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Electrical Remodeling (electrical + remodeling)

Distribution by Scientific Domains

Medical Sciences	100%

Kinds of Electrical Remodeling

atrial electrical remodeling

Selected Abstracts

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]

Inhibitors of the Na+/H+ Exchanger Cannot Prevent Atrial Electrical Remodeling in the Goat

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2004
YURI BLAAUW M.D.
Introduction: It has been suggested that blockade of the Na+/H+ exchanger (NHE1) can prevent atrial fibrillation (AF)-induced electrical remodeling and the development of AF. Methods and Results: AF was maintained by burst pacing in 10 chronically instrumented conscious goats. Intravenous and oral dosages of two NHE1 blockers (EMD87580 and EMD125021) resulted in plasma levels several magnitudes higher than required for effective NHE1 blockade. Shortening of atrial refractoriness immediately after 5 minutes of AF was not prevented by NHE1 blockade. In remodeled atria, increasing dosages of EMD87580 and EMD125021 did not reverse shortening of the atrial refractory period or reduce the duration of AF episodes. The cycle length during persistent AF also was not affected. Oral pretreatment with EMD87580 (8 mg/kg bid) starting 3 days before AF could not prevent electrical remodeling. After 24 and 48 hours of remodeling, the duration of AF paroxysms was 47 ± 32 seconds and 135 ± 63 seconds compared to 56 ± 17 seconds and 136 ± 52 seconds in placebo-treated animals (P > 0.8), respectively. Conclusion: In the goat model of AF, the Na+/H+ exchanger inhibitors EMD87580 and EMD125021 did not prevent or revert AF-induced electrical remodeling. This indicates that activation of the Na+/H+ exchanger is not involved in the intracellular pathways of electrical remodeling. This does not support the suggestion that blockers of the Na+/H+ exchanger may be beneficial for prevention and treatment of AF. (J Cardiovasc Electrophysiol, Vol. 15, pp. 440-446, April 2004) [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]

Changes in Left Ventricular Repolarization and Ion Channel Currents Following a Transient Rate Increase Superimposed on Bradycardia in Anesthetized Dogs

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2000
MICHAEL RUBART M.D.
Electrical Remodeling of the Heart due to Rate. Introduction: We previously demonstrated in dogs that a transient rate increase superimposed on bradycardia causes prolongation of ventricular refractoriness that persists for hours after resumption of bradycardia. In this study, we examined changes in membrane currents that are associated with this phenomenon. Methods and Results: The whole cell, patch clamp technique was used to record transmembrane voltages and currents, respectively, in single mid-myocardial left ventricular myocytes from dogs with 1 week of complete AV block; dogs either underwent 1 hour of left ventricular pacing at 120 beats/min or did not undergo pacing. Pacing significantly heightened mean phase 1 and peak plateau amplitudes by ,6 and ,3 mV, respectively (P < 0.02). and prolonged action potential duration at 90% repolarization from 235 ± 8 msec to 278 ± 8 msec (1 Hz; P = 0.02). Rapid pacing-induced changes in transmembrane ionic currents included (1) a more pronounced cumulative inactivation of the 4-aminopyridine-sensitive transient outward K+ current, I to over the range of physiologic frequencies, resulting from a ,30% decrease in the population of quickly reactivating channels; (2) increases in peak density of L-type Ca2+ currents, Ica.I.' by 15% to 35% between +10 and +60 mV; and (3) increases in peak density of the Ca2+ -activated chloride current, ICl.Ca' by 30% to 120% between +30 and +50 mV. Conclusion: Frequency-dependent reduction in Ito combined with enhanced ICa.I. causes an increase in net inward current that may he responsible for the observed changes in ventricular repolarization. This augmentation of net cation influx is partially antagonized by an increase in outward ICa.Cl. [source]

Alcohol-Induced Electrical Remodeling: Effects of Sustained Short-Term Ethanol Infusion on Ion Currents in Rabbit Atrium

