Pathophysiology of sepsis-triggered takotsubo syndrome.

Abstract

pathetic nerves exert a damaging infl uence on the cardiomyocytes; (b) the sympathetic nerves are disrupted and thus they do not exert any stimulation on the cardiomyocytes, but the injurious infl uence on the cardiomyocytes is exerted by the noradrenaline spillover? (c) One wonders whether ‘ disrupted ’ sympathetic nerves secrete larger amounts of norepinephrine, except if the authors imply by ‘ disruption ’ of the sympathetic nerves an enhanced state of stimulation, with resultant increased norepinephrine secretion and spillover; (d) Do the authors imply ‘ cardiac sympathetic denervation ’ by ‘ cardiac sympathetic disruption ’ ? (e) Of course it is conceivable that a population of the cardiac sympathetic nerve terminals are partially disrupted, and non-functioning (partial cardiac sympathetic denervation), while other populations of such terminals are in a state of heightened function with intense stimulation of cardiomyocytes, and profuse nonadrenaline spillover. I will appreciate very much the response of the authors on the above.