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Activation Sequence (activation + sequence)

Distribution by Scientific Domains
Medical Sciences91%

Kinds of Activation Sequence

  • atrial activation sequence
    		•

    Selected Abstracts

    Ablation of Posteroseptal and Left Posterior Accessory Pathways Guided by Left Atrium,Coronary Sinus Musculature Activation Sequence

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008
    RÓBERT PAP M.D.
    Introduction: While some posteroseptal and left posterior accessory pathways (APs) can be ablated on the tricuspid annulus or within the coronary venous system, others require a left-sided approach. "Fragmented" or double potentials are frequently recorded in the coronary sinus (CS), with a smaller, blunt component from left atrial (LA) myocardium, and a larger, sharp signal from the CS musculature. Methods and Results: Forty patients with posteroseptal or left posterior AP were included. The LA,CS activation sequence was determined at the earliest site during retrograde AP conduction. Eleven APs (27.5%) were ablated on the tricuspid annulus (right endocardial), 9 (22.5%) inside the coronary venous system (epicardial), and 20 (50%) on the mitral annulus (left endocardial). A "fragmented" or double "atrial" potential was recorded in all patients inside the CS at the earliest site during retrograde AP conduction. Sharp potential from the CS preceded the LA blunt component (sharp/blunt sequence) in all patients with an epicardial AP, and in 10 of 11 (91%) patients with a right endocardial AP. Therefore, 18 of 19 (95%) APs ablated by a right-sided approach produced this pattern. The reverse sequence (blunt/sharp) was recorded in 19 of 20 (95%) patients with a left endocardial AP. Conclusion: During retrograde AP conduction, the sequence of LA,CS musculature activation,as deduced from analysis of electrograms recorded at the earliest site inside the CS,can differentiate posteroseptal and left posterior APs that require left heart catheterization from those that can be eliminated by a totally venous approach. [source]

    Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node Preparation

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2002
    ATSUSHI IWASA
    IWASA, A., et al.: Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node Preparation. Junctional tachycardia is observed during radiofrequency ablation of the slow pathway. The authors investigated the atrial activation sequence during junctional tachycardia induced with thermal stimulation in canine blood-perfused atrioventricular node (AVN) preparation. The canine heart was isolated (n = 7) and cross-circulated with heparinized arterial blood of the support dog. The activation sequence in the region of Koch's triangle (15 × 21 mm) was determined by recording 48 unipolar electrograms. Atrial sites anterior to the coronary sinus ostium (site AN), close to the His-potential recording site (site N) and superior to site N (site F), were subjected to a continuous temperature rise from 38°C to 50°C with a heating probe. The temperature of the tissue adjacent to the heating site was monitored simultaneously. Junctional tachycardia at a rate of 92 ± 12 beats/min with the His potential preceding the atrial one in the His-bundle electrogram was induced during thermal stimulation at site AN (temperature 42.1°C ± 0.9°C) in all seven preparations, whereas junctional tachycardia was induced during stimulation at site N in one and at site F in none. In each case, the temperature rose only at the site of stimulation. The earliest activation site during junctional tachycardia induced by site AN stimulation was at the His-potential recording site in five preparations and the middle of Koch's triangle in the other two. After creating an obstacle between sites AN and N, atrial tachycardia at a rate of 85 ± 11 beats/min was induced during site AN stimulation. The earliest activation site during this tachycardia was site AN. Thus, junctional tachycardia induced by thermal stimulation was suggested to originate from the AN thermal stimulation site. The impulse from the stimulation site appeared to conduct via the posterior input to the compact AVN and junctional tachycardia was generated. When the posterior input was interrupted, atrial tachycardia was generated. [source]

    Conduction Properties of the Crista Terminalis and Its Influence on the Right Atrial Activation Sequence in Patients with Typical Atrial Flutter

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2002
    HIROSHIGE 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]

    Modulation of rabbit sinoatrial node activation sequence by acetylcholine and isoproterenol investigated with optical mapping technique