ALCOHOLISM, Issue 10 2009
Roman Laszlo
Background:, In some patients, above-average alcohol consumption before occurrence of atrial fibrillation (AF) in terms of a "holiday heart syndrome" (HHS) can be determined. There is evidence that long before development of apparent alcohol-induced cardiomyopathy, above-average alcohol consumption generates an arrhythmogenic substrate which abets the onset of AF. Changes of atrial current densities in terms of an electrical remodeling after sustained short-term ethanol infusion in rabbits as a potential part of HHS pathophysiology were examined in this study. Methods:, Rabbits of the ethanol group (EG) received sustained short-term intravenous alcohol infusion for 120 hours (during infusion period, blood alcohol level did not fall below 158 mg/dl), whereas NaCl 0.9% was infused in the placebo group (PG). Using patch clamp technique in whole-cell mode, atrial current densities were measured and compared between both groups. Results:, Ethanol infusion did not alter current densities of Ito [58.7 ± 5.0 pA/pF (PG, n = 20 cells) vs. 53.9 ± 5.0 pA/pF (EG, n = 24)], Isus [11.3 ± 1.4 pA/pF (PG, n = 20) vs. 10.2 ± 1.0 pA/pF (EG, n = 24)], and IK1 [,1.6 ± 0.3 pA/pF (PG, n = 17) vs. ,2.0 ± 0.3 pA/pF (EG, n = 22)]. However, alcohol infusion resulted in a remarkable reduction of ICa,L current densities [,28.4 ± 1.8 pA/pF (PG, n = 20) vs. ,15.2 ± 1.4 pA/pF (EG, n = 22)] and INa [,75.4 ± 3.6 pA/pF (PG, n = 17) vs. ,35.4 ± 4.4 pA/pF (EG, n = 21)], respectively. Conclusion:, Sustained short-term ethanol infusion in rabbits alters atrial current densities. HHS might be favored by alcohol-induced atrial electrical remodeling. [source]

Evidence for Electrical Remodeling of the Native Conduction System with Cardiac Resynchronization Therapy

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2007
CHARLES A. HENRIKSON M.D.
Background:Cardiac resynchronization therapy (CRT) improves hemodynamics and decreases heart failure symptoms. However, the potential of CRT to bring about electrical remodeling of the heart has not been investigated. Methods and Results:We studied 25 patients, of whom 17 had a nonischemic cardiomyopathy, and 8 had an ischemic cardiomyopathy; 16 had left bundle branch block (LBBB), 1 right bundle branch block (RBBB), and 8 nonspecific intraventricular conduction delay. During routine device clinic visits, patients with chronic biventricular pacing (>6 months) were reprogrammed to VVI 40 to allow for native conduction to resume. After 5 minutes of native rhythm, a surface electrocardiogram (ECG) was recorded, and then the previous device settings were restored. This ECG was compared to the preimplant ECG. Preimplant mean ejection fraction was 19% (range, 10%,35%), and follow-up mean ejection fraction was 35% (12.5%,65%). Mean time from implant to follow-up ECG was 14 months (range, 6,31). The QRS interval prior to CRT was 155 ± 29 ms, and shortened to 144 ± 31 ms (P = 0.0006), and the QRS axis shifted from ,1 ± 59 to ,26 ± 53 (P = 0.03). There was no significant change in PR or QTc interval, or in heart rate. Conclusion:CRT leads to a decrease in the surface QRS duration, without affecting other surface ECG parameters. The reduced electrical activation time may reflect changes in the specialized conduction system or in intramyocardial impulse transmission. [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]

Electrical and Structural Remodeling in Left Ventricular Hypertrophy,A Substrate for a Decrease in QRS Voltage?

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2007
Ljuba Bacharova M.D., M.B.A., Ph.D.
Electrical remodeling in advanced stages of cardiovascular diseases creates a substrate for triggering and maintenance of arrhythmias. The electrical remodeling is a continuous process initiated already in the early stages of cardiological pathology. The aim of this opinion article was to discuss the changes in electrical properties of myocardium in left ventricular hypertrophy (LVH), with special focus on its early stage, as well as their possible reflection in the QRS amplitude of the electrocardiogram. It critically appraises the classical hypothesis related to the QRS voltage changes in LVH. The hypothesis of the relative voltage deficit is discussed in the context of supporting evidence from clinical studies, animal experiments, and simulation studies. The underlying determinants of electrical impulse propagation which may explain discrepancies between "normal" ECG findings and increased left ventricular size/mass in LVH are reviewed. [source]

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

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]

Reversal of Electrical Remodeling After Cardioversion of Persistent Atrial Fibrillation

