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Atrial Activation (atrial + activation)
Terms modified by Atrial Activation Selected AbstractsRelationship Between Connexins and Atrial Activation During Human Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2004M.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] Irregular Atrial Activation During Atrioventricular Nodal Reentrant Tachycardia:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2003Evidence of an Upper Common Pathway Controversy continues regarding the precise nature of the reentrant circuit of AV nodal reentrant tachycardia, especially the existence of an upper common pathway. In this case report, we show that marked variation and irregularity in atrial activation (maximum AA interval variation of 80 msec) can exist with fixed and constant activation of the His bundle and ventricles during AV nodal reentrant tachycardia in a 45-year-old female patient. We propose that irregular atrial activation is due to variable and inconsistent conduction from the AV node to the atria through the perinodal transitional cell envelope extrinsic to the reentrant circuit. Our observations support the concept of an upper common pathway, at least in some patients with AV nodal reentrant tachycardia.(J Cardiovasc Electrophysiol, Vol. 14, pp. 309-313, March 2003) [source] Is the Coronary Sinus Really Reflective of Left Atrial Activation?JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2001JEFFREY E. OLGIN M.D. [source] Differential Diagnosis of Supraventricular Tachycardia with Concentric Atrial ActivationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2000TSE-MIN LU M.D. [source] Typical Atrial Flutter Ablation: Conduction Across the Posterior Region of the Inferior Vena Cava Orifice May Mimic Unidirectional Isthmus BlockJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2000MARCO SCAGLIONE M.D. Atrial Flutter Mapping. Introduction: The aim of this study was to map the low right atrium before and after radiofrequency ablation of the inferior vena cava-tricuspid annulus (IVC-TA) isthmus in patients with typical atrial flutter (AFI) to better understand the electrophysiologic meaning of incomplete or unidirectional block following the ablation procedure and its relationship with AFI recurrence. Methods and Results: We performed atrial mapping in 12 patients using a "basket" catheter in the IVC orifice, Halo catheter in the right atrium, and multipolar catheters in the coronary sinus (CS) and His region. In patients in sinus rhythm, atrial activation was analyzed during pacing from the CS and low lateral right atrium (KLRA) before and after ablation. Atrial activation propagated across the isthmus and posterior region of the IVC orifice simultaneously before ablation. Mapping during AFI in four patients showed that the crista terminalis was a site of functional block. After ablation, evaluation of Halo catheter recordings in three patients showed apparent unidirectional counterclockwise block, whereas analysis of basket catheter recordings demonstrated complete bidirectional block. The apparent conduction over the isthmus during pacing from proximal CS was due to conduction along the posterior part of the IVC orifice, which activated the LLRA despite complete isthmus block. Conclusion: Our results demonstrate that limited endocardial mapping may yield a pattern compatible with unidirectional block in the IVC-TA isthmus, although bidirectional block is present at this anatomic level. [source] Electrophysiologic characteristics and radiofrequency ablation of focal atrial tachycardia arising from para-Hisian regionINTERNATIONAL JOURNAL OF CLINICAL PRACTICE, Issue 3 2007Y. Zhou Summary This study describes the electrophysiologic characteristics and radiofrequency ablation of focal atrial tachycardia (AT) arising from para-Hisian region in 14 (6.0%) patients of a consecutive series of 224 patients patients. Inverted or biphasic P wave in V1 and uncharacteristic P wave in inferior leads were observed during tachycardia, suggesting that there isn't a characteristic P-wave morphology for para-Hisian AT. During electrophysiological study, tachycardia could be induced with programmed atrial extrastimuli in 11 patients while a spontaneous onset and offset with ,warm-up and cool-down' phenomenon were seen in other three patients. Moreover, the tachycardias were sensitive to intravenous administration of adenosine triphosphate in all patients. On the basis of these