    ACTA PHYSIOLOGICA, Issue 4 2009
    D. V. Abramochkin
    Abstract Aims:, Changes in the rabbit sinoatrial node (SAN) activation sequence with the cholinergic and adrenergic factors were studied. The correlation between the sinus rhythm rate and the leading pacemaker site shift was determined. The hypothesis concerning the cholinergic suppression of nodal cell excitability as one of the mechanisms associated with pacemaker shift was tested. Methods:, A high-resolution optical mapping technique was used to register beat-to-beat changes in the SAN activation pattern under the influence of the cholinergic and adrenergic factors. Results:, Acetylcholine (10 ,m) and strong intramural parasympathetic nerve stimulation caused a pacemaker shift as well as rhythmic slowing and the formation of an inexcitable region in the central part of SAN. In this region the generation of action potentials was suppressed. The slowing of the sinus rhythm (which exceeded 12.8 ± 3.1% of the rhythm control rate) always accompanied the pacemaker shift. Isoproterenol (10, 100 nm, 1 ,m) and sympathetic postganglionic nerve stimulation also evoked a pacemaker shift but without formation of an inexcitable zone. The acceleration of the sinus rhythm, which exceeded 10.5 ± 1.3% of the control rate of the rhythm, always accompanied the shift. Conclusions:, Both cholinergic and adrenergic factors cause pacemaker shifts in the rabbit SAN. While modest changes in the sinus rhythm do not coincide with the pacemaker shift, greater changes always accompany the shift and may be caused by it, according to one hypothesis. The formation of an inexcitable zone at the place where the leading pacemaker is situated is one of the mechanisms associated with pacemaker shift. [source]

    Ablation of Posteroseptal and Left Posterior Accessory Pathways Guided by Left Atrium,Coronary Sinus Musculature Activation Sequence

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008
    RÓBERT PAP M.D.
    Introduction: While some posteroseptal and left posterior accessory pathways (APs) can be ablated on the tricuspid annulus or within the coronary venous system, others require a left-sided approach. "Fragmented" or double potentials are frequently recorded in the coronary sinus (CS), with a smaller, blunt component from left atrial (LA) myocardium, and a larger, sharp signal from the CS musculature. Methods and Results: Forty patients with posteroseptal or left posterior AP were included. The LA,CS activation sequence was determined at the earliest site during retrograde AP conduction. Eleven APs (27.5%) were ablated on the tricuspid annulus (right endocardial), 9 (22.5%) inside the coronary venous system (epicardial), and 20 (50%) on the mitral annulus (left endocardial). A "fragmented" or double "atrial" potential was recorded in all patients inside the CS at the earliest site during retrograde AP conduction. Sharp potential from the CS preceded the LA blunt component (sharp/blunt sequence) in all patients with an epicardial AP, and in 10 of 11 (91%) patients with a right endocardial AP. Therefore, 18 of 19 (95%) APs ablated by a right-sided approach produced this pattern. The reverse sequence (blunt/sharp) was recorded in 19 of 20 (95%) patients with a left endocardial AP. Conclusion: During retrograde AP conduction, the sequence of LA,CS musculature activation,as deduced from analysis of electrograms recorded at the earliest site inside the CS,can differentiate posteroseptal and left posterior APs that require left heart catheterization from those that can be eliminated by a totally venous approach. [source]

    Mapping of Epicardial Activation in a Rabbit Model of Chronic Myocardial Infarction:

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2007
    Endocardial, Epicardial Pacing, Response to Atrial
    Introduction: This study examines the consequences of a large transmural apical infarct on the epicardial electrical activity in isolated rabbit hearts. Methods and Results: Hearts were isolated 8 weeks after coronary artery ligation. Membrane voltage from the epicardial surface of the left ventricle (LV) including the infarct was monitored using the voltage sensitive dye RH237. Optical action potentials were detected from the epicardial surface of the infarct; the signal amplitude was ,20% of those in the noninfarcted zone (NZ). Epicardial activation mapping of the LV free wall showed that during right atrial (RA) pacing, the activation sequence was not significantly different between infarcted and sham-operated groups. However, direct stimulation of the epicardium in the NZ revealed an area of slow conduction velocity (CV ,5 cm/s,1, ,10% of normal values) at the margin of the infarct zone (IZ). Within the IZ, CV was ,50% of normal. A prominent endocardial rim of myocardium in the infarct was not the source of epicardial optical signals because chemical ablation of the endocardium did not affect the epicardial activation pattern. Concluson: Therefore, remnant groups of myocytes in the mid-wall and epicardium of the infarct scar support normal electrical activation during RA pacing. Areas of delayed conduction emerge only on epicardial stimulation. [source]