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2004
MERRITT H. RAITT M.D.
Introduction: In animals, atrial fibrillation results in reversible atrial electrical remodeling manifested as shortening of the atrial effective refractory period, slowing of intra-atrial conduction, and prolongation of sinus node recovery time. There is limited information on changes in these parameters after cardioversion in patients with persistent atrial fibrillation. Methods and Results: Thirty-eight patients who had been in atrial fibrillation for 1 to 12 months underwent electrophysiologic testing 10 minutes and 1 hour after cardioversion. At 1 week, 19 patients still in sinus rhythm returned for repeat testing. Reverse remodeling of the effective refractory period was not uniform across the three atrial sites tested. At the lateral right atrium, there was a highly significant increase in the effective refractory period between 10 minutes and 1 hour after cardioversion (drive cycle length 400 ms: 204 ± 17 ms vs 211 ± 20 ms, drive cycle length 550 ms: 213 ± 18 ms vs 219 ± 23 ms, P < 0.001). The effective refractory period at the coronary sinus and distal coronary sinus did not change in the first hour but had increased by 1 week. The corrected sinus node recovery time did not change in the first hour but was shorter at 1 week (606 ± 311 ms vs 408 ± 160 ms, P = 0.009). P wave duration also was shorter at 1 week (135 ± 18 ms vs 129 ± 13 ms, P = 0.04) consistent with increasing atrial conduction velocity. Conclusion: The atrial effective refractory period increases, sinus node function improves, and atrial conduction velocity goes up in the first week after cardioversion of long-standing atrial fibrillation in humans. Reverse electrical remodeling of the effective refractory period occurs at different rates in different regions of the atrium. (J Cardiovasc Electrophysiol, Vol. 15, pp. 507-512, May 2004) [source]

Inhibitors of the Na+/H+ Exchanger Cannot Prevent Atrial Electrical Remodeling in the Goat

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]

Effect of Electrical and Structural Remodeling on Spatiotemporal Organization in Acute and Persistent Atrial Fibrillation

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 10 2002
JOSEPH G. AKAR M.D.
Spatiotemporal Organization in Atrial Fibrillation.Introduction: Atrial fibrillation (AF) may originate from discrete sites of periodic activity. We studied the effect of structural and electrical remodeling on spatiotemporal organization in acute and persistent AF. Methods and Results: Atrial effective refractory periods (AERPs) were recorded from five different sites at baseline and after pacing in acute AF (n = 8 dogs) and persistent AF (n = 8). Four persistent AF dogs subsequently were cardioverted to sinus rhythm to allow AERP recovery. Periodicity was quantified by calculating power spectra on left atrial electrograms obtained from a 64-electrode basket catheter. Left atrial size was measured by intracardiac echocardiography and structural changes were assessed by electron microscopy. Mean AERPs decreased after pacing in acute (128 ± 16 msec to 108 ± 29 msec, P < 0.001) and persistent AF (135 ± 16 msec to 104 ± 24 msec, P < 0.0001). AERP recovery was established after 7 days of sinus rhythm. Structural changes were mild in acute AF, severe in persistent AF, and remained severe after AERP recovery. A single dominant frequency was identified in 94% of acute AF bipoles, 57% in persistent AF, and 76% after AERP recovery. Average correlation coefficient was 0.82 among acute AF bipoles, 0.63 in persistent AF, and 0.73 after AERP recovery. Conclusion: Transition from acute to persistent AF is associated with loss of spatiotemporal organization. A single dominant frequency recruits the majority of the left atrium in acute AF. Persistent AF, however, is associated with structural remodeling and dominant frequency dispersion. Recovery of refractoriness only partially restores spatiotemporal organization, indicating a major role for structural remodeling in the maintenance of persistent AF. [source]

