Key result
T ± ϵ feedback control applied to the Luo-Rudy I model dramatically reduced fast pacing-induced cardiac alternans and increased average cytosolic calcium levels when ϵ exceeded a critical threshold.
Computational modeling suggests that T ± ϵ feedback control can effectively suppress cardiac alternans and improve average cytosolic calcium levels, potentially enhancing cardiac contractions.
Caution against clinical translation; leaves open efficacy of T ± ϵ feedback for alternans in vivo.
Using the Luo-Rudy I model, the recently proposed T ± ϵ feedback control for suppressing cardiac alternans is investigated. It is shown that cardiac alternans, induced by fast pacing (of period T ), can be dramatically reduced by small changes of fixed magnitude ( ) under feedback control when exceeds a critical threshold. Detail information on various ionic currents and cytosolic calcium concentration ( [ Ca ] i ) are examined when the cardiac cell is under control. In particular, the alternans in ionic currents and [Ca] i are also reduced under the control. Furthermore, when exceeds the threshold value, the average [Ca] i level is significantly higher when the alternans is under control, suggesting a possible physiological improvement of cardiac contractions.
No takes yet. Share an insight, caveat, or question.
Liang et al. (2016) studied Cardiac alternans. T ± ϵ feedback control was evaluated on Suppression of cardiac alternans and changes in ionic currents and cytosolic calcium concentration. T ± ϵ feedback control applied to the Luo-Rudy I model dramatically reduced fast pacing-induced cardiac alternans and increased average cytosolic calcium levels when ϵ exceeded a critical threshold.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: