scholarly journals Noninvasive imaging of three-dimensional cardiac activation sequence during pacing and ventricular tachycardia

Heart Rhythm ◽  
2011 ◽  
Vol 8 (8) ◽  
pp. 1266-1272 ◽  
Author(s):  
Chengzong Han ◽  
Steven M. Pogwizd ◽  
Cheryl R. Killingsworth ◽  
Bin He
Keyword(s):  
Ventricular Tachycardia ◽  
Noninvasive Imaging ◽  
Three Dimensional ◽  
Activation Sequence

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
Keyword(s):  
Ventricular Tachycardia ◽  
Clinical Medicine ◽  
Three Dimensional ◽  
Left Ventricular ◽  
Canine Heart ◽  
Cardiovascular Research ◽  
Computed Tomography Images ◽  
Electrical Imaging ◽  
Ectopic Beats ◽  
Activation Sequence

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.

Three-dimensional activation sequence of cesium-induced ventricular arrhythmias

1997 ◽  
Vol 273 (3) ◽  
pp. H1377-H1385 ◽  
Author(s):  
Y. Murakawa ◽  
K. Sezaki ◽  
T. Yamashita ◽  
Y. Kanese ◽  
M. Omata
Keyword(s):  
Ventricular Tachycardia ◽  
Ventricular Arrhythmia ◽  
Purkinje Cells ◽  
Ventricular Arrhythmias ◽  
Three Dimensional ◽  
Cesium Chloride ◽  
Recording System ◽  
Anesthetized Dogs ◽  
Myocardial Muscle ◽  
Activation Sequence

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.

Noninvasive three-dimensional electrocardiographic imaging of ventricular activation sequence

2005 ◽  
Vol 289 (6) ◽  
pp. H2724-H2732 ◽  
Author(s):  
Xin Zhang ◽  
Indiresha Ramachandra ◽  
Zhongming Liu ◽  
Basharat Muneer ◽  
Steven M. Pogwizd ◽  
...  
Keyword(s):  
Surface Potential ◽  
Body Surface ◽  
Cardiac Arrhythmias ◽  
Experimental Studies ◽  
Three Dimensional ◽  
Electrocardiographic Imaging ◽  
Ventricular Activation ◽  
Body Surface Potential ◽  
Life Threatening ◽  
Activation Sequence

Imaging the myocardial activation sequence is critical for improved diagnosis and treatment of life-threatening cardiac arrhythmias. It is desirable to reveal the underlying cardiac electrical activity throughout the three-dimensional (3-D) myocardium (rather than just the endocardial or epicardial surface) from noninvasive body surface potential measurements. A new 3-D electrocardiographic imaging technique (3-DEIT) based on the boundary element method (BEM) and multiobjective nonlinear optimization has been applied to reconstruct the cardiac activation sequences from body surface potential maps. Ultrafast computerized tomography scanning was performed for subsequent construction of the torso and heart models. Experimental studies were then conducted, during left and right ventricular pacing, in which noninvasive assessment of ventricular activation sequence by means of 3-DEIT was performed simultaneously with 3-D intracardiac mapping (up to 200 intramural sites) using specially designed plunge-needle electrodes in closed-chest rabbits. Estimated activation sequences from 3-DEIT were in good agreement with those constructed from simultaneously recorded intracardiac electrograms in the same animals. Averaged over 100 paced beats (from a total of 10 pacing sites), total activation times were comparable (53.3 ± 8.1 vs. 49.8 ± 5.2 ms), the localization error of site of initiation of activation was 5.73 ± 1.77 mm, and the relative error between the estimated and measured activation sequences was 0.32 ± 0.06. The present experimental results demonstrate that the 3-D paced ventricular activation sequence can be reconstructed by using noninvasive multisite body surface electrocardiographic measurements and imaging of heart-torso geometry. This new 3-D electrocardiographic imaging modality has the potential to guide catheter-based ablative interventions for the treatment of life-threatening cardiac arrhythmias.

Three-dimensional nonfluoroscopic guidance for right coronary cusp ventricular tachycardia ablation

Heart Rhythm ◽  
2008 ◽  
Vol 5 (2) ◽  
pp. 326-327
Author(s):  
Miguel A. Arias ◽  
Eduardo Castellanos ◽  
Alberto Puchol ◽  
Belén Santos
Keyword(s):  
Ventricular Tachycardia ◽  
Three Dimensional ◽  
Ventricular Tachycardia Ablation ◽  
Coronary Cusp ◽  
Right Coronary Cusp

The mechanisms of ventricular tachycardia in humans determined by intraoperative recording of the electrical activation sequence

1985 ◽  
Vol 8 (2) ◽  
pp. 163-172 ◽  
Author(s):  
Jay W. Mason ◽  
Edward B. Stinson ◽  
Philip E. Oyer ◽  
Roger A. Winkle ◽  
Steven Hunt ◽  
...  
Keyword(s):  
Ventricular Tachycardia ◽  
Electrical Activation ◽  
Intraoperative Recording ◽  
Activation Sequence

Abstract 16807: Role of Rotor Activation Within the Pulmonary Vein as the Driving Sources for Atrial Fibrillation: Three-dimensional Analysis using a Non-contact Mapping System

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Hiroshige Yamabe ◽  
Hisanori Kanazawa ◽  
Tadashi Hoshiyama ◽  
Miwa Ito ◽  
Shozo Kaneko ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Pulmonary Vein ◽  
Three Dimensional ◽  
Recording Site ◽  
Contact Mapping ◽  
Proximal Half ◽  
Mapping System ◽  
Endocardial Mapping ◽  
Activation Sequence

Background: It has been suggested rotor which is located within the pulmonary vein (PV) acted as the driving sources of atrial fibrillation (AF). However, it has never been confirmed whether or not the rotor exists within PV in human. Objectives: We analyzed the activation sequence within the PV during AF and examined how the PV acted as the driving sources of AF. Methods: Selective endocardial mapping of left superior PV (LSPV) was performed during AF in 11 paroxysmal AF patients using a non-contact mapping system (EnSite 3000). Presence of rotor activation was defined when the circular activation around the functional block line once completed its whole reentrant activation. We analyzed the relation between the pivoting activation and the rotor activation. To define the preferable site of rotor and pivoting activation, we also analyzed the relation between the location of rotor and pivoting activation and region of the complex fractionated electrogram (CFE) recording site. Results: Rotor activation was observed with a mean number of 4.6±3.6 times/sec. CFE was observed at the roof (n=5), ridge (n=11) and carina (n=7) of the proximal half of LSPV with a mean area of 9.1±3.4 cm2. The number of rotor activation observed at the CFE area was significantly higher than that at the non-CFE area (4.1±3.9 vs. 0.7±1.2 times/sec, p=0.025). Total frequency of pivoting activation was 37.0±14.7 times/sec. Pivoting activation involved in the rotor activation was significantly lower than that not involved in the rotor activation (8.8±8.1 vs. 27.7±15.8 times/sec, p=0.0116). Regarding the CFE area, pivoting activation involved in the rotor activation was also significantly lower than that not involved in the rotor activation (8.4±8.2 vs. 24.1±12.0 times/sec, p=0.0105). However, there was no difference between the frequencies of pivoting activation with and without rotor activation in the non-CFE area (1.0±2.0 vs. 3.6±6.1 times/sec, p=NS). Conclusions: Rotor activation was observed at the proximal portion of the LSPV coincided with the location of CFE area. However, most of pivoting activation was not involved in the rotor activation. These suggest that AF was driven by the other meandering propagation associated with frequent non-stable pivoting activation over the CFE area.

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