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Pacing Protocol (pacing + protocol)

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Medical Sciences	77%

Selected Abstracts

Decremental Ramp Atrial Extrastimuli Pacing Protocol for the Induction of Atrioventricular Nodal Re-entrant Tachycardia and Other Supraventricular Tachycardias

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 10 2006
BHARAT K. KANTHARIA M.D.
Aim: The primary aim of this study was to evaluate the utility of decremental ramp atrial extrastimuli pacing protocol (PRTCL) for induction of atrioventricular nodal re-entrant tachycardia (AVNRT), and other supraventricular tachycardias (SVTs), compared to standard (STD) methods. Methods: The study cohort of 121 patients (age 57.51 ± 14.02 years) who presented with documented SVTs and/or symptoms of palpitations and dizziness, and underwent invasive electrophysiological evaluation was divided into Group I (AVNRT, n = 42) and Group II (Control, n = 79). The PRTCL involved a train of six atrial extrastimuli, delivered in a decremental ramp fashion. The STD methods included continuous burst and rapid incremental pacing up to atrioventricular (AV) block cycle length, and single and occasionally double atrial extrastimuli. Prolongation in the Atrio-Hisian (,-AH) intervals achieved by both methods were compared, as were induction frequencies. Results: In Group I, three categories of responses,(1) induction of AVNRT, (2) induction of echo beats only, and (3) none,were observed in 29 (69%), 11 (26%), and 2 (5%) patients with the PRTCL, when compared with 14 (33%), 16 (38%), and 12 (29%) patients with STD methods in the baseline state without the use of pharmacological agents. The ,-AH intervals for each of these three categories were larger using PRTCL versus STD methods; 293.3 ± 95.2 ms versus 192.9 ± 61.4 ms (P < 0.005), 308.6 ± 68.5 ms versus 189. 9 ± 64.9 ms (P < 0.0005), and 203.0 ± 86.3 ms versus 145.8 ± 58.9 ms (P = NS), respectively. In Group II, in one patient with dual AV nodal physiology but no clinical tachycardia, the PRTCL induced nonsustained (12 beats) AVNRT. Additionally, in this group, both PRTCL and STD methods induced atrial tachycardia in two patients and orthodromic AV re-entrant tachycardia in one patient. Conclusion: Decremental ramp atrial extrastimuli pacing PRTCL demonstrates a superior response for induction of typical AVNRT as compared to STD techniques. Because of easy and reliable induction of AVNRT and echo beats by the PRTCL, we recommend it as a method to increase the likelihood of induction of AVNRT. For induction of other SVTs, the PRTCL and the STD methods are comparable. [source]

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]

Regional variations in action potential alternans in isolated murine Scn5a+/, hearts during dynamic pacing

ACTA PHYSIOLOGICA, Issue 2 2010
G. D. K. Matthews
Abstract Aim:, Clinical observations suggest that alternans in action potential (AP) characteristics presages breakdown of normal ordered cardiac electrical activity culminating in ventricular arrhythmogenesis. We compared such temporal nonuniformities in monophasic action potential (MAP) waveforms in left (LV) and right ventricular (RV) epicardia and endocardia of Langendorff-perfused murine wild-type (WT), and Scn5a+/, hearts modelling Brugada syndrome (BrS) for the first time. Methods:, A dynamic pacing protocol imposed successively incremented steady pacing rates between 5.5 and 33 Hz. A signal analysis algorithm detected sequences of >10 beats showing alternans. Results were compared before and following the introduction of flecainide (10 ,m) and quinidine (5 ,m) known to exert pro- and anti-arrhythmic effects in BrS. Results:, Sustained and transient amplitude and duration alternans were both frequently followed by ventricular ectopic beats and ventricular tachycardia or fibrillation. Diastolic intervals (DIs) that coincided with onsets of transient (tr) or sustained (ss) alternans in MAP duration (DI*) and amplitude (DI,) were determined. Kruskal,Wallis tests followed by Bonferroni-corrected Mann,Whitney U -tests were applied to these DI results sorted by recording site, pharmacological conditions or experimental populations. WT hearts showed no significant heterogeneities in any DI. Untreated Scn5a+/, hearts showed earlier onsets of transient but not sustained duration alternans in LV endocardium compared with RV endocardium or LV epicardium. Flecainide administration caused earlier onsets of both transient and sustained duration alternans selectively in the RV epicardium in the Scn5a+/, hearts. Conclusion:, These findings in a genetic model thus implicate RV epicardial changes in the arrhythmogenicity produced by flecainide challenge in previously asymptomatic clinical BrS. [source]