    A Single Pulmonary Vein as Electrophysiological Substrate of Paroxysmal Atrial Fibrillation

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2006
    HE HUANG M.D.
    Introduction: It has been demonstrated that pulmonary veins (PVs) play an important role in initiation and maintenance of paroxysmal atrial fibrillation (AF). However, it is not clearly known whether a single PV acts as electrophysiological substrate for paroxysmal AF. Methods and Results: This study included five patients with paroxysmal AF. All patients underwent complete PV isolation with continuous circular lesions (CCLs) around the ipsilateral PVs guided by a three-dimensional mapping system. Irrigated radiofrequency (RF) delivery was performed during AF on the right-sided CCLs in two patients and on the left-sided CCLs in three patients. The incomplete CCLs resulted in a change from AF to atrial tachycardia (AT), which presented with an identical atrial activation sequence and P wave morphology. Complete CCLs resulted in AF termination with persistent PV tachyarrhythmias within the isolated PV in all five patients. PV tachyarrhythmia within the isolated PV was PV fibrillation from the left common PV (LCPV) in two patients, PV tachycardia from the right superior PV (RSPV) in two patients, and from the left superior PV in one patient. All sustained PV tachyarrhythmias persisted for more than 30 minutes, needed external cardioversion for termination in four patients and a focal ablation in one patient. After the initial procedure, an AT from the RSPV occurred in a patient with PV fibrillation within the LCPV, and was successfully ablated. Conclusion: In patients with paroxysmal AF, sustained PV tachyarrhythmias from a single PV can perpetuate AF. Complete isolation of all PV may provide good clinical outcome during long-term follow-up. [source]

    Relationship Between Regional Shortening and Asynchronous Electrical Activation in a Three-Dimensional Model of Ventricular Electromechanics

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003
    TARAS P. USYK Ph.D.
    Introduction: Asynchronous electrical activation can cause abnormalities in perfusion and pump function. An electromechanical model was used to investigate the mechanical effects of altered cardiac activation sequence. Methods and Results: We used an anatomically detailed three-dimensional computational model of the canine ventricular walls to investigate the relationship between regional electrical activation and the timing of fiber shortening during normal and ventricular paced beats. By including a simplified Purkinje fiber network and anisotropic impulse conduction in the model, computed electrical activation sequences were consistent with experimentally observed patterns. Asynchronous time courses of regional strains during beats stimulated from the left or right ventricular epicardium showed good agreement with published experimental measurements in dogs using magnetic resonance imaging tagging methods. When electrical depolarization in the model was coupled to the onset of local contractile tension development by a constant time delay of 8 msec, the mean delay from depolarization to the onset of systolic fiber shortening was 14 msec. However, the delay between the onset of fiber tension and initial shortening varied significantly; it was as late as 60 msec in some regions but was also as early as ,50 msec (i.e., 42 msec before depolarization) in other regions, particularly the interventricular septum during free-wall pacing. Conclusion: The large variation in delay times was attributable to several factors including local anatomic variations, the location of the site relative to the activation wavefront, and regional end-diastolic strain. Therefore, we conclude that these factors, which are intrinsic to three-dimensional ventricular function, make the regional sequence of fiber shortening an unreliable surrogate for regional depolarization or electromechanical activation in the intact ventricles. (J Cardiovasc Electrophysiol, Vol. 14, pp. S196-S202, October 2003, Suppl.) [source]

    Altered T Wave Dynamics in a Contracting Cardiac Model

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003
    NICOLAS P. SMITH Ph.D.
    Introduction: The implications of mechanical deformation on calculated body surface potentials are investigated using a coupled biophysically based model. Methods and Results: A cellular model of cardiac excitation-contraction is embedded in an anatomically accurate two-dimensional transverse cross-section of the cardiac ventricles and human torso. Waves of activation and contraction are induced by the application of physiologically realistic boundary conditions and solving the bidomain and finite deformation equations. Body surface potentials are calculated from these activation profiles by solving Laplace's equation in the passive surrounding tissues. The effect of cardiac deformation on electrical activity, induced by contraction, is demonstrated in both single-cell and tissue models. Action potential duration is reduced by 7 msec when the single cell model is subjected to a 10% contraction ramp applied over 400 msec. In the coupled electromechanical tissue model, the T wave of the ECG is shown to occur 18 msec earlier compared to an uncoupled excitation model. To assess the relative effects of myocardial deformation on the ECG, the activation sequence and tissue deformation are separated. The coupled and uncoupled activation sequences are mapped onto the undeforming and deforming meshes, respectively. ECGs are calculated for both mappings. Conclusion: Adding mechanical contraction to a mathematical model of the heart has been shown to shift the T wave on the ECG to the left. Although deformation of the myocardium resulting from contraction reduces the T wave amplitude, cell stretch producing altered cell membrane kinetics is the major component of this temporal shift. (J Cardiovasc Electrophysiol, Vol. 14, pp. S203-S209, October 2003, Suppl.) [source]