findings, the mechanism is suggestive of triggered activity or micro-reentry, but automaticity cannot be conclusively excluded. Radiofrequency energy was delivered to the earliest site of atrial activation during AT. Ablating energy was carefully titrated, starting at 5 W and increasing gradually upto a maximum of 40 W, to achieve the ceasing of tachycardia. The long-term outcome was a 100% success rate in these 14 patients and there were no irreversible complications associated with ablation. Thus, the mapping and ablation of focal AT arising from para-Hisian region is safe and effective, delivery of radiofrequency energy in a titrated manner and continuous monitoring of atrioventricular (AV) conduction advocated to minimise the risk of damage to the anterograde AV conduction. [source] A Novel Pacing Maneuver to Localize Focal Atrial TachycardiaJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2007F.R.A.C.P., UWAIS MOHAMED M.B.B.S. Background: Although focal atrial tachycardias cannot be entrained, we hypothesized that atrial overdrive pacing (AOP) can be an effective adjunct to localize the focus of these tachycardias at the site where the post-pacing interval (PPI) is closest to the tachycardia cycle length (TCL). Methods: Overdrive pacing was performed in nine patients during atrial tachycardia, and in a comparison group of 15 patients during sinus rhythm. Pacing at a rate slightly faster than atrial tachycardia in group 1 and sinus rhythm in group 2 was performed from five standardized sites in the right atrium and coronary sinus. The difference between the PPI and tachycardia or sinus cycle length (SCL) was recorded at each site. The tachycardia focus was then located and ablated in group 1, and the atrial site with earliest activation was mapped in group 2. Results: In both groups the PPI-TCL at the five pacing sites reflected the distance from the AT focus or sinus node. In group 1, PPI-TCL at the successful ablation site was 11 ± 8 msec. In group 2, PPI-SCL at the site of earliest atrial activation was 131 ± 37 msec (P < 0.001 for comparison). In groups 1 and 2, calculated values at the five pacing sites were proportional to the distance from the AT focus or sinus node, respectively. Conclusions: The PPI-TCL after-AOP of focal atrial tachycardia has a direct relationship to proximity of the pacing site to the focus, and may be clinically useful in finding a successful ablation site. [source] Atrial Tachycardia Originating from the Upper Left Atrial Septum: Demonstration of Transseptal Interatrial Conduction Using the Infolded Atrial WallsJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2006KOJI KUMAGAI M.D. We report a rare case of atrial tachycardia (AT) originating from the upper left atrial septum. Electroanatomic mapping of both atria demonstrated that the earliest atrial activation during AT occurred at the upper left atrial septum 26 msec before the onset of the P wave, followed by the mid-right atrial septum (10 msec before the onset of the P wave) and then the upper right atrial septum just adjacent to the left septal AT site (1 msec before the onset of the P wave), indicating detour pathway conduction from the upper left to the upper right atrium. Embryologically, it was suggested that the superior components of the secondary atrial septum are made by the infolded atrial walls and could develop a transseptal detour pathway involving the left-side atrial septal musculature, the superior rim of the oval fossa and the right-side atrial septal musculature. A single radiofrequency application targeting the upper left atrial septum successfully abolished the AT. [source] Orthodromic Pacemaker-Mediated Tachycardia in a Biventricular System Without an Atrial ElectrodeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2004ANTONIO BERRUEZO M.D. Pacemaker-mediated tachycardia is a well-known complication of dual-chamber devices. In this report, we describe for the first time a case of orthodromic pacemaker-mediated tachycardia in a patient in whom a biventricular system without an atrial electrode had been implanted. Retrograde atrial activation was directly produced by the dislodged coronary vein electrode in the AV groove, resulting in simultaneous capture of the left atrium and left ventricle. During tachycardia, AV nodal conduction was via the anterograde pathway of the circuit and limited the ventricular response. Subsequently, right ventricular activation was sensed by the right ventricular electrode that triggered biventricular pacing and left atrial capture, perpetuating the tachycardia. Because the left atrial threshold was higher than the left ventricular threshold, the problem could be resolved easily by lowering the output of the coronary vein electrode. [source] Relationship Between Connexins and Atrial Activation During Human Atrial FibrillationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2004M.