Current hypotheses regarding the pathophysiology behind the takotsubo syndrome

Re: On the quest of unravelling the pathophysiology of takotsubo syndrome

“…We thank Prof. Madias for his insightful comments regarding our recent review article on the pathophysiology behind the takotsubo syndrome [1]. Herein we provide our thoughts on the five matters he raises in his letter [2]: 1) We agree that assessment of patients very early in the course of takotsubo is of great value and we support the implementation of "focused cardiac ultrasound", i.e.…”

Plausible speculations on the pathophysiology of Takotsubo syndrome

“…Accordingly the latter could be viewed as ECG evidence of dyskinesis, and not due to ischemic injury, akin the situation observed in myocardial aneurysms, consequent to chronic transmural myocardial infarction [20]. According to the above cited chain of events the apical and mid-ventricular regional contraction abnormalities could be envisaged either as consequent to the basal hypercontractility, or could be thought as occurring as "part and parcel" of the TTS phenotype, along the line previously proposed [2], irrespective of the basal hyperkinesis, as an evolutionary adaptive cardioprotective response to the heightened intracardiac systolic stretch [2,9,15]. Thus, ME could be viewed as a consequence of this relentless systolic myocardial stress, and may be playing a modulating effect on the diagnoses of "myocardial ischemia" or "metabolic glucose impairment", detected by imaging modalities, which may be partially (doubt, totally) due to a "partial volume" effect, as discussed above [14].…”

“…Specifically what is needed is knowledge based on: 1) effects on the disease attributes of repeated administration of lower doses of catecholamines, rather than the traditional single larger dose injection (such single large doses of catecholamines triggering TTS in animals [1,2,9,10], but also leading to excessive mortality, makes one wonder whether they constitute animal experiments of catecholamine toxicity, rather than animal models of TTS); 2) consequences of continuous intravenous infusion of various doses of catecholamines; 3) effects of other catecholamines than the ones tried so far (epinephrine, norepinephrine, isoprenaline) [1,2,9]; 4) results of electrical stimulation of the autonomic (both sympathetic and parasympathetic) [11] neural routes to the heart; 5) effects of stimulation of various brain areas known to elicit TTS phenotypes; 6) implementation of subarachnoid hemorrhage animal TTS models; 7) phenotypic TTS effects of the enforced immobilization; 8) serial blood sampling of epinephrine and norepinephrine in the rat models of TTS, resulting from neural simulation or enforced immobilization, 9) implementation of the above in male and female intact animals, 10) implementation of the above in female ovariectomized animals; and 11) implementation of the above in female ovariectomized animals, which had undergone chronic ERT. In the clinical domain, the whole catecholamine hypothesis of the causation of TTS [12] need to be reexamined, since in spite of its early seemingly unconditional acceptance, it is currently undergoing scrutiny, with many expressing doubts about a certain pathogenetic role of high blood bound catecholamines triggering TTS [10].…”

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“…[1][2][3] It was first described in 1990 by Sato and associates. 4,5 The term "takotsubo" stands for octopus (Tako) pot (Tsubo) and resembles a widebased clay jar with a narrow neck and round bottom.…”