CardiomyopathyEmotional, Neurohormonal, and Hemodynamic Responses to Mental Stress in Tako-Tsubo Cardiomyopathy
Section snippets
Methods
From January 2012 to April 2014, 56 patients (18 patients with TTC, 19 healthy controls, and 19 HF control patients) participated in the study. Patients with TTC were identified from the echocardiography patient database belonging to the Elisabeth Tweesteden Hospital, Tilburg, The Netherlands. Patients who were admitted with a diagnosis of TTC in the preceding 5 years were approached by a cardiologist for participation in the study. The diagnosis of TTC was based on the Mayo Clinic diagnostic
Results
Characteristics of the study sample are listed in Table 1. Patients with TTC were on average older compared with the healthy control group and, thus, less likely to be used. Age and gender were adjusted for multivariable analyses. As listed in Table 1, patients with TTC were also more likely to have hypertension and use β-adrenergic blocking agents, ACE inhibitors, antiplatelet medication, and lipid-lowering medication. Patients with TTC did not differ from patients with HF on any of the
Discussion
Patients with TTC showed higher norepinephrine and dopamine levels during mental stress and exercise compared with healthy controls, suggesting sympathetic neurohormonal hyper-reactivity. Responses of the HPA axis and hemodynamic reactivity were not elevated in TTC. The emotional responses to mental stress were not exaggerated in TTC, and the results even showed a blunted arousal response compared with healthy controls. These findings provide preliminary evidence of hyper-reactivity of the
Acknowledgment
Dounya Schoormans, PhD is acknowledged for assistance with the cortisol assays.
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Cited by (31)
Chromogranin-A serum levels in patients with takotsubo syndrome and ST elevation acute myocardial infarction
2020, International Journal of CardiologyCitation Excerpt :On this basis, high CgA values were expected in TTS; however, CgA levels were significantly lower in TTS than in anterior-STEMI patients. As already speculated by other authors, [3,7,28–31] SNS activation in TTS might be mainly through the neuro-cardiac axis rather than via the systemic hormones spillover of adrenal origin, directly inducing a paracrine CA/CgA release from the intrinsic cardiac nerve terminals, and in fact the left ventricular anterior wall is rich with sympathetic terminations [32]. In this view, CgA might be expressed by the myocytes as local agent able to cross-talk with intracardiac catecholamines [15,16,24], and therefore circulating levels might not be elevated, at least within the first 24 h. Interestingly, we found that CgA levels in TTS patients positively correlated with NT-pro-BNP (Fig. 2A) likely suggesting that CgA is co-secreted with the B natriuretic peptide [33]; therefore, it may be hypothesized that initial CgA production is mainly driven by cardiac production rather than the extra-cardiac one (Fig. 3).
Diagnosis and study of rare heart diseases: imaging multimodality – stress cardiomyopathy
2019, Revista Colombiana de CardiologiaAutonomic function in Takotsubo syndrome long after the acute phase
2017, International Journal of CardiologyPotentially stress-induced acute splanchnic segmental arterial mediolysis with a favorable spontaneous outcome
2017, Journal of Vascular Surgery Cases and Innovative TechniquesCitation Excerpt :Slavin and Yaeger concluded that SAM might be caused by iatrogenic or accidental exposure to catecholamine release. Second, experimental studies have shown an excess of catecholamine release during acute mental stress in patients suffering from takotsubo,5 a rare reversible cardiomyopathy that is triggered by acute stress (such as intense fear) in two of three cases. Those data, combined with our observation of SAM following an acute psychological stress, suggest that SAM might be due to intake of adrenergic agonists or catecholamine hyper-reactivity.
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