Ping Jia

Noninvasive electrocardiographic imaging for cardiac electrophysiology and arrhythmia

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 hearts 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.

Noninvasive Electrocardiographic Imaging (ECGI): Application of the Generalized Minimal Residual (GMRes) Method

AbstractElectrocardiographic imaging (ECGI) is a developing imaging modality for cardiac electrophysiology and arrhythmias. It reconstructs epicardial potentials, electrograms, and isochrones from electrocardiographic body-surface potentials noninvasively. Current ECGI methodology employs Tikhonov regularization, which imposes constraints on the reconstructed potentials or their derivatives. This approach can sometimes reduce spatial resolution by smoothing the solution. Accuracy depends on a priori knowledge of solution characteristics and determination of an optimal regularization parameter. These properties led us to implement an independent, iterative approach for ECGI—the generalized minimal residual (GMRes) method—which does not apply constraints. GMRes was applied to experimental data during activation/repolarization of normal and infarcted hearts. GMRes reconstructions were compared to Tikhonov reconstructions and to measured “gold standards” in isolated hearts. Overall, the accuracy of GMRes solutions was similar to Tikhonov regularization. However, in certain cases GMRes recovered localized potential features (e.g., multiple potential minima), which were lost in the Tikhonov solution. Simultaneous use of these two complementary methods in clinical ECGI will ensure reliability and maximal extraction of diagnostic information in the absence of a priori information about a patients condition.© 2003 Biomedical Engineering Society. PAC2003: 8719Hh, 8757Gg

Heart-surface reconstruction and ECG electrodes localization using fluoroscopy, epipolar geometry and stereovision: application to noninvasive imaging of cardiac electrical activity

To date there is no imaging modality for cardiac arrhythmias which remain the leading cause of sudden death in the United States (>300,000/yr.). Electrocardiographic imaging (ECGI), a noninvasive modality that images cardiac arrhythmias from body surface potentials, requires the geometrical relationship between the heart surface and the positions of body surface ECG electrodes. A photographic method was validated in a mannequin and used to determine the three-dimensional coordinates of body surface ECG electrodes to within 1 mm of their actual positions. Since fluoroscopy is available in the cardiac electrophysiology (EP) laboratory where diagnosis and treatment of cardiac arrhythmias is conducted, a fluoroscopic method to determine the heart surface geometry was developed based on projective geometry, epipolar geometry, point reconstruction, b-spline interpolation and visualization. Fluoroscopy-reconstructed hearts in a phantom and a human subject were validated using high-resolution computed tomography (CT) imaging. The mean absolute distance error for the fluoroscopy-reconstructed heart relative to the CT heart was 4 mm (phantom) and 10 mm (human). In the human, ECGI images of normal cardiac electrical activity on the fluoroscopy-reconstructed heart showed close correlation with those obtained on the CT heart. Results demonstrate the feasibility of this approach for clinical noninvasive imaging of cardiac arrhythmias in the interventional EP laboratory.

Endocardial Potential Mapping from a Noncontact Nonexpandable Catheter: A Feasibility Study

AbstractIn previous studies, we established methodology for reconstructing endocardial potentials, electrograms and isochrones from a non-contact intracavitary probe during a single beat. The probe was too large to be introduced percutaneously. Here we examine the possibility of similar mapping with a small multielectrode catheter that could be introduced percutaneously and does not expand inside the cavity. Cavity geometry and endocardial potentials were recorded in an isolated canine left ventricle. Simulated catheter probes were introduced into the cavity. Probe potentials were computed from the measured endocardial potentials and perturbed to include measurement noise, geometrical errors, and limited electrode density. Endocardial potentials were then reconstructed from the perturbed probe potentials and compared to the actual measured potentials. Of all probes simulated, a 3.0 mm (9F) catheter that assumes a curved geometry (e.g., a J shape) inside the cavity performed best (better than a larger 7.6 mm cylinder simulating an inflatable probe). Without bending, a straight cylindrical probe of the same size (9F, 3.0 mm) did not perform well. Sixty probe electrodes were needed for accurate reconstruction. The J-probe reconstruction was very robust in the presence of noise (10%) and of geometry errors (3 mm shift, 10° rotation). The results demonstrate the feasibility of accurate single-beat endocardial mapping using a 9F percutaneous multielectrode catheter that assumes a J shape in the cavity without the need for expansion (e.g., into a balloon or a “basket”). The robustness of the procedure to noise and geometrical errors suggests its applicability in the clinical EP laboratory and the possibility of determining probe position in vivo using current imaging modalities.

RV electrical activation in heart failure during right, left, and biventricular pacing.

