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Human Atrial Fibrillation (human + atrial_fibrillation)

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Medical Sciences100%

Selected Abstracts

Characterization of the Electroanatomical Substrate in Human Atrial Fibrillation: The Relationship between Changes in Atrial Volume, Refractoriness, Wavefront Propagation Velocities, and AF Burden

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2007
PIPIN KOJODJOJO M.R.C.P.
Introduction: Progressive remodeling occurs in experimental models of AF whereby slowing of conduction, shortening of refractoriness, and atrial dilatation are associated with an increased vulnerability to atrial fibrillation (AF). This study investigates the relative changes in atrial geometry and electrophysiology with increasing AF burden in humans. Methods and Results: Patients undergoing ablation of AF or left-sided accessory pathways were recruited. Atrial volumes were determined by echocardiography. Wavefront propagation velocities (WPV), specifically in the direction of activation, were calculated from pre-ablation activation (CartoÔ) maps of both atria. Dispersion, adaptation of, and effective refractoriness (ERP) were measured at 3 sites. A composite arrhythmogenic index (Atrial Volume/WPV × ERP) was derived to compare the degree of electroanatomical remodeling with AF burden. Fifty-nine patients (22 paroxysmal AF, 19 recurrent persistent AF, and 18 controls) were recruited. AF subjects had slower right atrial WPV (P = 0.01), but no difference in left atrial WPV compared with controls. ERP was reduced globally (P < 0.05), with increased dispersion (P < 0.05). WPV and ERP did not distinguish between patients with paroxysmal or persistent AF. Biatrial volumes were greater only in patients with persistent AF (P < 0.01). There was a stepwise increase in the AI with increasing AF burden (P < 0.0001). Conclusion: An arrhythmogenic substrate exists in human AF, characterized by globally decreased refractoriness with greater dispersion, slower right atrial conduction, and atrial dilatation. Persistence of AF is not accompanied by any further electrical remodeling, but only atrial dilatation. The degree of electroanatomical remodeling is associated with the clinical pattern of AF. [source]

Relationship Between Connexins and Atrial Activation During Human Atrial Fibrillation

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2004
M.R.C.P., PRAPA KANAGARATNAM Ph.D.
Introduction: Gap junctional connexin proteins (connexin40 [Cx40], connexin43 [Cx43]) are a determinant of myocardial conduction and are implicated in the development of atrial fibrillation (AF). We hypothesized that atrial activation pattern during AF is related to connexin expression and that this relationship is altered by AF-induced remodeling in the fibrillating atria of chronic AF. Methods and Results: Isochronal activation mapping was performed during cardiac surgery on the right atria of patients in chronic AF (n = 13) using an epicardial electrode array. The atrial activation pattern was categorized using a complexity score based on the number of propagating wavefronts of activation and by grouping atria into those capable of uniform planar activation (simple) and those that were not (complex). The activation pattern was correlated with the levels of Cx43 and Cx40 signal measured by immunoconfocal quantification of biopsies from the mapped region. We studied the impact of electrical remodeling by comparing these findings with the unremodeled atria of patients in sinus rhythm during pacing-induced sustained AF (n = 17). In chronic AF, atria with complex activation had lower Cx40 signal than atria showing simple activation (0.013 ± 0.006 ,m2/,m2 vs 0.027 ± 0.009 ,m2/,m2, P < 0.02), with the relative connexin signal (Cx40/Cx40+Cx43) correlating with complexity score (P = 0.01, r =,0.74). This relationship did not occur in the unremodeled atria, and increased heterogeneity of distribution of Cx40 labeling in chronic AF was the only evidence of connexin remodeling that we detected in the overall group. Conclusion: The pattern of atrial activation is related to immunoconfocal connexin signal only in the fully remodeled atria of chronic AF. This suggests that intercellular coupling and pattern of atrial activation are interrelated, but only in conjunction with the remodeling of atrial electrophysiology that occurs in chronic AF. (J Cardiovasc Electrophysiol, Vol. 15, pp. 206-213, February 2004) [source]

Centrifugal Gradients of Rate and Organization in Human Atrial Fibrillation

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2009
DAVID E. KRUMMEN M.D.
Introduction:Animal studies show that atrial fibrillation (AF) may emanate from sites of high rate and regularity, with fibrillatory conduction to adjacent areas. We used simultaneous mapping to find evidence for potential drivers in human AF defined as sites with higher rate and regularity than surrounding tissue. Materials and Methods:In 24 patients (age 61 ± 10 years; 12 persistent), we recorded AF simultaneously from 32 left atrial bipolar basket electrodes in addition to pulmonary veins (PV), coronary sinus, and right atrial electrodes. We measured AF cycle length (CL) by Fourier transform and electrogram regularity at each electrode, referenced to patient-specific atrial anatomy. Results:We analyzed 10,298 electrode-periods. Evidence for potential AF drivers was found in 11 patients (five persistent). In persistent AF, these sites lay at the coronary sinus and left atrial roof but not PVs, while in paroxysmal AF six of nine sites lay at PVs (P < 0.05). During ablation, a subset of patients experienced AF CL prolongation or termination with a focal lesion; in each case this lesion mapped to potential driver sites on blinded analysis. Conversely, sequential mapping failed to reveal these sites, possibly due to fluctuations in dominant frequency at driver locations in the context of migratory AF. Conclusions:Simultaneous multisite recordings in human AF reveal evidence for drivers that lie near PVs in paroxysmal but not persistent AF, and were sites where ablation slowed or terminated AF in a subset of patients. The future work should determine if real-time ablation of AF-maintaining regions defined in this fashion eliminates AF. [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]

Pilot Study: Noninvasive Monitoring of Oral Flecainide's Effects on Atrial Electrophysiology during Persistent Human Atrial Fibrillation Using the Surface Electrocardiogram

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2005
Daniela Husser M.D.
Background: The relation between flecainide's plasma level and its influence on human atrial electrophysiology during acute and maintenance therapy of atrial fibrillation (AF) is unknown. Therefore, this study determined flecainide plasma levels and atrial fibrillatory rate obtained from the surface ECG during initiation and early maintenance of oral flecainide in patients with persistent lone AF and assessed their relationship. Methods and Results: In 10 patients (5 males, mean age 63 ± 14 years, left atrial diameter 46 ± 3 mm) with persistent lone AF, flecainide was administered as a single oral bolus (day 1) followed by 200,400 mg/day (days 2,5). The initial 300 mg flecainide bolus resulted in therapeutic plasma levels in all patients (range 288,629 ng/ml) with no side effects. Flecainide plasma levels increased on day 3 and remained stable thereafter. Day 5 plasma levels were lower (508 ± 135 vs 974 ± 276 ng/ml, P = 0.009) in patients with daily mean flecainide doses of 200 mg compared to patients with higher maintenance doses. Fibrillatory rate obtained from the surface electrocardiogram measuring 378 ± 17 fpm at baseline was reduced to 270 ± 18 fpm (P < 0.001) after the flecainide bolus but remained stable thereafter. Fibrillatory rate reduction was independent of flecainide plasma levels or clinical variables. Conclusion: A 300 mg oral flecainide bolus is associated with electrophysiologic effects that are not increased during early maintenance therapy in persistent human lone AF. In contrast to drug plasma levels, serial analysis of fibrillatory rate allows monitoring of individual drug effects on atrial electrophysiology. [source]