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ABSTRACT: AF Cycle Length Detection Analysis. Introduction: Experimental models have demonstrated that atrial fibrillation (AF) may be due to one or more rapid drivers (source) producing AF. These drivers may be characterized by rapid and regular cycle lengths (CLs), producing fibrillatory conduction to the rest of the atria. The ability to reliably identify such drivers would be invaluable. The purpose of this study was to develop and validate a CL variability detection (CLVD) analysis capable of accurately determining beat-to-beat CLs of atrial electrograms (AEGs) during AF, and then to compare this analysis with dominant frequency (DF) analysis. Methods and Results: We analyzed 6 episodes of AF in 6 dogs (sterile pericarditis model) due either to a single, stable left atrial reentrant circuit, or unstable reentrant circuits causing fibrillatory conduction to the rest of the atria. During AF, AEGs were recorded simultaneously from 400 to 420 electrodes on both atria. CLs from over 20,000 AEGs were manually measured, and compared to CLs detected using both the CLVD and DF analyses. There was significant correlation between (1) CLs measured manually and the CLVD analysis (mean CL: correlation coefficient [CC]= 0.96, standard deviation [SD]: CC = 0.89); and (2) mean CL measured manually and the DF analysis (CC = 0.84). However, there was poor correlation between SD of CLs measured manually and the organization index (OI) by DF analysis (CC =-0.59). Conclusion: The CLVD analysis was validated as being accurate for detecting both rate and degree of regularity of AEGs during AF, and more accurate than DF analysis. (J Cardiovasc Electrophysiol, Vol. pp. 1-8).
Journal of Cardiovascular Electrophysiology 11/2012; · 3.06 Impact Factor
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ABSTRACT: Interventricular mechanical dyssynchrony (VVMD) is a strong predictor of cardiac resynchronization therapy (CRT) response. However, no simple and reliable clinical method of measuring VVMD during CRT implant is currently available. We tested the hypothesis that the EnSite™ NavX™ system (St. Jude Medical, St. Paul, MN, USA) can be used intraoperatively to determine VVMD, thereby facilitating CRT optimization.
During CRT implant, the leads in the right atrium (RA), right ventricle (RV), and left ventricle (LV) were connected to the EnSite™ NavX™ system to record the real-time 3D motion of the lead electrodes. The distances from RA to RV lead electrodes (RA-RV) and RA to LV lead electrodes (RA-LV) were computed over ten cardiac cycles during each of RV pacing and biventricular (BiV) pacing, respectively. The degree of synchrony was computed from the distance waveforms between RA-RV and RA-LV by a cross-covariance method to characterize VVMD. Septal-to-posterior wall motion delay (SPWMD) from M-mode echocardiography (echo) was measured for reference at each pacing intervention. VVMD was present in all five patients undergoing CRT implant.
Four of the five patients demonstrated clear improvement in EnSite™ NavX™-derived VVMD during BiV versus RV pacing, which corresponded to the SPWMD results by echo.
It is feasible to characterize VVMD and resynchronization in CRT patients with the EnSite™ NavX™ system during implant, demonstrating its potential as a tool for intraoperative CRT optimization.
Journal of Interventional Cardiac Electrophysiology 06/2012; 35(2):189-96. · 1.17 Impact Factor
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ABSTRACT: Vanoxerine is a promising, new, investigational antiarrhythmic drug. The purpose of this study was to test the hypothesis that oral dosing of vanoxerine would first terminate induced atrial flutter (AFL) and atrial fibrillation (AF), and then prevent their reinduction.
In 5 dogs with sterile pericarditis, on the fourth day after creating the pericarditis, we performed electrophysiologic (EP) studies at baseline, measuring atrial excitability, refractoriness (AERP), and conduction time (CT) when pacing from the right atrial appendage, Bachmann's bundle (BB), and the posteroinferior left atrium at cycle lengths (CLs) of 400, 300, and 200 ms. Then, after induction of AFL or AF, all dogs received hourly oral doses of vanoxerine: 90 mg, followed by 180 mg and 270 mg. Blood was obtained to determine plasma vanoxerine concentrations at baseline, every 30 minutes, when neither AFL nor AF were inducible, and, finally, 1 hour after the 270 mg dose. Then we repeated the baseline EP studies.