    Estimation of Entrainment Response Using Electrograms from Remote Sites: Validation in Animal and Computer Models of Reentrant Tachycardia

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2003
    PETER E. HAMMER M.S.
    Estimation of Entrainment Response. Introduction: Studies suggest that entrainment response (ER) of reentrant tachycardia to overdrive pacing can be estimated using signals from sites other than the paced site. Methods and Results: A formula for estimation of ER using remote sites against the difference between the postpacing interval (PPI) and tachycardia cycle length (TCL) determined solely from the paced site signal was validated in experimental data and using a simple two-dimensional cellular automata model of reentry. The model also was used to study the behavior and features of entrained surfaces, including the resetting of tachycardia phase by single premature paced stimuli. Experimental results from 1,484 remote sites in 115 pacing sequences showed the average of the median ER estimate error at each pacing site was,2 ± 5 msec, and the median ER estimate was within 10 msec of PPI,TCL for 94% of pacing sites. From simulation results, ER at the paced site was accurately estimated from >99.8% of 20,764 remote sites during pacing at 24 sites and three paced cycle lengths. Intervals measured from remote electrograms revealed whether the site was activated orthodromically or nonorthodromically during pacing, and results of simulations illustrated that the portion of the surface activated nonorthodromically during pacing increased with distance from the pacing site to the circuit. The phenomenon of nonorthodromic activation of reentrant circuits predicted by modeling was discernible in measurements taken from the animal model of reentrant tachycardia. Results also showed that, for single premature stimuli that penetrated the tachycardia circuit, phase reset of the tachycardia was linearly related to distance between the central obstacle and the paced site. Conclusion: The ER is a complex but predictable perturbation of the global activation sequence of reentrant tachycardias. This predictability allows calculations of the response from anywhere on the perturbed surface. These findings suggest new techniques for measurement of the ER, which may lend themselves to computer-based methods for accurate and rapid mapping of reentrant circuits. [source]

    Lack of Effect of Conduction Direction on Action Potential Durations in Anisotropic Ventricular Strips of Pig Heart

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2002
    GUILLERMO BERTRAN B.Sc.
    Anisotropy and Repolarization.Introduction: The influence of activation sequence on the rate of rise of the depolarization phase of action potentials in atrial or ventricular muscles has been well established. However, whether myocardial fiber orientation is important in modulating the repolarization process is unclear. Methods and Results: We examined the influence of activation sequence on the repolarization phase of action potentials in epicardial tissues from the right and left ventricles of domestic pigs. Whereas cells from the right ventricle exhibited direction-dependent differences in action potential duration at 30%, 50%, and 90% of full repolarization (190.6 ± 31.1 msec vs 181.8 ± 32.8 msec, 240.3 ± 23.5 msec vs 236.7 ± 25.4 msec, and 291.3 ± 23.7 msec vs 287.4 ± 25.1 msec for longitudinal and transverse propagation, respectively; P < 0.001), a similar duration of repolarization during both directions of propagation was observed in cells from the left ventricle at 50% and 90% of full repolarization (241.4 ± 39.4 msec and 285.5 ± 39.5 msec vs 240.4 ± 38.9 msec and 284.9 ± 39.6 msec for longitudinal and transverse propagation respectively; P = NS). A slight but significant difference was found at 30% of full repolarization in cells from the left ventricle (190.4 ± 39.0 msec vs 187.0 ± 38.0 msec for longitudinal and transverse propagation, respectively; P < 0.05). In the left ventricle, the duration of repolarization did not change as the distance between the recording site and stimulation site increased. Conclusion: The direction of wavefront propagation with respect to fiber orientation may not play an important role in modulating the duration of repolarization in epicardial cells from the left ventricle. [source]

