2012 Proceedings - International Tissue Elasticity Conference

073 ELECTROMECHANICAL WAVE IMAGING OF CANINE AND HUMAN PATHOLOGICAL HEARTS
IN VIVO.
Jean Provost 1 , Alok Gambhir 1 , Alexandre Costet 1 , Julien Grondin 1 , Stanley J. Okrasinski 1 ,
Hasan Garan 1 , Elisa E. Konofagou 1 .
1 Columbia University, New York, NY, USA.
Background: Although arrhythmia and conduction disorders are a major cause of death and disability,
there is no imaging method currently available to the clinician that can map the electrical activation
sequence of the heart noninvasively. Electromechanical Wave Imaging (EWI) is an ultrasound–based
method that can map the electromechanical wave (EW), i.e., the transient deformations occurring in
response to the electrical activation. Recently, we have shown that a direct correlation between the
electrical activation sequence and the EW exists in normal canine hearts [1]. For EWI to become useful
clinically, it is critical to determine whether this correlation is maintained in presence of disease.
Aims: In this study, we aim at validating that EWI can map the activation sequence of the heart in
presence of disease, both in canine and human hearts in vivo.
Methods: Four conditions were studied in a total of 12 canine hearts: Progressive ischemia (n=5), left
bundle branch block (LBBB) (n=1), ventricular fibrillation (VF) (n=2), atrio–ventricular block (AVB) (n=4).
Progressive ischemia was induced by occluding the left–anterior descending coronary artery at 20% flow
decrements; LBBB and AVB were induced by radio–frequency (RF) ablation under fluoroscopy, and VF
occurred spontaneously. A pacemaker was implanted in the right ventricle (RV) of AVB canines. EWI was
performed during progressive ischemia, LBBB, and VF in an acute setting (open–chest) while AVB
canines were studied chronically, in a closed–chest setting. A customized acquisition system was used to
pace the heart and to map the endocardial electrical activation times using a high–resolution, 64–electrode,
basket catheter (Boston Scientific, Nattick, MA). EWI was also performed on three human subjects (n=3)
with heart failure undergoing cardiac resynchronization therapy with LBBB, AVB and/or
cardiomyopathy, during sinus rhythm, and left–ventricular (LV) or RV pacing. EWI was performed using
the automated composite technique (ACT) on a Ultrasonix MDP system with a 3.3MHz phased–array
(Ultrasonix, Burnaby, BC) at 500 fps or with virtual–source sequence (VSS) using a Verasonics system
(Verasonics, Richmond, WA) at 2000 fps. For the VSS sequence, RF frames were reconstructed using a
customized delay–and–sum algorithm implemented on a graphics processing unit (Nvidia, Santa Clara,
CA). Strains were estimated using RF cross–correlation and a least–squares estimator. Up to four views
were combined in multi-plane 3D EWI representations.
Results: In canines with progressive ischemia, the propagation of the EW was impeded in the ischemic
region when the flow occlusion reached 60%. In canines with LBBB, the EW propagation was first
observed in the RV and propagated in the LV; a strong correlation (R=0.83) was found between the EW
and the electrical activation times measured using the basket catheter. In canines with VF, the EW
dominant frequency was in good agreement with the electrical activation dominant frequency. In canines
with AVB, the EW was mapped in conscious canines in all four chambers transthoracically; independent
activation of the atria and paced ventricles was observed, in agreement with the expected normal (atria)
and paced (ventricles) activations.
In patients, EWI could identify the location of the pacing site transmurally. Indeed, during LV pacing
only, the EW originated from the epicardium of the LV lateral wall near the base. During RV pacing, the
EW originated from the apex of the RV. Both origins were in agreement with the transmural location of
the pacing leads. During sinus rhythm with LBBB, the propagation of the EW originated in the RV. In
patients with advanced heart failure (NYHA class IV) region in the lateral wall of the LV did not undergo
the EW. This phenomenon was not observed in patients with mild heart failure (NYHA class I).
Conclusions: These results demonstrate that EWI can be used to characterize LBBB, AVB, fibrillation
and ischemia. Moreover, the results observed in canines were reproduced in the clinical setting.
Therefore, EWI has the potential to assist in the diagnosis and treatment monitoring of conduction
disorders, and more specifically in patients undergoing CRT.
Acknowledgements: Supported in part by NIH R01EB006042, R21HL096094, and R01HL114358).
References:
[1] J. Provost et al.: Proceedings of the National Academy of Sciences. 108(21), pp. 8565–8570, 2011.
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