Four dogs had inducible, sustained AFL, and 1 dog only had induced, nonsustained AF. In 4 AFL episodes, oral vanoxerine terminated the AFL and then rendered it noninducible after an average of 111 minutes (range 75-180 minutes) after the first dose was administered. The mean vanoxerine plasma level at the point of noninducibility was 84 ng/mL, with a narrow range of 76-99 ng/mL. In the dog with induced, nonsustained AF, it was no longer inducible at a drug level of 75 ng/mL. Vanoxerine did not significantly (1) prolong the AERP except at BB, and then only at the faster pacing CLs; (2) change atrial excitability thresholds; (3) prolong atrial conduction time, the PR interval, the QRS complex or the QT interval.
Orally administered vanoxerine effectively terminated AFL and rendered it noninducible. It also suppressed inducibility of nonsustained AF. These effects occurred at consistent plasma drug levels. Vanoxerine's insignificant or minimal effects on measured electrophysiologic parameters are consistent with little proarrhythmic risk.
Journal of Cardiovascular Electrophysiology 05/2011; 22(11):1266-73. · 3.06 Impact Factor
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ABSTRACT: The mean, median, and minimum local atrial activation (A-A) intervals have been used to determine the local atrial effective refractory period (AERP) during atrial fibrillation (AF), the underlying assumption being that AF is due to multiple reentrant wavelets.
We tested the hypothesis that when AF is due to a single, rapid, stable reentrant circuit (driver), the minimum and mean local A-A intervals will be similar at sites in the reentrant circuit, but will vary widely at sites with fibrillatory conduction, making these latter intervals unreliable indicators of AERP.
During sustained AF due to a left atrial (LA) driver in 6 sterile pericarditis dogs, electrograms were recorded from 186 bipolar electrodes from both atria. A-A intervals were measured from each recording site during 1.2 seconds of AF. Minimum A-A intervals as well as temporal (within site) and spatial (between sites) variability were determined from all sites.
A-A intervals from each site during AF demonstrated that (1) 90-100% of right atrial (RA) sites and 18-39% of LA sites showed considerable (SD > 6 ms) temporal variability; (2) RA and LA sites with fibrillatory conduction (SD > 6 ms) showed considerable (a) spatial variability (RA: 9-36 ms; LA: 5-27 ms) and (b) variability of the minimum A-A intervals (RA: 14-35 ms; LA 11-28 ms).
During AF due to a driver, areas with fibrillatory conduction manifested considerable variability in the mean and the minimum A-A intervals. Therefore, it is unlikely that any of the A-A intervals reflect AERP.
Journal of Cardiovascular Electrophysiology 03/2011; 22(3):310-5. · 3.06 Impact Factor
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ABSTRACT: Cardiac resynchronization therapy (CRT) restores synchrony in heart failure patients. However, a significant proportion of patients implanted with CRT devices do not realize any benefit from CRT. Placing a left ventricular (LV) lead at the sites of electrical or mechanical delay has been advocated to maximize response to CRT, but there is currently no technique described to measure mechanical delay in real-time. We describe a novel technique that can be used intraoperatively to assess mechanical and electrical activation of the coronary sinus for guidance of LV pacing site optimization during CRT implantation.
Journal of Cardiovascular Electrophysiology 12/2009; 21(2):219-22. · 3.06 Impact Factor
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ABSTRACT: Vanoxerine produces potent block of cardiac hERG, sodium, and L-type calcium channels. Block is strongly frequency dependent, is unassociated with transmural dispersion of repolarization, and occurs at concentrations safe in humans. Therefore, we proposed that vanoxerine might be antiarrhythmic. In these studies, we tested the hypothesis that vanoxerine would terminate induced atrial fibrillation (AF) and atrial flutter (AFL) in dogs with sterile pericarditis (SP).
