scholarly journals Noninvasive reconstruction of the three-dimensional ventricular activation sequence during pacing and ventricular tachycardia in the canine heart

2012 ◽  
Vol 302 (1) ◽  
pp. H244-H252 ◽  
Author(s):  
Chengzong Han ◽  
Steven M. Pogwizd ◽  
Cheryl R. Killingsworth ◽  
Bin He

Single-beat imaging of myocardial activation promises to aid in both cardiovascular research and clinical medicine. In the present study we validate a three-dimensional (3D) cardiac electrical imaging (3DCEI) technique with the aid of simultaneous 3D intracardiac mapping to assess its capability to localize endocardial and epicardial initiation sites and image global activation sequences during pacing and ventricular tachycardia (VT) in the canine heart. Body surface potentials were measured simultaneously with bipolar electrical recordings in a closed-chest condition in healthy canines. Computed tomography images were obtained after the mapping study to construct realistic geometry models. Data analysis was performed on paced rhythms and VTs induced by norepinephrine (NE). The noninvasively reconstructed activation sequence was in good agreement with the simultaneous measurements from 3D cardiac mapping with a correlation coefficient of 0.74 ± 0.06, a relative error of 0.29 ± 0.05, and a root mean square error of 9 ± 3 ms averaged over 460 paced beats and 96 ectopic beats including premature ventricular complexes, couplets, and nonsustained monomorphic VTs and polymorphic VTs. Endocardial and epicardial origins of paced beats were successfully predicted in 72% and 86% of cases, respectively, during left ventricular pacing. The NE-induced ectopic beats initiated in the subendocardium by a focal mechanism. Sites of initial activation were estimated to be ∼7 mm from the measured initiation sites for both the paced beats and ectopic beats. For the polymorphic VTs, beat-to-beat dynamic shifts of initiation site and activation pattern were characterized by the reconstruction. The present results suggest that 3DCEI can noninvasively image the 3D activation sequence and localize the origin of activation of paced beats and NE-induced VTs in the canine heart with good accuracy. This 3DCEI technique offers the potential to aid interventional therapeutic procedures for treating ventricular arrhythmias arising from epicardial or endocardial sites and to noninvasively assess the mechanisms of these arrhythmias.

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Long Yu ◽  
Qi Jin ◽  
Zhaoye Zhou ◽  
Liqun Wu ◽  
Bin He

Introduction: Ventricular arrhythmias have been a major threat to human health in developed countries. Each year, more than 300,000 sudden cardiac death cases have been reported in the U.S. alone. The aim of this study is to evaluate a novel Cardiac Electrical Sparse Imaging technique (CESI) for noninvasive mapping and localizing the origin of ventricular arrhythmias in patients undergoing cardiac catheter ablation. Method: Pre-surgical ECG mapping and CT scans were performed in patients (n=13) with symptomatic Premature Ventricular Contraction (PVC, >10,000 beats /24h). Data analysis was performed upon the ectopic beats (n=130) to image the foci and propagation pattern. The imaged activation patterns were compared with the Local Activation Time (LAT) determined from CARTO 3 system and the CESI imaged initiation sites were compared with the last ablation sites. Results: Good correlation was obtained between the CESI imaged activation and the measured LAT with an averaged Correlation Coefficient of 0.79±0.04 and Relative Error of 0.23±0.05 over 130 beats analyzed. The Relative Temporal Shrinkage was as low as 0.01±0.01, indicating 99% of the temporal resolution was preserved. PVCs were found to originate from RV, RVOT and LV. The focal mechanism was well captured with the foci localized 8±0.9 mm away from the last successful ablation sites. In each individual patient, the activation sequence could be imaged with only one beat and the propagation pattern remained stable among all recorded beats. Conclusion: The present results indicate that CESI is feasible to image the activation pattern and localize the ectopic foci in both RV and LV. The imaged activation patterns are in good agreement with the intra-cardiac measured ones over the endocardial surface, and the localized initiators showed concordance with the real ablation outcome. The present promising results suggest the CESI technique can potentially assist clinical management of ventricular arrhythmias.


2001 ◽  
Vol 281 (2) ◽  
pp. H490-H505 ◽  
Author(s):  
Adam W. Cates ◽  
William M. Smith ◽  
Raymond E. Ideker ◽  
Andrew E. Pollard

Interactions between peripheral conduction system and myocardial wave fronts control the ventricular endocardial activation sequence. To assess those interactions during sinus and paced ventricular beats, we recorded unipolar electrograms from 528 electrodes spaced 0.5 mm apart and placed over most of the perfused rabbit right ventricular free wall endocardium. Left ventricular contributions to electrograms were eliminated by cryoablating that tissue. Electrograms were systematically processed to identify fast (P) deflections separated by >2 ms from slow (V) deflections to measure P-V latencies. By using this criterion during sinus mapping ( n = 5), we found P deflections in 22% of electrograms. They preceded V deflections at 91% of sites. Peripheral conduction system wave fronts preceded myocardial wave fronts by an overall P-V latency magnitude that measured 6.7 ± 3.9 ms. During endocardial pacing ( n = 8) at 500 ms cycle length, P deflections were identified on 15% of electrodes and preceded V deflections at only 38% of sites, and wave fronts were separated by a P-V latency magnitude of 5.6 ± 2.3 ms. The findings were independent of apical, basal, or septal drive site. Modest changes in P-V latency accompanied cycle length accommodation to 125-ms pacing (6.8 ± 2.6 ms), although more pronounced separation between wave fronts followed premature stimulation (11.7 ± 10.4 ms). These results suggested peripheral conduction system and myocardial wave fronts became functionally more dissociated after premature stimulation. Furthermore, our analysis of the first ectopic beats that followed 12 of 24 premature stimuli revealed comparable separation between wave fronts (10.7 ± 5.5 ms), suggesting the dissociation observed during the premature cycles persisted during the initiating cycles of the resulting arrhythmias.