Supervulnerable Phase Immediately After Termination of Atrial Fibrillation

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2002
MATTIAS DUYTSCHAEVER M.D.
Supervulnerable Phase After Termination of AF.Introduction: Recent studies with the implantable atrial cardioverter have shown that atrial fibrillation (AF) recurs almost immediately after successful cardioversion in about 27% of cases. In the present study, we determined the electrophysiologic properties of the caprine atrium immediately after spontaneous termination of AF both before and after 48 hours of AF-induced electrical remodeling. Methods and Results: In eight goats, atrial effective refractory period (AERP), intra-atrial conduction velocity, and atrial wavelength were measured during sinus rhythm both before (t = 0) and after 48 hours (t = 48) of electrically maintained AF (baseline). After baseline, a 5-minute paroxysm of AF was induced, during which the refractory period (RPAF) was determined. AERP, conduction velocity, and atrial wavelength also were measured immediately after spontaneous restoration of sinus rhythm (post-AF values). Both in normal and remodeled atria, immediately after AF, AERP and conduction velocity were markedly decreased compared with baseline (P < 0.01). In normal atria, post-AF AERP (107 ± 14 msec) gradually prolonged from its AF value (114 ± 17 msec) to its baseline value (138 ± 13 msec). Conduction velocity decreased from 130 ± 9 cm/sec to 117 ± 9 cm/sec. After 48 hours of AF, AERP had shortened to 74 ± 8 msec. RPAF was 89 ± 9 msec. Surprisingly, immediately after termination of AF, AERP shortened further to 58 ± 6 msec (P < 0.01). Post-AF conduction velocity decreased from 136 ± 11 cm/sec to 122 ± 10 cm/sec (P < 0.01). As a result, the post-AF atrial wavelength became as short as 7.1 ± 1 cm. These changes were transient, and all parameters gradually returned to baseline within 1 to 2 minutes after conversion of AF. Conclusion: Due to a combined decrease in AERP and conduction velocity, marked shortening of the atrial wavelength occurs during the first minutes after conversion of AF. In electrically remodeled atria, this results in a transient ultrashort value of AERP (< 60 msec) and atrial wavelength (7.1 cm). These observations imply a highly vulnerable substrate for reentry immediately after termination of AF. During this supervulnerable phase, both early and later premature beats reinitiated immediate recurrences of AF. [source]

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

Atrial Fibrillation in the Goat Induces Changes in Monophasic Action Potential and mRNA Expression of Ion Channels Involved in Repolarization

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000
HUUB M.W. VAN DER VELDEN PH.D.
MAP Changes and Ion Channel Expression in Goat AF. Introduction: Sustained atrial fibrillation (AF) is characterized by a marked shortening of the atrial effective refractory period (AKRP) and a decrease or reversal of its physiolonic adaptation to heart rate. The aim of the present study was to investigate whether the AF-induced changes in AKKP in the goat are associated with changes in the atrial monophasic action potential (MAP) and whether an abnormal expression of specific ion channels underlies such changes. Methods and Results: Following thoracotomy, MAPs were recorded from the free wall of the right atrium hoth before induction of AF (control) and after cardioversion of sustained AF (>2 months) in chronically instrumented goats. In control goats. MAP duration at 80% repolarization (MAPD80) shortened (P < 0.01) from 132 ± 4 msec during slow pacing (400-msec interval) to 86 ± 10 msec during fast pacing (180 msec). After cardioversion of sustained AF, the MAPD80, during slow pacing was as short as 67 ± 5 msec (electrical remodeling). Increasing the pacing rate resulted in prolongation (P = 0.02) of the MAPD80 to 91 ± 6 msec. Also. MAPD20 (20% repolarization) shortened (P = 0.05) from 32 ± 4 msec (400 msec) to 14 ± 7 msec (180 msec) in the control goats, whereas it prolonged (P = 0.03) from 20 ± 3 msec (400 msec) to 33 ± 5 msec (180 msec) in sustained AF, mRNA expression of the L-type Ca2+ channel ,1c gene and Kv1.5 potassium channel gene, which underlie Ica, and Ikur respectively, was reduced in sustained.AF compared with sinus rhythm hy 32% (P = 0.01) and 45% (P < 0.01). respectively. No significant changes were found in the mRNA levels of the rapid Na+ channel, the Na+/Ca2+ exchanger, or the Kv4.2/4.3 channels responsible for I10. Conclusion: AF-induced electrical remodeling in the goat comprises shortening of MAPD and reversal of its physiologic rate adaptation. Changes in the time course of reploarization of the action potential are associated with changes in mRNA expression of the , subunit genes of the L.-type Ca2+ channel and the Kvl.5 potassium channel. [source]

Alcohol-Induced Electrical Remodeling: Effects of Sustained Short-Term Ethanol Infusion on Ion Currents in Rabbit Atrium