In 9 SP dogs, 11 episodes each of sustained (>10 minutes) AF and AFL were induced. Electrophysiological studies were performed before and after infusion of vanoxerine, which effectively terminated AF and AFL in 19 of 22 episodes. Simultaneous multisite mapping during 3 AF and 3 AFL episodes demonstrated that termination of each arrhythmia occurred with termination of the driver (a reentrant circuit) following an increase in tachycardia CL. Except for conduction in an area of slow conduction in the driver's reentrant circuit, vanoxerine did not significantly affect intraatrial or atrioventricular conduction time, QRS duration, or QT/QTc intervals. Ventricular refractoriness prolonged minimally during ventricular pacing at 400 and 333 ms (176 +/- 16 ms to 182 +/- 16 ms; 173 +/- 11 ms to 178 +/- 18 ms, respectively). Vanoxerine minimally increased (mean 0.7 mA) atrial stimulus threshold for capture.
Vanoxerine effectively terminated induced, sustained AF and AFL in the canine SP model, and produced insignificant or minimal changes in refractoriness, conduction time, or stimulus threshold, consistent with little proarrhythmic risk.
Journal of Cardiovascular Electrophysiology 10/2009; 21(3):311-9. · 3.06 Impact Factor
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ABSTRACT: Studies of atrial fibrillation (AF) have demonstrated that a stable rhythm of very short cycle length in the left atrium (LA) can cause fibrillatory conduction in the rest of the atria. We tested the hypothesis that fast Fourier transform (FFT) analysis of atrial electrograms (AEGs) during this AF will rapidly and reliably identify LA-to-right atrium (RA) conduction pathway(s) generated by the driver. METHODS AND RESULTS: During induced atrial tachyarrhythmias in the canine sterile pericarditis and rapid ventricular pacing-induced congestive heart failure models, 380-404 AEGs were recorded simultaneously from epicardial electrodes on both atria. FFT analysis of AEGs during AF demonstrated a dominant frequency peak in the LA (driver), and multiple frequency peaks in parts of the LA and the most of the RA. Conduction pathways from the LA driver to the RA varied from study-to-study. They were identified by the presence of multiple frequency peaks with one of the frequency peaks at the same frequency as the driver, and traveled (1) inferior to the inferior vena cava (IVC); (2) between the superior vena cava and the right superior pulmonary vein (RSPV); (3) between the RSPV and the right inferior pulmonary vein (RIPV); (4) between the RIPV and the IVC; and (5) via Bachmann's bundle. Conduction pathways identified by FFT analysis corresponded to the conduction pathways found in classical sequence of activation mapping. Computation time for FFT analysis for each AF episode took less than 5 minutes. CONCLUSION: FFT analysis allowed rapid and reliable detection of the LA-to-RA conduction pathways in AF generated by a stable and rapid LA driver.
Journal of Cardiovascular Electrophysiology 02/2009; 20(6):667-74. · 3.06 Impact Factor
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ABSTRACT: In the canine sterile pericarditis model, typically only atrial fibrillation (AF) is inducible on postoperative day 2.
In this model, we tested the hypothesis that on postoperative day 2, placing a fixed line of block (LoB) between the vena cavae critically alters the atrial substrate, favoring the induction of sustained atrial flutter (AFL) instead of AF.
In 6 sterile pericarditis dogs, sustained AF was induced by rapid atrial pacing. After terminating AF, a fixed LoB between the vena cavae was created (cryoablation), and AF reinduction was attempted. Simultaneous mapping from 400 to 420 electrodes on the right and left atrial epicardium and the interatrial atrial septum was performed during all studies.
Before creation of the LoB, in all 6 dogs, rapid atrial pacing induced sustained AF because of a rapid (mean cycle length [CL] 110 +/- 10 ms), regular, left atrial reentrant driver, which caused fibrillatory conduction. After creation of the LoB, in 5 dogs, rapid atrial pacing now induced sustained AFL (mean CL 167 +/- 13 ms). In the 6th dog, AFL failed to develop because the left atrial driver that was induced before the LoB was still reproducibly induced despite the LoB.