Mechanism of Propensity to Atrial Fibrillation in Patients Undergoing Isthmus Ablation for Typical Atrial Flutter

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2005
HEMANTH RAMANNA M.D.
Background: Patients undergoing isthmus ablation for atrial flutter (AFL) may reveal postablation atrial fibrillation (AF). The electrophysiological mechanism is unclear. In patients with idiopathic AF, enhanced spatial dispersion of right atrial refractoriness was the substrate for the initiation of AF. We hypothesize that dispersion of right atrial refractoriness in patients undergoing AFL ablation is the major cause of postablation AF. Methods: Consecutive patients (n = 42) undergoing isthmus ablation for typical AFL were included. Twelve right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol, starting with one extrastimulus, followed by more aggressive pacing until AF was induced. Mean fibrillatory intervals were used to assess local refractoriness of each recording site. Spatial dispersion of right atrial refractoriness was calculated as the coefficient of dispersion (CD-value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). A CD-value of 3.0 or less was defined as normal, whereas CD-value greater than 3.0 was considered enhanced dispersion. PES and refractoriness analysis were followed by isthmus ablation. Results: Of the 42 patients, 29 had CD-value of 3.0 or less. In these 29 patients, AF was induced with 1 extrastimulus in only 1 patient, with 2 extrastimuli in 4 patients and burst pacing was required to induce AF in 24 of these 29 patients. Prior to the procedure, 5 of 29 patients had AF episodes, after ablation 6 of 29 patients. Of the 42 patients, 13 had CD-value greater than 3.0, AF was induced with a single extrastimulus in 11 patients, with 2 extrastimuli in the remaining 2 patients. Of the 13 patients, 11 had AF episodes both before and after ablation (P < 0.001). Conclusion: Enhanced spatial dispersion of right atrial refractoriness may be the substrate for propensity to AF in patients with AFL. The substrate was associated with enhanced inducibility of atrial fibrillation. [source]

On the Atrial Response to Focal Discharges in Man

JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2004
HEMANTH RAMANNA M.D.
Introduction: Triggers and vulnerability are key factors for the occurrence of atrial fibrillation (AF). The aim of this study was to assess spatial dispersion of atrial refractoriness and vulnerability in response to both focal discharges as well as programmed electrical stimulation in patients undergoing ablation of atrial arrhythmogenic foci. Methods and Results: Twenty-nine patients were studied, and 12 right atrial unipolar electrograms were recorded. Inducibility of AF was assessed by a pacing protocol that started with one extrastimulus, followed by more aggressive pacing until AF was obtained. Mean fibrillatory intervals were used to assess the local refractoriness of each recording site. Spatial dispersion of refractoriness was calculated as the coefficient of dispersion (CD value: standard deviation of the mean of all local mean fibrillatory intervals as a percentage of the overall mean fibrillatory interval). Based on our previous study, a CD value , 3.0 was defined as normal, whereas a CD value >3.0 was considered enhanced spatial dispersion of refractoriness. Fifteen of 29 patients had normal dispersion of refractoriness (mean CD value 1.65 ± 0.43), and AF was inducible with burst pacing only. These patients had focal discharges causing rapid atrial tachycardia with a focal activation pattern. Activation mapping of focal activity was possible in 14 of 15 patients. Focal triggering of AF occurred in only 1 of 15 patients. Fourteen of 29 patients had enhanced dispersion (mean CD value 4.2 ± 0.72). AF was inducible with a single extrastimulus in 11 of 14 patients (P < 0.001). Focal triggering of AF occurred in all 14 patients. Conclusion: Spatial dispersion of atrial refractoriness determines whether focal atrial discharges trigger AF with disorganized activity or, alternatively, only rapid atrial tachycardia. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1-8, June 2004) [source]

Decremental Ramp Atrial Extrastimuli Pacing Protocol for the Induction of Atrioventricular Nodal Re-entrant Tachycardia and Other Supraventricular Tachycardias

Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties

ACTA PHYSIOLOGICA, Issue 1 2010
P. Hakim
Abstract Aim:, In contrast to extensive reports on the roles of Nav1.5 , -subunits, there have been few studies associating the , -subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b,/, mice. Methods:, The following properties were compared in the hearts of wild-type (WT) and Scn3b,/, mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the ,3 protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts. Results:,Scn3b mRNA was expressed in the atria of WT but not Scn3b,/, hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the ,3 protein was expressed in WT and absent in Scn3b,/, cardiac myocytes. Lead I electrocardiograms from Scn3b,/, mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b,/, hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b,/, but hardly any WT hearts. Scn3b,/, hearts also demonstrated significantly longer sinus node recovery times than WT hearts. Conclusion:, These findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion. [source]