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Noninvasive volumetric substrate detection in post myocardial infarction

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The presence of injured tissue after myocardial infarction (MI) creates substrate responsible for life-threatening ventricular arrhythmia, such as ventricular tachycardia and fibrillation, which often lead to cardiac arrest and sudden death. However, arrhythmogenic mechanism of such substrate is not well defined, because its investigation requires quantitative, complete and detailed knowledge on the correlation of local abnormality in phenomenal electrical function and inherent tissue property during normal sinus rhythm. We have developed a physiological model-constrained framework which utilizes noninvasive body surface potential measurements and tomographic images for personalized imaging of volumetric cardiac electrophysiology, including electrical functioning, tissue property and arrhythmogenic substrate inside the heart. Under the guidance of a prior knowledge of general cardiac electrical activity, this framework extracts subject-specific information from personal data to reconstruct transmembrane potential dynamics and tissue excitability inside the 3D myocardium. Abnormalities in these two different electrophysiological quantities are localized for identifying the latent arrhythmogenic substrate, investigating its possible mechanisms, and therefore assessing arrhythmia susceptibility of individual subject. For four post-MI patients, quantitative evaluation of infarct extent and location is validated by gold standard provided by cardiologists, and exhibit notable improvements over existent results.

This talk is part of the Isaac Newton Institute Seminar Series series.

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