In this model of sustained AF, altering the substrate to create a fixed LoB between the vena cavae creates a substrate favoring the induction of AFL.
Heart rhythm: the official journal of the Heart Rhythm Society 01/2009; 5(12):1745-52. · 4.56 Impact Factor
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ABSTRACT: Atrial fibrillation (AF) and atrial flutter (AFL) are common following cardiac surgery and are associated with significant morbidity. We tested the hypothesis that suppression of the inflammatory response with steroids would significantly modify the inducibility of postoperative AF/AFL in the canine sterile pericarditis model.
Twenty-three dogs were studied daily from creation of pericarditis to the fourth postoperative day: 11 dogs were treated with oral prednisone (PRED) starting 2 days preoperatively until the end of the study; 12 dogs were controls (CON). EP testing was performed daily using epicardial electrodes placed at initial surgery. High-resolution (404 sites) epicardial mapping was performed during the terminal study. Baseline and daily CRP levels were obtained in all dogs.
Sustained AFL was absent in PRED (0%) versus CON dogs (91%; P < 0.001); AF induced in the early postoperative course in PRED dogs was of very short CL (mean 66 ms). Tissue inflammation was significantly attenuated in PRED dogs. Thresholds were lower in PRED versus CON dogs, significantly so on postoperative day (POD) 3. There was a trend toward lower ERPs in the PRED group at all CLs. CRP levels were markedly reduced in PRED versus CON dogs (peak CRP 78 +/- 7 mg/L vs 231 +/- 21 mg/L, P < 0.001), and returned to baseline in PRED dogs by POD 4, correlating with a virtual absence of sustained arrhythmia. During open chest mapping studies on POD 4, PRED dogs showed only nonsustained AF/AFL.
Prednisone eliminated postoperative AFL, affected all EP parameters studied, and attenuated the inflammatory response associated with pericarditis.
Journal of Cardiovascular Electrophysiology 02/2008; 19(1):74-81. · 3.06 Impact Factor
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ABSTRACT: The canine sterile pericarditis model is characterized by impaired conduction and atrial arrhythmia vulnerability. Electrical and structural remodeling processes caused by the inflammatory response likely promote these abnormalities. In the present study, we tested the hypothesis that altered distribution of atrial connexins is associated with markedly abnormal atrial conduction, thereby contributing to vulnerability to atrial flutter (AFL) and atrial fibrillation (AF) induction and maintenance. During rapid pacing and induced, sustained AFL or AF in five sterile pericarditis (SP) and five normal (NL) dogs, epicardial atrial electrograms were recorded simultaneously from both atria (380 electrodes) or from the right atrium (RA) and Bachmann's bundle (212 electrodes). Tissues from RA sites were subjected to immunostaining and immunoblotting to assess connexin (Cx) 40 and Cx43 distribution and expression. Transmural myocyte (alpha-actinin) and fibroblast (vimentin) volume were also assessed by immunostaining. RA pacing maps showed markedly abnormal conduction in SP, with uniform conduction in NL. Total RA activation time was significantly prolonged in SP vs. NL at 300-ms and 200-ms pacing-cycle lengths. Sustained arrhythmias were only inducible in SP [total: 4/5 (AFL: 3/5; AF: 1/5)]. In NL, Cx40, Cx43, alpha-actinin, and vimentin were homogeneously distributed transmurally. In SP, Cx40, Cx43, and alpha-actinin were absent epicardially, decreased midmyocardially, and normal endocardially. SP increased epicardial vimentin expression, suggesting fibroblast proliferation. Immunoblot analysis confirmed reduced expression of Cx40 and Cx43 in SP. The transmural gradient in the volume fraction of Cx40 and Cx43 in SP is associated with markedly abnormal atrial conduction and is likely an important factor in the vulnerability to induction and maintenance of AFL/AF in SP.
