J.J.E. Blauer, D. Swenson, K. Higuchi, G. Plank, R. Ranjan, N. Marrouche,, R.S. MacLeod.
Sensitivity and Specificity of Substrate Mapping: An In Silico Framework for the Evaluation of Electroanatomical Substrate Mapping Strategies, In Journal of Cardiovascular Electrophysiology, In Journal of Cardiovascular Electrophysiology, Vol. 25, No. 7, Note: Featured on journal cover., pp. 774--780. May, 2014.
- Voltage mapping is an important tool for characterizing proarrhythmic electrophysiological substrate, yet it is subject to geometric factors that influence bipolar amplitudes and thus compromise performance. The aim of this study was to characterize the impact of catheter orientation on the ability of bipolar amplitudes to accurately discriminate between healthy and diseased tissues. Methods and Results
- We constructed a three-dimensional, in-silico
, bidomain model of cardiac tissue containing transmural lesions of varying diameter. A planar excitation wave was stimulated and electrograms were sampled with a realistic catheter model at multiple positions and orientations. We carried out validation studies in animal experiments of acute ablation lesions mapped with a clinical mapping system. Bipolar electrograms sampled at higher inclination angles of the catheter with respect to the tissue demonstrated improvements in both sensitivity and specificity of lesion detection. Removing low voltage electrograms with concurrent activation of both electrodes, suggesting false attenuation of the bipolar electrogram due to alignment with the excitation wavefront, had little effect on the accuracy of voltage mapping. Conclusions
- Our results demonstrate possible mechanisms for the impact of catheter orientation on voltage mapping accuracy. Moreover, results from our simulations suggest that mapping accuracy may be improved by selectively controlling the inclination of the catheter to record at higher angles with respect to the tissue.
Keywords: arrhythmia, computer-based model, electroanatomical mapping, voltage mapping, bipolar electrogram
K.S. McDowell, F. Vadakkumpadan, R. Blake, J. Blauer, G.t Plank, R.S. MacLeod, N.A. Trayanova.
Mechanistic Inquiry into the Role of Tissue Remodeling in Fibrotic Lesions in Human Atrial Fibrillation, In Biophysical Journal, Vol. 104, pp. 2764--2773. 2013.
PubMed ID: 23790385
PubMed Central ID: PMC3686346
Atrial fibrillation (AF), the most common arrhythmia in humans, is initiated when triggered activity from the pulmonary veins propagates into atrial tissue and degrades into reentrant activity. Although experimental and clinical findings show a correlation between atrial fibrosis and AF, the causal relationship between the two remains elusive. This study used an array of 3D computational models with different representations of fibrosis based on a patient-specific atrial geometry with accurate fibrotic distribution to determine the mechanisms by which fibrosis underlies the degradation of a pulmonary vein ectopic beat into AF. Fibrotic lesions in models were represented with combinations of: gap junction remodeling; collagen deposition; and myofibroblast proliferation with electrotonic or paracrine effects on neighboring myocytes. The study found that the occurrence of gap junction remodeling and the subsequent conduction slowing in the fibrotic lesions was a necessary but not sufficient condition for AF development, whereas myofibroblast proliferation and the subsequent electrophysiological effect on neighboring myocytes within the fibrotic lesions was the sufficient condition necessary for reentry formation. Collagen did not alter the arrhythmogenic outcome resulting from the other fibrosis components. Reentrant circuits formed throughout the noncontiguous fibrotic lesions, without anchoring to a specific fibrotic lesion.
K.S. McDowell, F. Vadakkumpadan, R. Blake, J. Blauer, G. Plank, R.S. MacLeod, N.A. Trayanova.
Methodology for patient-specific modeling of atrial fibrosis as a substrate for atrial fibrillation, In Journal of Electrocardiology, Vol. 45, No. 6, pp. 640--645. 2012.
PubMed ID: 22999492
PubMed Central ID: PMC3515859
Personalized computational cardiac models are emerging as an important tool for studying cardiac arrhythmia mechanisms, and have the potential to become powerful instruments for guiding clinical anti-arrhythmia therapy. In this article, we present the methodology for constructing a patient-specific model of atrial fibrosis as a substrate for atrial fibrillation. The model is constructed from high-resolution late gadolinium-enhanced magnetic resonance imaging (LGE-MRI) images acquired in vivo from a patient suffering from persistent atrial fibrillation, accurately capturing both the patient's atrial geometry and the distribution of the fibrotic regions in the atria. Atrial fiber orientation is estimated using a novel image-based method, and fibrosis is represented in the patient-specific fibrotic regions as incorporating collagenous septa, gap junction remodeling, and myofibroblast proliferation. A proof-of-concept simulation result of reentrant circuits underlying atrial fibrillation in the model of the patient's fibrotic atrium is presented to demonstrate the completion of methodology development.
Keywords: Patient-specific modeling, Computational model, Atrial fibrillation, Atrial fibrosis