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Tachycardia Cycle Length (tachycardia + cycle_length)
Selected AbstractsFocal Atrial Tachycardia Originating from the Left Atrial Appendage: Electrocardiographic and Electrophysiologic Characterization and Long-Term Outcomes of Radiofrequency AblationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 5 2007WANG YUN-LONG M.D. Introduction: This study sought to investigate electrophysiologic characteristics and radiofrequency ablation (RFA) in patients with focal atrial tachycardia (AT) arising from the left atrial appendage (LAA). Methods: This study included seven patients undergoing RFA with focal AT. Activation mapping was performed during tachycardia to identify an earlier activation in the left atria and the LAA. The atrial appendage angiography was performed to identify the origin in the LAA before and after RFA. Results: AT occurred spontaneously or was induced by isoproterenol infusion rather than programmed extrastimulation and burst atrial pacing in any patient. The tachycardia demonstrated a characteristic P-wave morphology and endocardial activation pattern. The P wave was highly positive in inferior leads in all patients. Lead V1 showed upright or biphasic (±) component in all patients. Lead V2,V6 showed an isoelectric component in five patients or an upright component with low amplitude (<0.1 mV) in two patients. Earliest endocardial activity occurred at the distal coronary sinus (CS) ahead of P wave in all seven patients. Mean tachycardia cycle length was 381 ± 34 msec and the earliest endocardial activation at the successful RFA site occurred 42.3 ± 9.6 msec before the onset of P wave. RFA was acutely successful in all seven patients. Long-term success was achieved in seven of the seven over a mean follow-up of 24 ± 5 months. Conclusions: The LAA is an uncommon site of origin for focal AT (3%). There were consistent P-wave morphology and endocardial activation associated with this type of AT. The LAA focal ablation is safe and effective. Long-term success was achieved with focal ablation in all patients. [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] Mechanism of Repolarization Change During Initiation of Supraventricular TachycardiaJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2004YENN-JIANG LIN M.D. Introduction: Previous literature has documented the association between narrow QRS supraventricular tachycardia (SVT) and pronounced ST-T segment change. The aim of this study was to evaluate repolarization changes during SVT initiation and demonstrate the possible mechanism. Methods and Results: Fifty-one consecutive patients (20 men and 31 women; mean age 46.1 ± 16.4 years) with narrow QRS SVT (32 patients with AV nodal reentrant tachycardia and 19 patients with AV reentrant tachycardia) were included. We retrospectively analyzed the intracardiac recordings and ST-T segment changes on 12-lead surface ECGs during SVT initiation. Twenty-six (51%) patients developed ST segment repolarization changes during SVT initiation. Patients with shorter baseline sinus cycle length, shorter tachycardia cycle length, elevated systolic blood pressure before tachycardia induction, and greater reduction of systolic blood pressure had a higher incidence of repolarization changes. However, multivariate analysis showed that reduction of systolic blood pressure after SVT induction was the only independent predictor of repolarization changes. Furthermore, the maximal degree of ST segment depression during SVT correlated with the reduction of systolic blood pressure (r = 0.75, P < 0.001). Conclusion: Repolarization changes during SVT initiation were caused mainly by concurrent hemodynamic change after SVT initiation with abrupt cycle length shortening. [source] Estimation of Entrainment Response Using Electrograms from Remote Sites: Validation in Animal and Computer Models of Reentrant TachycardiaJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2003PETER 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] High-Resolution Mapping of Tachycardia Originating from the Superior Vena Cava: Evidence of Electrical Heterogeneity, Slow Conduction, and Possible Circus Movement ReentryJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2002DIPEN C. SHAH M.D. Superior Vena Cava Reentry. High-resolution mapping of a tachycardia originating from the superior vena cava (SVC) in a patient with atrial fibrillation is described. Unidirectional circuitous repetitive activation encompassing the full tachycardia cycle length was documented around a line of block within the myocardial sleeve of the SVC. Intermittent conduction to the right atrium resulted in an irregular atrial tachycardia. Evidence of electrical heterogeneity and slow conduction persisted in sinus