AJP Heart and Circulatory Physiology 09/2007; 293(2):H1231-41. · 3.71 Impact Factor
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ABSTRACT: Renin-angiotensin-aldosterone system activation may be involved in the pathogenesis of atrial arrhythmias in congestive heart failure (CHF). The effects of aldosterone blockade on atrial tachyarrhythmias have not been evaluated. This study's aim was to determine whether selective aldosterone blockade suppresses atrial tachyarrhythmia inducibility and modifies atrial electrical and/or structural remodeling in a canine model of rapid ventricular pacing (RVP)-induced CHF.
Dogs were assigned randomly to treatment with oral placebo or eplerenone (50 mg/day) and divided into four groups: two sham-operated (no RVP) and two RVP groups. After 5 weeks of no RVP or RVP at 230 beats/min along with concurrent placebo or eplerenone treatment, dogs underwent electrophysiologic and echocardiographic studies. Sustained atrial tachyarrhythmia inducibility (>10-minute duration), atrial effective refractory periods (ERPs), systolic and diastolic function, and left atrial and left ventricular (LV) chamber sizes were assessed. Placebo-treated RVP dogs developed CHF with LV systolic and diastolic dysfunction, left atrial and LV enlargement, increased atrial ERPs, and inducible sustained atrial tachyarrhythmias. Eplerenone treatment in RVP dogs significantly suppressed sustained atrial tachyarrhythmia inducibility, nonuniformly prolonged atrial ERPs and attenuated LV diastolic dysfunction without modifying left atrial or LV dilation or ejection fractions in CHF. Isoproterenol (2-4 microg/min) reversed eplerenone's atrial antiarrhythmic and ERP prolonging effects in CHF. Eplerenone did not alter atrial ERPs in sham (no RVP) dogs without CHF.
Eplerenone suppresses inducibility of sustained atrial tachyarrhythmias, selectively prolongs atrial ERPs, and attenuates LV diastolic remodeling in RVP-induced CHF. Aldosterone blockade may be a promising new approach for atrial tachyarrhythmia prevention in CHF.
Journal of Cardiovascular Electrophysiology 06/2006; 17(5):534-41. · 3.06 Impact Factor
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ABSTRACT: Knowledge of normal human cardiac excitation stems from isolated heart or intraoperative mapping studies under nonphysiological conditions. Here, we use a noninvasive imaging modality (electrocardiographic imaging) to study normal activation and repolarization in intact unanesthetized healthy adults under complete physiological conditions. Epicardial potentials, electrograms, and isochrones were noninvasively reconstructed. The normal electrophysiological sequence during activation and repolarization was imaged in seven healthy subjects (four males and three females). Electrocardiographic imaging depicted salient features of normal ventricular activation, including timing and location of the earliest right ventricular (RV) epicardial breakthrough in the anterior paraseptal region, subsequent RV and left ventricular (LV) breakthroughs, apex-to-base activation of posterior LV, and late activation of LV base or RV outflow tract. The repolarization sequence was unaffected by the activation sequence, supporting the hypothesis that in normal hearts, local action potential duration (APD) determines local repolarization time. Mean activation recovery interval (ARI), reflecting local APD, was in the typical human APD range (235 ms). Mean LV apex-to-base ARI dispersion was 42 ms. Average LV ARI exceeded RV ARI by 32 ms. Atrial images showed activation spreading from the sinus node to the rest of the atria, ending at the left atrial appendage. This study provides previously undescribed characterization of human cardiac activation and repolarization under normal physiological conditions. A common sequence of activation was identified, with interindividual differences in specific patterns. The repolarization sequence was determined by local repolarization properties rather than by the activation sequence, and significant dispersion of repolarization was observed between RV and LV and from apex to base.
