Introduction Takotsubo syndrome (TTS), also known as stress cardiomyopathy or “broken heart” syndrome, is a mysterious condition that often mimics an acute myocardial infarction. Both are characterized by left ventricular systolic dysfunction. However, this dysfunction is reversible in the majority of TTS patients. Purpose Recent studies surprisingly demonstrated that TTS, initially perceived as a benign condition, has a long-term prognosis akin to myocardial infarction. Therefore, the health consequences and societal impact of TTS are not trivial. The pathophysiological mechanisms of TTS are not yet completely understood. In the last decade, attention has been increasingly focused on the putative role of the central nervous system in the pathogenesis of TTS. Conclusion In this review, we aim to summarize the state of the art in the field of the brain–heart axis, regional structural and functional brain abnormalities, and connectivity aberrancies in TTS.

Indirect evidences in reviews and case reports on Takotsubo syndrome (TTS) support the fact that the existence of oxidative stress (OS) might be its common feature in the pre-acute stage. The sources of OS are exogenous (environmental factors including pharmacological and toxic influences) and endogenous, the combination of both may be present, and they are being discussed in detail. OS is associated with several pathological conditions representing TTS comorbidities and triggers. The dominant source of OS electrones are mitochondria. Our analysis of drug therapy related to acute TTS shows many interactions, e.g., cytostatics and glucocorticoids with mitochondrial cytochrome P450 and other enzymes important for OS. One of the most frequently discussed mechanisms in TTS is the effect of catecholamines on myocardium. Yet, their metabolic influence is neglected. OS is associated with the oxidation of catecholamines leading to the synthesis of their oxidized forms – aminochromes. Under pathological conditions, this pathway may dominate. There are evidences of interference between OS, catecholamine/aminochrome effects, their metabolism and antioxidant protection. The OS offensive may cause fast depletion of antioxidant protection including the homocystein-methionine system, whose activity decreases with age. The alteration of effector subcellular structures (mitochondria, sarco/endoplasmic reticulum) and subsequent changes in cellular energetics and calcium turnover may also occur and lead to the disruption of cellular function, including neurons and cardiomyocytes. On the organ level (nervous system and heart), neurocardiogenic stunning may occur. The effects of OS correspond to the effect of high doses of catecholamines in the experiment. Intensive OS might represent “conditio sine qua non” for this acute clinical condition. TTS might be significantly more complex pathology than currently perceived so far.

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Background Takotsubo cardiomyopathy (TTC) is a severe cardiologic disorder with an increasing incidence that often mimics acute coronary syndrome. Both of the entities are characterized by systolic dysfunction of the left ventricle myocardium. However, this dysfunction is reversible in most cases of TTC. Takotsubo syndrome affects predominantly postmenopausal females, typically with a direct link to emotional or physical stress factors. The pathophysiology of TTC remains unclear. In this study, we aimed to assess the pathophysiology of TTC using the invasive functional testing of coronary microcirculation. Methods Ten female patients diagnosed with TTC in line with interTAK Diagnostic Criteria were included in this pilot study. In all subjects we measured fractional and coronary flow reserve in the left anterior descending and left circumflex coronary arteries (FFR LAD, FFR LCx, CFR LAD, CFR LCx), and the index of microcirculatory resistance in the same arteries (iMR LAD, iMR LCx) in addition to acute and late (after 12 weeks) transthoracic echocardiography (TTE) and acute cardiac biomarkers (troponin and NT-proBNP). The results of the microcirculatory assessment were statistically compared with normal population values. Results In all subjects, the troponin level was elevated in the acute phase and repeated TTE revealed transient dysfunction of the left myocardial ventricle. Whilst fractional flow reserve was normal in both assessed epicardial artery territories for all patients (mean FFR LAD: 0.92±0.04; mean FFR LCx: 0.98±0.046), both mean values of coronary flow reserve disclosed pathological microcirculatory findings (CFR LAD: 1.9±1.197; CFR LCx: 1.75±0.742) and were pathological in nine out of ten subjects. Index of microcirculatory resistance revealed abnormal values in five out of ten patients for LAD (31.03±18.515) and three out of ten for LCx (23.8±17.86). Conclusions Our pilot study confirmed non-obstructive findings in the epicardial coronary arteries assessed by FFR. On the other hand, the investigation of both CFR and iMR, microcirculatory functional testing, revealed pathological findings in a significant number of evaluated subjects. From this aspect, our study validates further research in the field of microcirculatory functions as a possible mechanism in the origin of TTS. Acknowledgement/Funding Supported by MH CZ - DRO (FNBr, 65269705)

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