ABSTRACT
Conduction velocity (CV) slowing is associated with atrial fibrillation (AF) and reentrant ventricular tachycardia (VT). Clinical electroanatomical mapping systems used to localize AF or VT sources as ablation targets remain limited by the number of measuring electrodes and signal processing methods to generate high-density local activation time (LAT) and CV maps of heterogeneous atrial or trabeculated ventricular endocardium. The morphology and amplitude of bipolar electrograms depend on the direction of propagating electrical wavefront, making identification of low-amplitude signal sources commonly associated with fibrotic area difficulty. In comparison, unipolar electrograms are not sensitive to wavefront direction, but measurements are susceptible to distal activity. This study proposes a method for local CV calculation from optical mapping measurements, termed the circle method (CM). The local CV is obtained as a weighted sum of CV values calculated along different chords spanning a circle of predefined radius centered at a CV measurement location. As a distinct maximum in LAT differences is along the chord normal to the propagating wavefront, the method is adaptive to the propagating wavefront direction changes, suitable for electrical conductivity characterization of heterogeneous myocardium. In numerical simulations, CM was validated characterizing modeled ablated areas as zones of distinct CV slowing. Experimentally, CM was used to characterize lesions created by radiofrequency ablation (RFA) on isolated hearts of rats, guinea pig, and explanted human hearts. To infer the depth of RFA-created lesions, excitation light bands of different penetration depths were used, and a beat-to-beat CV difference analysis was performed to identify CV alternans. Despite being limited to laboratory research, studies based on CM with optical mapping may lead to new translational insights into better-guided ablation therapies.
ABSTRACT
Simulations of cardiac electrophysiological models in tissue, particularly in 3D require the solutions of billions of differential equations even for just a couple of milliseconds, thus highly demanding in computational resources. In fact, even studies in small domains with very complex models may take several hours to reproduce seconds of electrical cardiac behavior. Today's Graphics Processor Units (GPUs) are becoming a way to accelerate such simulations, and give the added possibilities to run them locally without the need for supercomputers. Nevertheless, when using GPUs, bottlenecks related to global memory access caused by the spatial discretization of the large tissue domains being simulated, become a big challenge. For simulations in a single GPU, we propose a strategy to accelerate the computation of the diffusion term through a data-structure and memory access pattern designed to maximize coalescent memory transactions and minimize branch divergence, achieving results approximately 1.4 times faster than a standard GPU method. We also combine this data structure with a designed communication strategy to take advantage in the case of simulations in multi-GPU platforms. We demonstrate that, in the multi-GPU approach performs, simulations in 3D tissue can be just 4× slower than real time.
ABSTRACT
Alternans-an arrhythmic response of cardiac tissue to periodic pacing-often serves as a precursor to a more dangerous, and potentially lethal, state of fibrillation. Suppression of alternans using feedback control may be a plausible method to prevent fibrillation. Several approaches based on impulsive control have been proposed previously, where feedback is applied for a brief instance of time during each pacing interval. This paper presents a continuous-time approach, where feedback current is applied at all times, which is capable of suppressing alternans in fibers of significantly greater length (up to at least 4 cm), compared with impulsive control (less than 1 cm), and for a wide range of pacing cycle lengths.