Proceedings of the National Academy of Sciences 05/2006; 103(16):6309-14. · 9.68 Impact Factor
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ABSTRACT: Cardiac resynchronization therapy (CRT) for congestive heart failure patients with delayed left ventricular (LV) conduction is clinically beneficial in approximately 70% of patients. Unresolved issues include patient selection, lead placement, and efficacy of LV pacing alone. Being an electrical approach, detailed electrical information during CRT is critical to resolving these issues. However, electrical data from patients have been limited because of the requirement for invasive mapping.
The purpose of this study was to provide observations and insights on the variable electrophysiologic responses of the heart to CRT using electrocardiographic imaging (ECGI).
ECGI is a novel modality for noninvasive epicardial mapping. ECGI was conducted in eight patients undergoing CRT during native rhythm and various pacing modes.
In native rhythm (six patients), ventricular activation was heterogeneous, with latest activation in the lateral LV base in three patients and in the anterolateral, midlateral, or inferior LV in the remainder of patients. Anterior LV was susceptible to block and slow conduction. Right ventricular pacing improved electrical synchrony in two of six patients. LV pacing in three of four patients involved fusion with intrinsic excitation resulting in electrical resynchronization similar to biventricular pacing. Although generally electrical synchrony improved significantly with biventricular pacing, it was not always accompanied by clinical benefit.
Results suggest that (1) when accompanied by fusion, LV pacing alone can be as effective as biventricular pacing for electrical resynchronization; (2) right ventricular pacing is not effective for resynchronization; and (3) efficacy of CRT depends strongly on the patient-specific electrophysiologic substrate.
Heart Rhythm 04/2006; 3(3):296-310. · 4.10 Impact Factor
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ABSTRACT: Different analysis techniques have been developed to help understand and characterize the mechanisms responsible for atrial arrhythmias. We tested the hypothesis that Fast Fourier Transform (FFT) analysis of recorded atrial electrograms (AEGs) will rapidly and accurately identify regular and irregular patterns of atrial activation, and, thereby, may provide evidence suggestive of underlying mechanisms of atrial tachyarrhythmias.
During induced atrial tachyarrhythmias in both the canine sterile pericarditis model and canine rapid ventricular pacing-induced congestive heart failure model; 380-404 AEGs were recorded simultaneously from epicardial electrodes on both atria. From AEGs, atrial activation sequences were determined during atrial flutter (AFL), focal atrial tachycardia (AT), and atrial fibrillation (AF). Four-second recording segments of each AEG were subjected to FFT analysis. Frequencies found during FFT analyses in all studies precisely corresponded to the cycle lengths of the AEGs. In AFL and AT, one dominant frequency peak was found throughout both atria. In AF due to multiple unstable reentry circuits, multiple and broad frequency peaks were found in both atria. In AF due to a stable rapid rhythm (driver) in the left atrium with fibrillatory conduction to the rest of the atria, one dominant frequency peak in areas with 1:1 conduction from the driver, and multiple and/or broad frequency peaks in areas with fibrillatory conduction produced by the driver were found. Computation time for all FFT analyses took <5 minutes.
FFT analysis accurately and rapidly identifies global atrial activation patterns during AFL, AT, and AF, thereby assisting in determining arrhythmia mechanisms.
Journal of Cardiovascular Electrophysiology 03/2006; 17(2):198-206. · 3.06 Impact Factor
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Anselma Intini,
Robert N Goldstein,
Ping Jia,
Charulatha Ramanathan, Kyungmoo Ryu,
Bartolomeo Giannattasio,
Robert Gilkeson,
Bruce S Stambler,
Pedro Brugada,
William G Stevenson,
Yoram Rudy,
Albert L Waldo
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ABSTRACT: We report the first clinical application of electrocardiographic imaging (ECGI), a new, noninvasive imaging modality for arrhythmias, in an athlete with focal ventricular tachycardia (VT) originating from a left ventricular (LV) diverticulum. A reconstructed map of the epicardial activation sequence during a single premature ventricular complex (PVC) of an identical QRS morphology to the clinical VT, generated from 224-electrode body surface ECGs and a chest CT (ECGI), localized the PVC to the site of the diverticulum. This correlated with subsequent maps obtained using standard techniques. We describe the first case that used ECGI to guide diagnosis and therapy of a clinical tachyarrhythmia.
