Insulin and takotsubo syndrome: plausible pathophysiologic, diagnostic, prognostic, and therapeutic roles.

The pathophysiology of takotsubo syndrome (TTS) is elusive. Heightened adrenergic surge via the sympathetic nervous system (mainly by norepinephrine secretion) and/or elevated blood-borne catecholamines (mainly epinephrine, secreted by the adrenals) probably mediate TTS. Patients with TTS have a low prevalence of diabetes mellitus (DM), and it has been postulated that DM, via its associated neuropathy, prevents the emergence of TTS. Insulin, in animal experiments, has been shown to greatly attenuate the effects of NE on the cardiomyocytes; also, insulin in a limited clinical experience, has been found to improve heart function in patients with neurogenic stress-cardiomyopathy and TTS. Accordingly, it is postulated that high levels of insulin encountered in patients with type 2 DM are at the roots of the protective effect of DM for the emergence of TTS. Thus, a role of insulin in the pathophysiology, diagnosis, prognosis, and therapy of TTS appears to be plausible, and needs exploration.