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] Irregular Atrial Activation During Atrioventricular Nodal Reentrant Tachycardia:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2003Evidence of an Upper Common Pathway Controversy continues regarding the precise nature of the reentrant circuit of AV nodal reentrant tachycardia, especially the existence of an upper common pathway. In this case report, we show that marked variation and irregularity in atrial activation (maximum AA interval variation of 80 msec) can exist with fixed and constant activation of the His bundle and ventricles during AV nodal reentrant tachycardia in a 45-year-old female patient. We propose that irregular atrial activation is due to variable and inconsistent conduction from the AV node to the atria through the perinodal transitional cell envelope extrinsic to the reentrant circuit. Our observations support the concept of an upper common pathway, at least in some patients with AV nodal reentrant tachycardia.(J Cardiovasc Electrophysiol, Vol. 14, pp. 309-313, March 2003) [source] Demonstration of Electrical and Anatomic Connections Between Marshall Bundles and Left Atrium in Dogs: Implications on the Generation of P Waves on Surface ElectrocardiogramJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2002CHIKAYA OMICHI M.D. Marshall Bundle and P Wave.Introduction: The muscle bundles within the ligament of Marshall (LOM) are electrically active. The importance of these muscle bundles (Marshall bundle [MB]) to atrial activation and the generation of the ECG P wave is unclear. Methods and Results: We used optical mapping techniques to study epicardial activation patterns in isolated perfused left atrium in four dogs. In another seven dogs, P waves were studied before and after in vivo radiofrequency (RF) ablation of the connection between coronary sinus (CS) and the LOM. Computerized mapping was performed before and after RF ablation. Optical mapping studies showed that CS pacing resulted in broad wavefronts propagating from the middle and distal LOM directly to the adjacent left atrium (LA). Serial sections showed direct connection between MB and LA near the orifice of the left superior pulmonary vein in two dogs. In vivo studies showed that MB potentials were recorded in three dogs. After ablation, the duration of P waves remained unchanged. In the other four dogs, MB potentials were not recorded. Computerized mapping showed that LA wavefronts propagated to the MB region via LA-MB connection and then excited the CS. After ablation, the activation of CS muscle sleeves is delayed, and P wave duration increased from 65.3 ± 14.9 msec to 70.5 ± 17.2 msec (P = 0.025). Conclusion: In about half of the normal dogs, MB provides an electrical conduit between LA free wall and CS. Severing MB alters the atrial activation and lengthens the P wave. MB contributes to generation of the P wave on surface ECG. [source] Focal Atrial Fibrillation: Experimental Evidence for a Pathophysiologic Role of the Autonomic Nervous SystemJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2001PATRICK SCHAUERTE M.D. Focal AF and Autonomic Nerves.Introduction: Focal paroxysmal atrial fibrillation (AF) was shown recently to originate in the pulmonary veins (PVs) and superior vena cava (SVC). In the present study, we describe an animal model in which local high-frequency electrical stimulation produces focal atrial activation and AF/AT (atrial tachycardia) with electrogram characteristics consistent with clinical reports. Methods and Results: In 21 mongrel dogs, local high-frequency electrical stimulation was performed by delivering trains of electrical stimuli (200 Hz, impulse duration 0.1 msec) to the PVs/SVC during atrial refractoriness. Atrial premature depolarizations (APDs), AT, and AF occurred with increasing highfrequency electrical stimulation voltage. APD/AT/AF originated adjacent to the site of high-frequency electrical stimulation and were inducible in 12 of 12 dogs in the SVC and in 8 of 9 dogs in the left superior PV (left inferior PV: 7/8, right