Heart Rhythm 12/2005; 2(11):1250-2. · 4.10 Impact Factor
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ABSTRACT: Dogs with rapid ventricular pacing (RVP)-induced congestive heart failure (CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis that rapid atrial activation in multiple regions and at different rates is responsible for sustained AF in this CHF model.
We studied 12 episodes of sustained (>10 minutes) AF induced in 12 dogs with CHF produced by 3-6 weeks of RVP at 230 beats/minute. High-density mapping of AF was performed using 382 unipolar atrial electrograms recorded simultaneously from epicardial electrodes on the right (RA) and left atria (LA) and Bachmann's bundle. AF mechanisms were based on Fast Fourier Transform (FFT) analysis and activation sequence mapping. A driver was defined as a rapid stable activation region with a single dominant frequency peak in FFT analysis. During AF, three FFT and activation patterns were seen: (1) a single LA driver (7.8 +/- 1.1 Hz) near the pulmonary veins (PVs) with irregular activation in the rest of the atria (n = 4); (2) simultaneous, multisite, biatrial drivers at differing frequencies (LA vs RA dominant frequency gradient: 1.3 +/- 0.8 Hz) near the PVs (8.4 +/- 0.3 Hz) and high RA (8.5 +/- 1.5 Hz) (n = 7); and (3) biatrial irregular activation with multiple and/or broadband frequency peaks without a dominant frequency. (LA: 7.1-11.4 Hz; RA: 5.9-7.7 Hz) (n = 1). Atrial drivers had either a focal activation pattern or were due to a macroreentrant circuit around the PVs.
In this CHF model, FFT analysis and activation sequence mapping demonstrate that sustained AF is characterized by single and multiple, stable LA and RA drivers with predominant sources in the PVs and high RA causing fibrillatory conduction.
Journal of Cardiovascular Electrophysiology 12/2005; 16(12):1348-58. · 3.06 Impact Factor
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ABSTRACT: Nonuniform conduction may cause block and/or delay, thereby providing a substrate for the onset and maintenance of reentrant atrial arrhythmias. We tested the hypothesis that linear triple-site, bipolar, rapid pacing (LTSBRP) of the right atrium generates more uniform wave-front propagation compared with single-site, bipolar, rapid pacing (SSBRP), thereby reducing and/or eliminating conduction block and delay that is otherwise present. Five dogs with pericarditis and three normal dogs were studied. Three plunge-wire electrode pairs were placed 5-7 mm apart in both perpendicular and parallel configurations at the superior aspect of the crista terminalis and were used to pace at 200- and 300-ms cycle lengths for < or =6 s. During pacing, 380 electrograms were recorded simultaneously from electrode arrays placed epicardially on the atria, which produced activation sequence maps for each pacing episode. Local conduction-velocity vectors were computed for each site during each episode. Histograms of absolute velocity vector angles from the x-axis (of the crista terminalis) were plotted to assess uniformity of wave-front propagation, and the magnitude of each vector was computed to assess the local speed. LTSBRP showed 1) more uniform linear activation wave fronts compared with SSBRP, 2) velocity vectors with a more uniform magnitude and direction compared with SSBRP, 3) a predominant absolute velocity vector angle vs. a scattered angle distribution with SSBRP, and 4) shorter right atrial activation time and faster mean epicardial speed than SSBRP for each pacing cycle length. LTSBRP created a more uniform wave-front propagation with less or no conduction block and/or delay compared with SSBRP.
AJP Heart and Circulatory Physiology 08/2005; 289(1):H374-84. · 3.71 Impact Factor
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ABSTRACT: Cardiac arrhythmias are a leading cause of death and disability. Electrocardiographic imaging (ECGI) is a noninvasive imaging modality that reconstructs potentials, electrograms, and isochrones on the epicardial surface from body surface measurements. We previously demonstrated in animal experiments through comparison with simultaneously measured epicardial data the high accuracy of ECGI in imaging cardiac electrical events. Here, images obtained by noninvasive ECGI are compared to invasive direct epicardial mapping in open heart surgery patients.