    Electrogram Polarity and Cavotricuspid Isthmus Block During Ablation of Typical Atrial Flutter

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2001
    HIROSHI TADA M.D.
    Electrogram Polarity in Atrial Flutter Ablation.Introduction: The atrial activation sequence around the tricuspid annulus has been used to assess whether complete block has been achieved across the cavotricuspid isthmus during radiofrequency ablation of typical atrial flutter. However, sometimes the atrial activation sequence does not clearly establish the presence or absence of complete block. The purpose of this study was to determine whether a change in the polarity of atrial electrograms recorded near the ablation line is an accurate indicator of complete isthmus block. Methods and Results: Radiofrequency ablation was performed in 34 men and 10 women (age 60 ± 13 years [mean ± SD]) with isthmus-dependent, counterclockwise atrial flutter. Electrograms were recorded around the tricuspid annulus using a duodecapolar halo catheter. Electrograms recorded from two distal electrode pairs (E1 and E2) positioned just anterior to the ablation line were analyzed during atrial flutter and during coronary sinus pacing, before and after ablation. Complete isthmus block was verified by the presence of widely split double electrograms along the entire ablation line. Complete bidirectional isthmus block was achieved in 39 (89%) of 44 patients. Before ablation, the initial polarity of E1 and E2 was predominantly negative during atrial flutter and predominantly positive during coronary sinus pacing. During incomplete isthmus block, the electrogram polarity became reversed either only at E2, or at neither E1 nor E2. In every patient, the polarity of E1 and E2 became negative during coronary sinus pacing only after complete isthmus block was achieved. In 4 patients (10%), the atrial activation sequence recorded with the halo catheter was consistent with complete isthmus block, but the presence of incomplete block was accurately detected by inspection of the polarity of E1 and E2. Conclusion: Reversal of polarity in bipolar electrograms recorded just anterior to the line of isthmus block during coronary sinus pacing after ablation of atrial flutter is a simple, quick, and accurate indicator of complete isthmus block. [source]

    Spatial Distribution and Frequency Dependence of Arrhythmogenic Vagal Effects in Canine Atria

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2000
    OLEG F. SHARIFOV Ph.D.
    Arrhythmogenic Vagal Effects in Dog Atria. introduction: Prior studies in isolated canine atria demonstrated that acetylcholine-induced reentrant atrial fibrillation (AF) was triggered by multifocal activity in the area of normal impulse origin (sinus node-crista terminalis). The aim of this study was to investigate the activation sequence in AF induced by vagal stimulation (VS) in intact dog hearts. Methods and Results: VS (10 to 50 Hz, 1 msec, 15 V, 5-sec trains) induced single or multiple atrial premature depolarizations (APDs), and/or AF in 8 of 10 open chest dogs. Occurrence of APDs and AF increased with increasing VS intensity. Epicardial mapping (254 unipolar electrodes) of both atria showed that APDs as a rule emerged from ectopic sites, often from the right atrial appendage. Activation mapping of the first 10 cycles of AF showed that only a small number (<3 to 4) of unstable reentrant circuits were possible at the same moment. Moreover, most sustained VS-induced AFs were accounted for by a single leading stable reentrant circuit that activated the remainder of the atria. Conclusion: (1) Occurrence of vagally induced APDs and AF increases with increasing frequency of VS. (2) VS-induced focal ectopic APDs are widely distributed over the atria. (3) A single APD can be sufficient for initiation of reentrant AF. (4) Despite its high rate of sustained AF, it may be maintained by single stable reentrant circuit. (5) The atrial septum can play an important role in both the initiation and the maintenance of VS-induced AF. [source]