Ion channel remodeling in gastrointestinal inflammation

NEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2010
H. I. Akbarali
Abstract Background,Gastrointestinal inflammation significantly affects the electrical excitability of smooth muscle cells. Considerable progress over the last few years have been made to establish the mechanisms by which ion channel function is altered in the setting of gastrointestinal inflammation. Details have begun to emerge on the molecular basis by which ion channel function may be regulated in smooth muscle following inflammation. These include changes in protein and gene expression of the smooth muscle isoform of L-type Ca2+ channels and ATP-sensitive K+ channels. Recent attention has also focused on post-translational modifications as a primary means of altering ion channel function in the absence of changes in protein/gene expression. Protein phosphorylation of serine/theronine or tyrosine residues, cysteine thiol modifications, and tyrosine nitration are potential mechanisms affected by oxidative/nitrosative stress that alter the gating kinetics of ion channels. Collectively, these findings suggest that inflammation results in electrical remodeling of smooth muscle cells in addition to structural remodeling. Purpose,The purpose of this review is to synthesize our current understanding regarding molecular mechanisms that result in altered ion channel function during gastrointestinal inflammation and to address potential areas that can lead to targeted new therapies. [source]

Evidence for Electrical Remodeling of the Native Conduction System with Cardiac Resynchronization Therapy

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]

Correlation of Electrical and Mechanical Reverse Remodeling after Cardiac Resynchronization Therapy

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009
Swapna Kamireddy M.D.
Background: Cardiac resynchronization therapy (CRT) improves clinical outcome in many patients with refractory heart failure (HF). This study examined whether CRT is associated with reverse electrical remodeling by surface electrocardiogram (ECG). Methods: Consecutive CRT recipients at the University of Pittsburgh Medical Center with >90 days of follow-up were included in this analysis. ECG data were abstracted from medical records. Subjects with a relative increase of ,15% in left ventricular ejection fraction (LVEF) after CRT were considered responders. Results: A total of 113 patients (age 69 ± 11 years, men 70%, white 92%) were followed for a mean duration of 407 ± 290 (92,1439) days. Overall, LVEF increased after CRT (29 ± 13% vs 24 ± 9%; P < 0.01) and 50% of patients were responders. The mean native QRS interval among responders was higher than in nonresponders (163 ± 32 ms vs 148 ± 29 ms; P < 0.01). More than 3 months after CRT, there was no change in the paced QRS duration compared to baseline. Paced QRS duration, however, decreased among responders and increased among nonresponders and was significantly different by response status (P < 0.001). There was a significant correlation between increase in LVEF and decrease in paced QRS width in the overall population (r =,0.3; P < 0.01). Conclusions: Among responders to CRT, the paced QRS width decreases significantly, whereas it increases among nonresponders. Given the paced nature of the QRS, the improved conduction probably reflects enhanced cell-to-cell coupling after CRT as opposed to improved conduction within the His-Purkinje system. These findings have significant implications as to the mechanisms of benefit from CRT. [source]

Ionic Mechanisms and Vectorial Model of Early Repolarization Pattern in the Surface Electrocardiogram of the Athlete

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2008
Eduardo C. Barbosa M.D.
Background: The electrocardiogram (ECG) of the athlete displays particular characteristics as a consequence of both electrophysiological and autonomic remodeling of the heart that follows continued physical training. However, doubts persist on how these changes directly interact during ventricular activation and repolarization ultimately affecting surface ECG waveforms in athletes. Objective: This article considers an in deep rationale for the electrocardiographic pattern known as early repolarization based on both electrophysiological mechanisms at cellular level and the vectorial theory of the cardiac activation. Methods: The mechanism by which the autonomic remodeling influences the cardiac electrical activation is reviewed and an insight model of the ventricular repolarization based on ionic models and the vectorial theory of the cardiac activation is proposed. Results: Considering the underlying processes related to ventricular electrical remodeling, we propose that, in athletes' heart: 1) vagal modulation increases regional electrophysiological differences in action potential phases 1 and 2 amplitudes, thus enhancing a voltage gradient between epicardial and endocardial fibers; 2) this gradient affects depolarization and repolarization timing sequences; 3) repolarization wave front starts earlier on ventricular wall and partially overcomes the end of depolarization causing an upward displacement of the J-point, ST segment elevation, and inscription of magnified T-waves amplitudes leading to characteristic surface ECG waveform patterns. Conclusions: In athletes, the association between epicardial to endocardial electrophysiological differences and early repolarization ECG pattern can be demonstrated by the vectorial theory of the ventricular activation and repolarization. [source]