Heart Rhythm ◽  
2011 ◽  
Vol 8 (8) ◽  
pp. 1266-1272 ◽  
Author(s):  
Chengzong Han ◽  
Steven M. Pogwizd ◽  
Cheryl R. Killingsworth ◽  
Bin He

1997 ◽  
Vol 273 (3) ◽  
pp. H1377-H1385 ◽  
Author(s):  
Y. Murakawa ◽  
K. Sezaki ◽  
T. Yamashita ◽  
Y. Kanese ◽  
M. Omata

To investigate the electrophysiological and electrocardiographic characteristics of ventricular arrhythmia due to abnormal repolarization, we studied the three-dimensional activation sequence of cesium-induced ventricular tachycardia (VT) in 10 anesthetized dogs using a 384-channel recording system. Seventeen monomorphic VT (mVT) and eight polymorphic VT (pVT) episodes induced by cesium chloride (2 or 3 mM/kg) were analyzed. Only a single arrhythmogenic focus was detected in most beats of VT, whereas two competing foci were temporarily observed in two episodes of pVT. The site of arrhythmogenic focus of mVT was the endocardium (5 of 17), the midmyocardium (4 of 17), or undetermined (8 of 17). Both endocardial and midmyocardial arrhythmogenic foci were also found in pVT, and most pVT (6 of 8) were associated with the transition of the site of arrhythmogenic focus. These results are consistent with the view that both myocardial muscle fibers and Purkinje cells can cause ventricular arrhythmia due to abnormal repolarization and that changing the site of arrhythmogenic focus is the main mechanism of pVT.


2007 ◽  
Vol 293 (1) ◽  
pp. H754-H761 ◽  
Author(s):  
Benjamin A. Coppola ◽  
James W. Covell ◽  
Andrew D. McCulloch ◽  
Jeffrey H. Omens

Abnormal electrical activation of the left ventricle results in mechanical dyssynchrony, which is in part characterized by early stretch of late-activated myofibers. To describe the pattern of deformation during “prestretch” and gain insight into its causes and sequelae, we implanted midwall and transmural arrays of radiopaque markers into the left ventricular anterolateral wall of open-chest, isoflurane-anesthetized, adult mongrel dogs. Biplane cineradiography (125 Hz) was used to determine the time course of two- and three-dimensional strains while pacing from a remote, posterior wall site. Strain maps were generated as a function of time. Electrical activation was assessed with bipolar electrodes. Posterior wall pacing generated prestretch at the measurement site, which peaked 44 ms after local electrical activation. Overall magnitudes and transmural gradients of strain were reduced when compared with passive inflation. Fiber stretch was larger at aortic valve opening compared with end diastole ( P < 0.05). Fiber stretch at aortic valve opening was weakly but significantly correlated with local activation time ( r2 = 0.319, P < 0.001). With a short atrioventricular delay, fiber lengths were not significantly different at the time of aortic valve opening during ventricular pacing compared with atrial pacing. However, ejection strain did significantly increase ( P < 0.05). We conclude that the majority of fiber stretch occurs after local electrical activation and mitral valve closure and is different from passive inflation. The increased shortening of these regions appears to be because of a reduced afterload rather than an effect of length-dependent activation in this preparation.


2005 ◽  
Vol 12 (2) ◽  
pp. 137-141 ◽  
Author(s):  
Corinna B. Brunckhorst ◽  
Etienne Delacretaz ◽  
Kyoko Soejima ◽  
William H. Maisel ◽  
Peter L. Friedman ◽  
...  

1991 ◽  
Vol 260 (5) ◽  
pp. H1596-H1611 ◽  
Author(s):  
A. S. Douglas ◽  
E. K. Rodriguez ◽  
W. O'Dell ◽  
W. C. Hunter

Understanding the relationship between structure and function in the heart requires a knowledge of the connection between the local behavior of the myocardium (e.g., shortening) and the pumping action of the left ventricle. We asked the question, how do changes in preload and afterload affect the relationship between local myocardial deformation and ventricular volume? To study this, a set of small radiopaque beads was implanted in approximately 1 cm3 of the isolated canine heart left ventricular free wall. Using biplane cineradiography, we tracked the motion of these markers through various cardiac cycles (controlling pre- and afterload) using the relative motion of six markers to quantify the local three dimensional Lagrangian strain. Two different reference states (used to define the strains) were considered. First, we used the configuration of the heart at end diastole for that particular cardiac cycle to define the individual strains (which gave the local “shortening fraction”) and the ejection fraction. Second, we used a single reference state for all cardiac cycles i.e., the end-diastolic state at maximum volume, to define absolute strains (which gave local fractional length) and the volume fraction. The individual strain versus ejection fraction trajectories were dependent on preload and afterload. For any one heart, however, each component of absolute strain was more tightly correlated to volume fraction. Around each linear regression, the individual measurements of absolute strain scattered with standard errors that averaged less than 7% of their range. Thus the canine hearts examined had a preferred kinematic (shape) history during ejection, different from the kinematics of filling and independent or pre-or afterload and of stroke volume.


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