    Reentry Within the Cavotricuspid Isthmus: An Isthmus Dependent Circuit

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2005
    YANFEI YANG
    Background: We describe a new cavotricuspid isthmus (CTI) circuit. Methods: This study includes 8 patients referred for atrial flutter (AFL) ablation whose tachycardia circuit was confined to the septal CTI and the os of the coronary sinus (CSOS) region. Entrainment mapping was performed within the CTI, CSOS, and other right atrial annular sites (tricuspid annulus (TA)). Electroanatomic mapping was available in 2 patients. Results: Sustained AFL occurred in all patients with mean tachycardia cycle length (TCL) of 318 ± 54 (276 , 420) ms. During tachycardia, fractionated or double potentials were recorded at either the septal CTI and/or the region of CSOS in all, and concealed entrainment with post-pacing interval (PPI) , TCL , 25 ms occurred in this area; but manifest entrainment with PPI > TCL was demonstrated from the anteroinferior CTI and other annular sites in 7/8 patients. In one, tachycardia continued with conduction block at the anteroinferior CTI during ablation. Up to three different right atrial activation patterns (identical TCL) were observed. The tachycardia showed a counterclockwise (CCW) pattern in 6, a clockwise pattern in 2, and simultaneous activation of both low lateral right atrium and septum in 5. Electroanatomic mapping was available in 2, showing an early area arising from the septal CTI in 1, and a CCW activation sequence along the TA in another. Radiofrequency application to the septal CTI terminated tachycardia in 4, and tachycardia no longer inducible in all. Conclusions: We describe a tachycardia circuit confined to the septal CTI/CSOS region, and hypothesize that this circuit involves slow conduction within the CTI and around the CSOS, which acts as a central obstacle. [source]

    Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node Preparation

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2002
    ATSUSHI IWASA
    IWASA, A., et al.: Atrial Activation Sequence During Junctional Tachycardia Induced by Thermal Stimulation of Koch's Triangle in Canine Blood-Perfused Atrioventricular Node Preparation. Junctional tachycardia is observed during radiofrequency ablation of the slow pathway. The authors investigated the atrial activation sequence during junctional tachycardia induced with thermal stimulation in canine blood-perfused atrioventricular node (AVN) preparation. The canine heart was isolated (n = 7) and cross-circulated with heparinized arterial blood of the support dog. The activation sequence in the region of Koch's triangle (15 × 21 mm) was determined by recording 48 unipolar electrograms. Atrial sites anterior to the coronary sinus ostium (site AN), close to the His-potential recording site (site N) and superior to site N (site F), were subjected to a continuous temperature rise from 38°C to 50°C with a heating probe. The temperature of the tissue adjacent to the heating site was monitored simultaneously. Junctional tachycardia at a rate of 92 ± 12 beats/min with the His potential preceding the atrial one in the His-bundle electrogram was induced during thermal stimulation at site AN (temperature 42.1°C ± 0.9°C) in all seven preparations, whereas junctional tachycardia was induced during stimulation at site N in one and at site F in none. In each case, the temperature rose only at the site of stimulation. The earliest activation site during junctional tachycardia induced by site AN stimulation was at the His-potential recording site in five preparations and the middle of Koch's triangle in the other two. After creating an obstacle between sites AN and N, atrial tachycardia at a rate of 85 ± 11 beats/min was induced during site AN stimulation. The earliest activation site during this tachycardia was site AN. Thus, junctional tachycardia induced by thermal stimulation was suggested to originate from the AN thermal stimulation site. The impulse from the stimulation site appeared to conduct via the posterior input to the compact AVN and junctional tachycardia was generated. When the posterior input was interrupted, atrial tachycardia was generated. [source]

    Conduction Properties of the Crista Terminalis and Its Influence on the Right Atrial Activation Sequence in Patients with Typical Atrial Flutter

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2002
    HIROSHIGE 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]

    Relationship Between Regional Shortening and Asynchronous Electrical Activation in a Three-Dimensional Model of Ventricular Electromechanics

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003
    TARAS P. USYK Ph.D.
    Introduction: Asynchronous electrical activation can cause abnormalities in perfusion and pump function. An electromechanical model was used to investigate the mechanical effects of altered cardiac activation sequence. Methods and Results: We used an anatomically detailed three-dimensional computational model of the canine ventricular walls to investigate the relationship between regional electrical activation and the timing of fiber shortening during normal and ventricular paced beats. By including a simplified Purkinje fiber network and anisotropic impulse conduction in the model, computed electrical activation sequences were consistent with experimentally observed patterns. Asynchronous time courses of regional strains during beats stimulated from the left or right ventricular epicardium showed good agreement with published experimental measurements in dogs using magnetic resonance imaging tagging methods. When electrical depolarization in the model was coupled to the onset of local contractile tension development by a constant time delay of 8 msec, the mean delay from depolarization to the onset of systolic fiber shortening was 14 msec. However, the delay between the onset of fiber tension and initial shortening varied significantly; it was as late as 60 msec in some regions but was also as early as ,50 msec (i.e., 42 msec before depolarization) in other regions, particularly the interventricular septum during free-wall pacing. Conclusion: The large variation in delay times was attributable to several factors including local anatomic variations, the location of the site relative to the activation wavefront, and regional end-diastolic strain. Therefore, we conclude that these factors, which are intrinsic to three-dimensional ventricular function, make the regional sequence of fiber shortening an unreliable surrogate for regional depolarization or electromechanical activation in the intact ventricles. (J Cardiovasc Electrophysiol, Vol. 14, pp. S196-S202, October 2003, Suppl.) [source]