OBJECTIVES To compare right ventricular (RV) activation during intrinsic conduction or pacing in heart failure (HF) patients. BACKGROUND RV activation during intrinsic conduction or pacing in patients with left ventricular (LV) dysfunction is unclear but may affect the prognosis. In cardiac resynchronization therapy (CRT), timed LV pacing (CRT-LV) may be superior to biventricular pacing (CRT-BiV), and is hypothesized to be due to the merging of LV-paced and right bundle branch-mediated wavefronts, thus avoiding perturbation of RV electrical activation. METHODS Epicardial RV activation duration (RVAD) (onset to end of free wall activation) was evaluated noninvasively by electrocardiographic imaging in healthy control subjects (n = 7) and compared with that of HF patients (LV ejection fraction 23 +/- 10%, n = 14). RVAD in HF was contrasted during RV pacing, CRT-BiV, and CRT-LV at optimized AV intervals. RESULTS During intrinsic conduction in HF (n = 12), the durations of QRS and precordial lead rS complexes were 158 +/- 24 and 77 +/- 17 ms, respectively, indicating delayed total ventricular depolarization but rapid initial myocardial activation. Echocardiography demonstrated no significant RV disease. RV epicardial voltage, activation patterns, and RVAD in HF did not differ from normal (RVAD 32 +/- 15 vs. 28 +/- 3 ms, respectively, p = 0.42). In HF, RV pacing generated variable areas of slow conduction and prolonged RVAD (78 +/- 33 ms, p < 0.001). RVAD remained delayed during CRT-BiV at optimized atrioventricular intervals (76 +/- 32 ms, p = 0.87). In contrast, CRT-LV reduced RVAD to 40 +/- 26 ms (p < 0.016), comparable to intrinsic conduction (p = 0.39) but not when atrioventricular conduction was poor or absent. CONCLUSIONS In HF patients without RV dysfunction treated with CRT, normal RV free wall activation in intrinsic rhythm indicated normal right bundle branch-mediated depolarization. However, the RV was vulnerable to the development of activation delays during RV pacing, whether alone or with CRT-BiV. These were avoided by CRT-LV in patients with normal atrioventricular conduction.

Confirmation of novel noninvasive high-density electrocardiographic mapping with electrophysiology study: Implications for therapy

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Spontaneous Migration of Left Ventricular Electrical Activation Wavefronts During Biventricular Pacing

Noninvasive three-dimensional mapping with electrocardiographic imaging (ECGI) was used to evaluate left ventricular (LV) activation during CRT in a 50-year-old male with nonischemic cardiomyopathy (LV ejection fraction 20%), left bundle branch block (QRS duration 138 ms) and PR interval of 220 ms. During continuous mapping, a change was detected on surface ECG leads, coinciding with a spontaneous shift in LV activation. The figure depicts 10 consecutive beats recorded in leads V1 and V2 (top). After beats 1–2, there is a subtle change to a different QRS morphology during beats

Confirmation of Novel Noninvasive High-Density Electrocardiographic Mapping With Electrophysiology StudyClinical Perspective

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Confirmation of Novel Noninvasive High-Density Electrocardiographic Mapping With Electrophysiology StudyClinical Perspective: Implications for Therapy

Background—Twelve lead ECGs have limited value in precisely identifying atrial and ventricular activation during arrhythmias, including accessory atrioventricular conduction activation. The aim of this study was to report a single center’s clinical experience validating a novel, noninvasive, whole heart, beat-by-beat, 3-dimensional mapping technology with invasive electrophysiological studies, including ablation, where applicable. Methods and Results—Using an electrocardiographic mapping (ECM) system in 27 patients, 3-dimensional epicardial activation maps were generated from >250 body surface ECGs using heart–torso geometry obtained from computed tomographic images. ECM activation maps were compared with clinical diagnoses, and confirmed with standard invasive electrophysiological studies mapping. (1) In 6 cases of Wolff–Parkinson–White syndrome, ECM accurately identified the ventricular insertion site of an accessory atrioventricular connection. (2) In 10 patients with premature ventricular complexes, ECM accurately identified their ventricular site of origin in 8 patients. In 2 of 10 patients transient premature ventricular complex suppression was observed during ablation at the site predicted by ECM as the earliest. (3) In 10 cases of atrial tachycardia/atrial flutter, ECM accurately identified the chamber of origin in all 10, and distinguished isthmus from nonisthmus dependent atrial flutter. (4) In 1 patient with sustained exercise induced ventricular tachycardia, ECM accurately identified the focal origin in the left ventricular outflow tract. Conclusions—ECM successfully provided valid activation sequence maps obtained noninvasively in a variety of rhythm disorders that correlated well with invasive electrophysiological studies.

Fluoroscopy-based method to determine heart geometry for functional imaging of cardiac electrical activity

A fluoroscopy based method for determining heart surface geometry has been developed and validated in phantom and human studies. Biplane fluoroscopic projections were calibrated independently. The heart contour was segmented in each projection and corresponding contour points were matched using epipolar geometry. Points in 3D were reconstructed from the corresponding contour points using point reconstruction. B-splines were approximated from the reconstructed points and meshed to form the heart surface. The fluoroscopy-reconstructed heart was validated in a phantom and human study by comparison to CT imaging. Mean, minimum, maximum and standard deviation of the absolute distance errors were computed for the fluoroscopy-reconstructed heart relative to the CT heart. The mean absolute distance error for the phantom was 4mm. The mean absolute distance error for the human subject was 10 mm. In addition to validating the geometry, we also evaluated in the human subject the feasibility of noninvasive imaging of normal cardiac electrical activity on the fluoroscopy-reconstructed heart by comparing the results to those obtained on the CT heart. Noninvasive images on the fluoroscopy-reconstructed heart by showed close correlation with those obtained on the CT heart (CC=0.70).