Three patients were studied during sinus rhythm and right ventricular endocardial and epicardial pacing (total of five datasets). Body surface potentials were acquired preoperatively or postoperatively using a 224-electrode vest. Heart-torso geometry was determined preoperatively using computed tomography. Intraoperative mapping was performed with two 100-electrode epicardial patches.
Noninvasive potential maps captured epicardial breakthrough sites and reflected general activation and repolarization patterns, localized pacing sites to approximately 1 cm and distinguished between epicardial and endocardial origin of activation. Noninvasively reconstructed electrogram morphologies correlated moderately with their invasive counterparts (cross correlation = 0.72 +/- 0.25 [sinus rhythm], 0.67 +/- 0.23 [endocardial pacing], 0.71 +/- 0.21 [epicardial pacing]). Noninvasive isochrones captured the sites of earliest activation, areas of slow conduction, and the general excitation pattern.
Despite limitations due to nonsimultaneous acquisition of the surgical and noninvasive data under different conditions, the study demonstrates that ECGI can capture important features of cardiac electrical excitation in humans noninvasively during a single beat. It also shows that general excitation patterns and electrogram morphologies are largely preserved in open chest conditions.
Heart Rhythm 05/2005; 2(4):339-54. · 4.10 Impact Factor
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ABSTRACT: The mechanisms of chronic atrial fibrillation (AF) are not well understood. We performed epicardial mapping of chronic AF in patients undergoing open heart surgery to test the hypothesis that chronic AF is due to a left atrial "driver" with a regular, short cycle length, resulting in fibrillatory conduction to the rest of the atria.
Nine patients with chronic AF (1 month to >15 years' duration) were studied at open heart surgery, 8 before and 1 during cardiopulmonary bypass. During AF, atrial electrograms (AEGs) were recorded for 1 to 5 minutes from 404 epicardial electrodes arranged in bipoles along with ECG lead II or ventricular electrogram. Four-second segments of each bipolar AEG were also subjected to fast Fourier transform analysis. Two patterns of atrial activation were present during AF. In pattern 1 (7/9 patients), AEGs from parts of the atria demonstrated a short, regular cycle length with identical beat-to-beat morphology, and the rest of the atria were activated irregularly, and AEGs that demonstrated constant morphology and cycle length were localized to parts of the left atria (5/7), the right atria (1/7), or both atria (1/7). In pattern 2 (2/9 patients), AEGs showed no evidence of regular activation or constant morphology.
In 9 patients with chronic AF, the commonest recorded AEG pattern showed an area of regular, rapid rhythm, consistent with the possibility that a driver causing fibrillatory conduction is one mechanism of AF in these patients.
Circulation 12/2004; 110(21):3293-9. · 14.74 Impact Factor
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ABSTRACT: Over 7 million people worldwide die annually from erratic heart rhythms (cardiac arrhythmias), and many more are disabled. Yet there is no imaging modality to identify patients at risk, provide accurate diagnosis and guide therapy. Standard diagnostic techniques such as the electrocardiogram (ECG) provide only low-resolution projections of cardiac electrical activity on the body surface. Here we demonstrate the successful application in humans of a new imaging modality called electrocardiographic imaging (ECGI), which noninvasively images cardiac electrical activity in the heart. In ECGI, a multielectrode vest records 224 body-surface electrocardiograms; electrical potentials, electrograms and isochrones are then reconstructed on the heart's surface using geometrical information from computed tomography (CT) and a mathematical algorithm. We provide examples of ECGI application during atrial and ventricular activation and ventricular repolarization in (i) normal heart (ii) heart with a conduction disorder (right bundle branch block) (iii) focal activation initiated by right or left ventricular pacing, and (iv) atrial flutter.
Nature Medicine 05/2004; 10(4):422-8. · 22.46 Impact Factor
