Pathophysiology of sepsis-triggered takotsubo syndrome

The comprehensive article by Y-Hassan et al, published ahead of print in the June 2014 issue of Acute Cardiac Care (1), about patients with sepsis-triggered (ST) takotsubo syndrome (TTS), which I immensely enjoyed, should be studied by all physicians caring for patients with suspected or established sepsis. The authors dealt with all the ramifications of the sepsis-TTS association, based on their experience, and a thorough review of the literature of ST-TTS, and sepsis-induced myocardial depression, which the authors convincingly mostly attribute to ST-TTS. I have one comment and one question for the authors to consider:

1. In their assessment of their cases, experience of others, and their critical review of the literature on sepsis-induced myocardial depression, they seem to focus primarily on the segmental ventricular dysfunction, as opposed to a pattern of generalized hypokinesis, ‘global left ventricular hypokinesia’, as they say in their introduction, which often occurs in patients with sepsis, and which if present only transiently followed by complete restoration of left (or right) ventricular function, it should not exclude a diagnosis of ST-TTS; are the authors in agreement with this?

2. Regarding the pathophysiology of ST-TTS, the authors attribute it to an ‘acute cardiac sympathetic disruption with noradrenaline spill-over’, and ‘intense activation of the local cardiac sympathetic nervous system leading to disruption of the cardiac sympathetic nerve terminals and causing noradrenaline spillover’, I should like to ask them whether they imply that: (a) the sympathetic nerves exert a damaging influence on the cardiomyocytes; (b) the sympathetic nerves are disrupted and thus they do not exert any stimulation on the cardiomyocytes, but the injurious influence 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.

Declaration of interest: The author reports no conflicts of interest. The author alone is responsible for the content and writing of the paper.