superior PV: 6/8; right inferior PV: 4/8). In the PVs, APDs occurred at 13 ± 8 V and AT/AF at 15 ± 9 V (P < 0.01; n = 25). In the SVC, APDs were elicited at 19 ± 6 V and AT/AF at 26 ± 6 V (P < 0.01; n = 12). High-frequency electrical stimulation led to local refractory period shortening in the PVs. The response to high-frequency electrical stimulation was blunted or prevented after beta-receptor blockade and abolished by atropine. In vitro, high-frequency electrical stimulation induced a heterogeneous response, with shortening of the action potential in some cells (from 89 ± 35 msec to 60 ± 22 msec; P < 0.001; n = 7) but lengthening of the action potential and development of early afterdepolarizations that triggered APD/AT in other cells. Action potential shortening was abolished by atropine. Conclusion: High-frequency electrical stimulation evokes rapid ectopic beats from the PV/SVC, which show variable degrees of conduction block to the atria and induce AF, resembling findings in patients with focal idiopathic paroxysmal AF. The occurrence of the arrhythmia in this animal model was likely due to alterations in local autonomic tone by high-frequency electrical stimulation. Further research is needed to prove absolutely that the observed effects of high-frequency electrical stimulation were caused by autonomic nerve stimulation. [source] Predicting the Arrhythmogenic Foci of Atrial Fibrillation Before Atrial Transseptal Procedure:JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2000Implication for Catheter Ablation Arrhythmosenic Foci of Atrial Fibrillation. Introduction: Use of endocardial atrial activation sequences from recording catheters in the right atrium. His bundle, and coronary sinus to predict the location of initiating foci of atrial fibrillation (AF) before an atrial transseptal procedure has not been reported. The purpose of the present study was to develop an algorithm using endocardial atrial activation sequences to predict the location of initiating foci of AF before transseptal procedure. Methods and Results: Seventy-five patients (60 men and 15 women, age 68 ± 12 years) with frequent episodes of paroxysmal AF were referred for radiofrequency ablation. By retrospective analysis, characteristics of the endocardial atrial activation sequences of right atrial, His-bundle, and coronary sinus catheters from the initial 37 patients were correlated with the location of initiating foci of AF, which were confirmed by successful ablation. The endocardial atrial activation sequences of the other 38 patients were evaluated prospectively to predict the location of initiating foci of AF before transseptal procedure using the algorithm derived from the retrospective analysis. Accuracy of the value <0 msee (obtained by subtracting the time interval between high right atrium and His-bundle atrial activation during atrial premature beats from that obtained during sinus rhythm) for discriminating the superior vena cava or upper portion of the crista terminalis from the pulmonary vein (PV) foci was 100%. When the interval between atrial activation ostial and distal pairs of the coronary sinus catheter of the atrial premature beats was <0 msec, the accuracy for discriminating left PV foci from right PV foci was 92% in the 24 foci from the left PVs and 100% in the 19 foci from the right PVs. Conclusion: Endocardial atrial activation sequences from right atrial, His-bundle, and coronary sinus catheters can accurately predict the location of initiating foci of AF before transseptal procedure. This may facilitate mapping and radiofrequency ablation of paroxysmal AF. [source] Typical Atrial Flutter Ablation: Conduction Across the Posterior Region of the Inferior Vena Cava Orifice May Mimic Unidirectional Isthmus BlockJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2000MARCO SCAGLIONE M.D. Atrial Flutter Mapping. Introduction: The aim of this study was to map the low right atrium before and after radiofrequency ablation of the inferior vena cava-tricuspid annulus (IVC-TA) isthmus in patients with typical atrial flutter (AFI) to better understand the electrophysiologic meaning of incomplete or unidirectional block following the ablation procedure and its relationship with AFI recurrence. Methods and Results: We performed atrial mapping in 12 patients using a "basket" catheter in the IVC orifice, Halo catheter in the right atrium, and multipolar catheters in the coronary sinus (CS) and His region. In patients in sinus rhythm, atrial activation was analyzed during pacing from the CS and low lateral right atrium (KLRA) before and after ablation. Atrial activation propagated across the isthmus and posterior region of the IVC orifice simultaneously before ablation. Mapping during AFI in four patients showed that the crista terminalis was a site of functional block. After ablation, evaluation of Halo catheter recordings in three patients showed apparent unidirectional counterclockwise block, whereas analysis of basket catheter recordings demonstrated complete bidirectional block. The apparent conduction over the isthmus during pacing from proximal CS was due to conduction along the posterior part of the IVC orifice, which activated the LLRA despite complete isthmus block. Conclusion: Our results demonstrate that limited endocardial mapping may yield a pattern compatible with unidirectional block in the IVC-TA isthmus, although bidirectional block is present at this anatomic level. [source] Time-Domain and Morphological Analysis of the P Wave.PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2008Part II: Effects of Atrial Pacing on P-Wave Features Background: The aim of this study was to compare time-domain and morphological descriptors of paced and spontaneous P wave in patients prone to atrial fibrillation (AF). Methods: Nineteen patients (nine women, aged 72 ± 10 years) affected by paroxysmal AF and implanted with dual-chamber pacemakers (PM) were studied. Two 5-minute recordings were performed during spontaneous and paced rhythm. Electrocardiogram (ECG) signals were acquired using a 32-lead mapping system. Patients were grouped into two classes: no previous AF and previous AF groups, according to the number of AF episodes in the 6 months before the analysis. Results and Conclusion:During atrial pacing P wave appeared prolonged and morphologically more complex with respect to sinus rhythm. We also found that in patients at lower risk for AF, the atrial pacing changes the atrial activation to a greater extent than in patients at higher risk for AF. Finally, all time-domain and morphological descriptors of the P wave except one succeed in discriminating "no previous AF" and "previous AF" patients in spontaneous rhythm, while no significant differences have been observed during pacing for any parameters. [source] "Left-Variant" Adenosine-Sensitive Atrial Reentrant Tachycardia Ablated from the Left Coronary Aortic SinusPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2008KIYOSHI OTOMO M.D. Adenosine-sensitive reentrant atrial tachycardia (AT) is usually amenable to ablation at the right superoseptum near the His bundle. We report a case with "left-variant" adenosine-sensitive reentrant AT. The AT was reproducibly induced by atrial extrastimulation with negative correlation between the coupling interval and return cycle, and was terminated by atrial extrastimulation and bolus of 2 mg of adenosine 5'-triphosphate. Ablations at the right superoseptum were unsuccessful; however, the AT was successfully ablated from the left coronary aortic sinus (LCAS) where the earliest atrial activation was recorded. Ablation at the LCAS might be effective in this entity resistant to right-sided ablation. [source] Atrial Activation Occurring Immediately after Successful Cardioversion of Atrial FibrillationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1 2008ARTURO MARTÍN PEÑATO MOLINA M.D. Background and Objective: Electrical defibrillation is very effective in interrupting atrial fibrillation (AF). However, its mechanism is not completely understood. We report our observations in patients subjected to external electriocardioversion (ECV) of atrial fibrillation and contrast them with recent theories about defibrillation mechanism. Methods: In 13 consecutive patients transthoracic electrical cardioversion for AF was performed during an electrophysiological study (11 monophasic -200,360 J- and 9 biphasic shocks -50,150 J-). About 10,16 electrograms were obtained with multipolar catheters recording right atrium, coronary sinus, and right pulmonary artery. AF was defined by interelectrogram intervals and changing sequences among recordings, indicating complete lack of organization. We evaluated the presence of propagated activations immediately (<300 ms) after successful shocks (,1 discrete electrogram in all recordings). In unsuccessful shocks we evaluated changes in electrogram morphology (discrete/fragmented) and interelectrogram intervals before and after defibrillation. Results: About 16/20 shocks terminated AF. In 6/16 one or two cycles of atrial activation were recorded just after the shock and before AF ended. In 10/16 AF was interrupted immediately after the shock. 