In addition, cardiovascular b-adrenoreceptor responsiveness is decreased and adrenoreceptor responsiveness is increased in postmenopausal women. Therefore, sympathetic dominance replaces parasympathetic one as the main regulator of the cardiovascular system in postmenopausal women. These changes would affect cardiovascular responses during acute stress, including heart rate increases and vasoconstriction, and might help explain the increased incidence of TTC in these patients. Studies exploring pathophysiological features of TTC mainly converge towards a common pathway, i.e. namely sympathetic nervous system activation. However, up to now, all previous studies only collected indirect measurement of SNS activity and none has been able to provide data about baroreflex function in TTC patients. Plasma catecholamine levels at presentation are usually markedly higher among patients with stress-induced cardiomyopathy. This is particularly the case for catecholamines, their precursor and neuronal metabolites, during acute phase. We hypothesized that elevated nerve firing, as assessed by microneurography in our study, coupled possibly with impaired neuronal NE reuptake, is probably responsible for the known high catecholamine levels observed in these patients. Finally, our results indicate that elevated sympathetic activity during the acute phase of TTC is associated with a marked alteration in sympathetic baroreflex function favoring substantially greater response in sympathetic nerve firing to spontaneous fluctuation in diastolic blood pressure. It has been suggested in a case report that afferent baroreflex failure could be associated to TTC. In this previously published case-report, lesions of both solitary tract nuclei, where impulses arising from baroreceptors converge, preceded TTC. However the patient had disseminated encephalomyelitis associated to this brainstem involvement and thus the causality relationship is questionable. Our study provides the first evidence that TTC is effectively associated to a decrease of the spontaneous baroreflex control of sympathetic activity. We have only used heart failure patient as control patient, because there are known to have elevated SNS activity. Our hypothesis was that if Takotsubo patient have a higher SNS activity than patient know to have the most elevated activity then our study would be clinically relevant. However from a pathophysiological perspective having a “clinically matched” group of female subject with acute coronary syndrome, or a “real” control group of age matched healthy female subjects without cardiac disease could have been interesting. However data from the literature show that these type of patients have a lover SNS activity than heart failure patient. Hence using these type of control patient would have facilitated positive results. In this study we did not analyze baroreflex control of MSNA after FDA-approved Compound Library pharmacological intervention. It appears complicated to use this technique in patients with low ejection fraction since drugs delivered for that purpose.