AF. It is anticipated that insights gleaned from mechanistic studies will facilitate the development of improved pharmacological approaches to treat AF and to prevent the progression of arrhythmia. (PACE 2003; 26[Pt. II]:1572,1575) [source]

Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001
RIK WILLEMS
WILLEMS, R. et al.: Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep Model. In different animal models rapid atrial stimulation led to a shortening and maladaptation to rate of the atrial effective refractory period (AERP). This atrial electrical remodeling resulted in an increased vulnerability to atrial fibrillation (AF). These experimental findings formed the rationale for a stringent pursuit of sinus rhythm in patients with AF, since this would prevent or reverse atrial remodeling. This study tested the hypothesis that a reduction of arrhythmia burden would lead to a decreased vulnerability for AF. Different rapid atrial pacing protocols in a sheep model were used. During 15 weeks, 13 animals were continuously rapid paced and 7 animals were intermittently burst-paced, resulting in rapid atrial activation during 100% versus 33 ± 4% of the time, respectively. In the continuously paced group, 77% of the animals developed sustained AF (i.e., >1 hour) versus only 29% in the burst-paced group (P < 0.05). However, there was no difference in mean AERP shortening over time, nor maximal AERP shortening per animal, between both protocols. Minimal AERP was 103 ± 5 ms in the continuously paced group and 107 ± 5 in the burst-paced group (P = NS). Significant changes could be identified in effect on P wave duration, AVN function, and atrial dilation. Conduction slowing was more pronounced in the continuously paced group with a maximal P wave duration of 136 ± 4 ms in this group versus 116 ± 5 in the burst-paced group (P < 0.05). In the continuously paced group, the right atrial area significantly increased from 2.5 ± 0.1 cm2 at baseline to 4.2 ± 0.2 cm2. In the burst-paced group there was no significant atrial dilatation (from 2.6 ± 0.1 to 2.8 ± 0.1 cm2). In conclusion, limiting atrial arrhythmia burden slowed the development of sustained AF in this sheep model. This was not mediated by a decreased influence on atrial refractoriness but seemed to be dependent on smaller changes in atrial conduction and dimensions. [source]

Effect of Obesity on P-Wave Parameters in a Chinese Population

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2010
Ph.D., Tong Liu M.D.
Objective: To study the association between obesity and P-wave duration and dispersion (Pd) in order to evaluate the potential risk for atrial fibrillation development in Chinese subjects using the definitions applied for Asian populations. Methods: The study population consisted of 40 obese (body mass index (BMI) , 25 Kg/m2, according to the World Health Organization classification for the Asian population) subjects and 20 age- and sex-matched normal weight controls. Maximum P-wave duration (Pmax), minimum P-wave duration (Pmin), and Pd were carefully measured using a 12-lead electrocardiogram, while the presence of interatrial block (IAB; P , 110 ms) was assessed. Results: There were no significant differences between the two groups regarding age, sex, history of hypertension or diabetes, and hyperlipidemia. Compared to controls, BMI, left atrial diameter (LAD), and interventricular septal thickness were increased, while Pmax (111.9 ± 9.3 vs 101.1 ± 6.0 ms, P < 0.01) and Pd (47.9 ± 9.3 vs 31.8 ± 6.9 ms, P < 0.01) were significantly prolonged in the obese group. Pmin was similar between the two groups. The prevalence of IAB was significantly greater in the obese subjects. Pearson's correlation analysis showed that there were positive correlations between Pd and BMI (r = 0.6, P < 0.001), as well as between Pd and LAD (r = 0.366, P < 0.05). Conclusion: Our data suggest that obesity is associated with increased Pmax and Pd, and increased prevalence of IAB, parameters that have been associated with atrial fibrillation. The correlation of these electrocardiogram parameters with LAD indicates an association between increased BMI and atrial remodeling in Asian subjects. Ann Noninvasive Electrocardiol 2010;15(3):259,263 [source]

Update on Atrial Fibrillation: Part I

CLINICAL CARDIOLOGY, Issue 2 2008
Irina Savelieva M.D.
Abstract Atrial fibrillation (AF) is an epidemic, affecting 1% to 1.5% of the population in the developed world. Projected data from the population-based studies suggest that the prevalence of AF will grow at least 3-fold by 2050. The health and economic burden imposed by AF and AF-related morbidity is enormous. Atrial fibrillation has a multiplicity of causes ranging from genetic to degenerative, but hypertension and heart failure are the commonest and epidemiologically most prevalent conditions associated with AF as both have been shown to create an arrhythmogenic substrate. Several theories emerged regarding the mechanism of AF, which can be combined into two groups: the single focus hypothesis and the multiple sources hypothesis. Several lines of evidence point to the relevance of both hypotheses to the mechanism of AF, probably with a different degree of involvement depending on the variety of AF (paroxysmal or persistent). Sustained AF alters electrophysiological and structural properties of the atrial myocardium such that the atria become more susceptible to the initiation and maintenance of the arrhythmia, a process known as atrial remodeling. Angiotensin II has been recognized as a key element in atrial remodeling in association with AF opening the possibility of exploitation of "upstream" therapies to prevent or delay atrial remodeling. The clinical significance of AF lies predominantly in a 5-fold increased risk of stroke. The limitations of warfarin prompted the development of new antithrombotic drugs, which include anticoagulants, such as direct oral thrombin inhibitors (dabigatran) and factor Xa inhibitors (rivaroxaban, apixaban). Novel mechanical approaches for the prevention of cardioembolic stroke have recently been evaluated: percutaneous left atrial appendage occluders, minimally invasive surgical isolation of the left atrial appendage, and implantation of carotid filtering devices. Copyright © 2008 Wiley Periodicals, Inc. [source]

Search for the Optimal Right Ventricular Pacing Site: Design and Implementation of Three Randomized Multicenter Clinical Trials

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2009
GERRY KAYE M.D.
Background: The optimal site to permanently pace the right ventricle (RV) has yet to be determined. To address this issue, three randomized prospective multicenter clinical trials are in progress comparing the long-term effects of RV apical versus septal pacing on left ventricular (LV) function. The three trials are Optimize RV Selective Site Pacing Clinical Trial (Optimize RV), Right Ventricular Apical and High Septal Pacing to Preserve Left Ventricular Function (Protect Pace), and Right Ventricular Apical versus Septal Pacing (RASP). Methods: Patients that require frequent or continuous ventricular pacing are randomized to RV apical or septal pacing. Optimize RV excludes patients with LV ejection fraction <40% prior to implantation, whereas the other trials include patients regardless of baseline LV systolic function. The RV septal lead is positioned in the mid-septum in Optimize RV, the high septum in Protect Pace, and the mid-septal inflow tract in RASP. Lead position is confirmed by fluoroscopy in two planes and adjudicated by a blinded panel. The combined trials will follow approximately 800 patients for up to 3 years. Results: The primary outcome in each trial is LV ejection fraction evaluated by radionuclide ventriculography or echocardiography. Secondary outcomes include echo-based measurements of ventricular/atrial remodeling, 6-minute hall walk distance, brain natriuretic peptide levels, and clinical events (atrial tachyarrhythmias, heart failure, stroke, or death). Conclusion: These selective site ventricular pacing trials should provide evidence of the importance of RV pacing site in the long-term preservation of LV function in patients that require ventricular pacing and help to clarify the optimal RV pacing site. [source]