4/20 shocks did not interrupt the arrhythmia. After these shocks, transient organization of recorded activity with longer interelectrogram cycle length and disappearance of fragmented activity were transiently observed. Conclusion: Our clinical findings in atrial defibrillation in vivo reproduce experimental data that show myocardial activations early after successful direct current shocks. These observations suggest that successful defibrillation depends not only on the immediate effects of the shock, but also on transient effects on electrophysiological properties of the myocardium, capable of interrupting persistent or reinitiated activations. [source] Ectopic Atrial Rhythm with Exit Block Following Catheter Ablation for Focal Atrial Tachycardias in a Patient with Prior Surgery for Atrial Septal DefectPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2002KIMIE OHKUBO OHKUBO, K., et al.: Ectopic Atrial Rhythm with Exit Block Following Catheter Ablation for Focal Atrial Tachycardias in a Patient with Prior Surgery for Atrial Septal Defect. The patient was a 40-year-old woman with a history of surgery for atrial septal defect and catheter ablation for typical atrial flutter. An electrophysiological study was performed because she had palpitation and syncope. She had ectopic atrial rhythm originating from low lateral RA. Two focal atrial tachycardias ([1] superior vena cava-RA junction and [2] a low posteroseptal RA) were successfully ablated. Following catheter ablation for the second atrial tachycardia, she developed junctional rhythm because ectopic atrial rhythm showed exit block. However, atrial activation of junctional rhythm could conduct into the ectopic atrial rhythm focus and reset the rhythm when atrial activation of junctional rhythm reached the blocked line after atrial refractoriness by preceding ectopic atrial rhythm. [source] Conduction Properties of the Crista Terminalis and Its Influence on the Right Atrial Activation Sequence in Patients with Typical Atrial FlutterPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2002HIROSHIGE YAMABE YAMABE, H., et al.: Conduction Properties of the Crista Terminalis and Its Influence on the Right Atrial Activation Sequence in Patients with Typical Atrial Flutter. The conduction properties of the crista terminalis (CT) and its influence on the right atrial activation sequence were analyzed in 14 patients with typical atrial flutter (AF). Atrial mapping was performed with 35 points of the right atrium during typical AF and during atrial pacing performed after linear ablation of inferior vena cava-tricuspid annulus (IVCTA) isthmus. Atrial pacing was delivered from the septal isthmus at cycle lengths of 600 ms and the tachycardia cycle length (TCL). The right atrial activation sequence and the conduction interval (CI) from the septal to lateral portion of the IVC-TA isthmus were analyzed. During AF, the conduction block line (CBL) (detected by the appearance of double potentials along the CT and craniocaudal activation on the side anterior to CT) was observed along the CT in all patients. The TCL and CI during AF were 254 ± 19 and 207 ± 14 ms, respectively. During pacing at a cycle length of 600 ms, the CBL was observed along the CT in four patients, however, a short-circuiting activation across the CT was observed in the remaining ten patients. The CI during pacing at 600 ms was 134 ± 38 ms, shorter than that during AF (P < .0001). During pacing at the TCL, the CBL was observed along the CT in all patients. The presence of the CBL along the CT prevented a short-circuiting activation across the CT and resulted in the same right atrial activation as observed during AF. With the formation of the CBL, the CI significantly increased to 206 ± 17 ms and was not different from that during AF. These data suggest that the conduction block along the CT is functional. It was presumed that presence of conduction block at the CT has some relevance to the initiation of typical AF though it was not confirmed. [source] Effect of Different Pacing Protocols on the Induction of Atrial Fibrillation in a Transvenously Paced Sheep ModelPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001RIK 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] | ||||||||||