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Comput Cardiol. 2008;35(4749156):773-776.

An Artificial Multi-Channel Model for Generating Abnormal Electrocardiographic Rhythms.

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1
Harvard-MIT Division of Health Sciences and Technology (HST), Cambridge, MA 02142, USA.

Abstract

We present generalizations of our previously published artificial models for generating multi-channel ECG so that the simulation of abnormal rhythms is possible. Using a three-dimensional vectorcardiogram (VCG) formulation, we generate the normal cardiac dipole for a patient using a sum of Gaussian kernels, fitted to real VCG recordings. Abnormal beats are then specified either as new dipoles, or as perturbations of the existing dipole. Switching between normal and abnormal beat types is achieved using a hidden Markov model (HMM). Probability transitions can be learned from real data or modeled by coupling to heart rate and sympathovagal balance. Natural morphology changes form beat-to-beat are incorporated as before from varying the angular frequency of the dipole as a function of the inter-beat (RR) interval. The RR interval time series is generated using our previously described model whereby time-and frequency-domain heart rate (HR) and heart rate variability (HRV) characteristics can be specified. QT-HR hysteresis is simulated by coupling the Gaussian kernels associated with the T-wave in the model with a nonlinear factor related to the local HR (determined from the last n RR intervals). Morphology changes due to respiration are simulated by coupling the RR interval to the angular frequency of the dipole. We demonstrate an example of the use of this model by simulating T-Wave Alternans (TWA). The magnitude of the TWA effect is modeled as a disturbance on the T-loop of the dipole with a magnitude that differs in each of the three VCG planes. The effect is then turned on or off using a HMM. The values of the transition matrix are determined by the local heart rate, such that when the HR ramps up towards 100 BPM, the probability of observing a TWA effect rapidly but smoothly increases. In this way, no 'sudden' switching from non-TWA to TWA is observed, and the natural tendency for TWA to be associated with a critical HR-related activation level is simulated. Finally, to generate multi-lead signals, the VCG is mapped to any set of clinical leads using a Dower-like transform derived from a least-squares optimization between known VCGs and known lead morphologies. ECGs with calibrated amounts of TWA were generated by this model and included in the PhysioNet/CinC Challenge 2008 data set.

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