Key result
Severe cooling of simulated human atrial tissue to ~5°C for ~200ms successfully terminated all electrical activity and scroll waves by substantially decreasing tissue excitability.
Why the study?
Little is known about how ambient temperature influences cardiac electrophysiological properties such as resting membrane potential, excitability, action potential characteristics, restitution, and conduction velocity beyond action potential prolongation.
Does ambient temperature variation affect the electrophysiological properties of human atrial cardiomyocytes in silico?
Does ambient temperature variation affect the electrophysiological properties of human atrial cardiomyocytes in silico?
Heterogeneous electrophysiological responses to temperature changes in human atria may explain proarrhythmic substrate development during mild hypothermia and suggest brief, severe hypothermia as a potential AF treatment strategy.
May alter arrhythmia risk assessment in temperature extremes; leaves open clinical translation pending higher-level validation.
Ambient temperature has a profound influence on cellular electrophysiology through direct control over the gating mechanisms of different ion channels. In the heart, low temperature is known to favour prolongation of the action potential. However, not much is known about the influence of temperature on other important characterisation parameters such as the resting membrane potential (RMP), excitability, morphology and characteristics of the action potential (AP), restitution properties, conduction velocity (CV) of signal propagation, etc. Here we present the first, detailed, systematic in silico study of the electrophysiological characterization of cardiomyocytes from different regions of the normal human atria, based on the effects of ambient temperature (5 −50° C ). We observe that RMP decreases with increasing temperature. At ∼ 48° C , the cells lose their excitability. Our studies show that different parts of the atria react differently to the same changes in temperature. In tissue simulations a drop in temperature correlated positively with a decrease in CV, but the decrease was region-dependent, as expected. In this article we show how this heterogeneous response can provide an explanation for the development of a proarrhythmic substrate during mild hypothermia. We use the above concept to propose a treatment strategy for atrial fibrillation that involves severe hypothermia in specific regions of the heart for a duration of only ∼ 200ms.
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Majumder et al. (2020) studied Atrial fibrillation. Temperature alteration (5-50°C) vs. 37°C was evaluated on Scroll wave termination and action potential characteristics. Severe cooling of simulated human atrial tissue to ~5°C for ~200ms successfully terminated all electrical activity and scroll waves by substantially decreasing tissue excitability.
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