    Altered T Wave Dynamics in a Contracting Cardiac Model

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2003
    NICOLAS P. SMITH Ph.D.
    Introduction: The implications of mechanical deformation on calculated body surface potentials are investigated using a coupled biophysically based model. Methods and Results: A cellular model of cardiac excitation-contraction is embedded in an anatomically accurate two-dimensional transverse cross-section of the cardiac ventricles and human torso. Waves of activation and contraction are induced by the application of physiologically realistic boundary conditions and solving the bidomain and finite deformation equations. Body surface potentials are calculated from these activation profiles by solving Laplace's equation in the passive surrounding tissues. The effect of cardiac deformation on electrical activity, induced by contraction, is demonstrated in both single-cell and tissue models. Action potential duration is reduced by 7 msec when the single cell model is subjected to a 10% contraction ramp applied over 400 msec. In the coupled electromechanical tissue model, the T wave of the ECG is shown to occur 18 msec earlier compared to an uncoupled excitation model. To assess the relative effects of myocardial deformation on the ECG, the activation sequence and tissue deformation are separated. The coupled and uncoupled activation sequences are mapped onto the undeforming and deforming meshes, respectively. ECGs are calculated for both mappings. Conclusion: Adding mechanical contraction to a mathematical model of the heart has been shown to shift the T wave on the ECG to the left. Although deformation of the myocardium resulting from contraction reduces the T wave amplitude, cell stretch producing altered cell membrane kinetics is the major component of this temporal shift. (J Cardiovasc Electrophysiol, Vol. 14, pp. S203-S209, October 2003, Suppl.) [source]

    Predicting the Arrhythmogenic Foci of Atrial Fibrillation Before Atrial Transseptal Procedure:

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2000
    Implication 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]

    Excitation of the Intrinsic Conduction System Through His and Interventricular Septal Pacing

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 4 2006
    TIMOTHY G LASKE
    Background: Direct His bundle pacing results in rapid synchronous ventricular activation. However, clinical experiences with such pacing have been associated with long procedure times and compromised pacing and sensing performance. Methods: We evaluated myocardial activation sequences (AS) for pacing of the His bundle and peri-His region and assessed acute pacing performance using custom-designed plunge electrodes. Unipolar pacing was performed in isolated swine hearts (n = 10) using four quadripolar stimulation/sensing electrodes implanted into the interventricular septum and equally spaced between the membranous septum and the coronary sinus ostium (zones 1,4, respectively; electrode depth (ED) 1 = most distal, ED 4 = most proximal). Optimal pacing sites were defined as: pacing thresholds ,1.5 V, a P-R ratio of ,0.5, and ,50% occurrence of an intrinsic midseptal left ventricular (LV) endocardial electrical breakout (BO) and activation pattern. Results: Pacing thresholds improved with greater depth of electrode location within the septum (ED 1: 1.51 ± 0.8 V vs ED 4: 5.2 ± 3.8 V, P < 0.001), as did the P-R ratio (0.34 ± 0.6 vs 0.78 ± 1.0, P < 0.05). His potentials were only observed in zone 1 and 2 electrodes (0.12 and 0.02 mV, respectively). Only electrodes in zones 1 and 2 produced LV endocardial electrical BOs in the midseptal region that demonstrated an intrinsic-like endocardial AS. Depth 1 and 2 electrodes (11.75 and 8.75 mm, respectively) in zone 1 satisfied all three optimal pacing site requirements. Conclusions: This study has shown that LV activation patterns similar to sinus rhythm may be achieved without direct activation of the His bundle, while maintaining acceptable pacing and sensing performance. These data indicate that pacing systems designed to stimulate the tissues below the point at which the His bundle penetrates the central fibrous body may provide improved system efficiency and LV performance in comparison to both direct His bundle pacing and traditional pacing sites. [source]