rhythm and was exaggerated by premature stimulation but did not reproduce the activation pattern during tachycardia. All the available evidence is best compatible with circus movement reentry within the SVC, with marked slow and anisotropic conduction responsible for the restricted dimensions of the reentrant circuit. These findings may suggest a similar substrate and arrhythmia mechanism in the myocardium of the pulmonary veins. [source] Abnormal Atrioventricular Node Conduction and Atrioventricular Nodal Reentrant Tachycardia in Patients Older Versus Younger Than 65 Years of AgePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2009MIHAELA GRECU M.D. Study Objective: We examined the possible role of atrioventricular node (AVN) conduction abnormalities as a cause of AVN reentrant tachycardia (RT) in patients >65 years of age. Study Population: Slow pathway radiofrequency catheter ablation (RFCA) was performed in 104 patients. Patients in group 1 (n = 14) were >65 years of age and had AV conduction abnormalities associated with structural heart disease. Patients in group 2 (n = 90) were <65 years of age and had lone AVNRT. Results: Patients in group 1 versus group 2 (66% vs. 46% men) had a first episode of tachycardia at an older age than in group 2 (68 ± 16.8 vs 32.5 ± 18.8 years, P = 0.007). The history of arrhythmia was shorter in group 1 (5.4 ± 3.8 vs 17.5 ± 14, P = 0.05) and was associated with a higher proportion of patients with underlying heart disease than in group 2 (79% vs 3%, P < 0.001). The electrophysiological measurements were significantly shorter in group 2: atrial-His interval (74 ± 17 vs 144 ± 44 ms, P = 0.005), His-ventricular (HV) interval (41 ± 5 vs 57 ± 7 ms, P = 0.001), Wenckebach cycle length (329 ± 38 vs 436 ± 90 ms, P = 0.001), slow pathway effective refractory period (268 ± 7 vs 344 ± 94 ms, P = 0.005), and tachycardia cycle length (332 ± 53 vs 426 ± 56 ms, P = 0.001). The ventriculoatrial block cycle length was similar in both groups. The immediate procedural success rate was 100% in both groups, and no complication was observed in either group. One patient in group 2 had recurrence of AVNRT. One patient with a 98-ms HV interval underwent permanent VVI pacemaker implantation before RFCA procedure. Conclusion: In patients undergoing RFCA for AVNRT at >65 years of age had a shorter history of tachycardia-related symptoms than patients with lone AVNRT. The longer AVN conduction intervals and refractory period might explain the late development of AVNRT in group 1. [source] Reentry Within the Cavotricuspid Isthmus: An Isthmus Dependent CircuitPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 8 2005YANFEI 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] 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] Mechanisms of Transition Between Double Paroxysmal Supraventricular TachycardiasJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2001JEN-YUAN KUO M.D. Double Paroxysmal Supraventricular Tachycardias. Introduction: Coexistence of double tachycardias in one patient has been infrequently reported. Furthermore, the mechanisms of transition between double paroxysmal supraventricular tachycardias have not been well studied. Methods and Results: Thirty-five patients with two paroxysmal supraventricular tachycardias were studied. Group IA consisted of 3 patients with spontaneous transition between AV reciprocating tachycardia (AVRT) and AV nodal reentrant tachycardia (AVNRT). Group IB consisted of 13 patients without spontaneous transition between AVRT and AVNRT. Group IIA consisted of 5 patients with spontaneous transition between AVNRT and atrial tachycardia (AT). Group IIB consisted of 14 patients without spontaneous transition between AVNRT and AT. The absolute values of differences between the two tachycardia cycle lengths were significantly smaller in patients with than in those without transition between the two tachycardias (25 ± 8 msec vs 90 ± 46 msec, P < 0.05, IA vs IB; 21 ± 25 msec vs 99 ± 57 msec, P < 0.01, IIA vs IIB). The cutoff point of 25 msec had 80% positive predictive value for transition between the two tachycardias. Transition between two tachycardias occurred due to a spontaneous premature atrial complex (30%), conduction block at one limb of tachycardia (20%), or tachycardiainduced tachycardia (50%). Absence of transition between two tachycardias might be explained by the absence of a spontaneous premature atrial complex, longer cycle length of the first tachycardia, larger difference between two tachycardia cycle lengths, or induction of each tachycardia under different situations. Conclusion: Double supraventricular tachycardias with similar tachycardia cycle lengths are vulnerable to transition between different tachycardias. [source] | ||||||||||