Journal
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 56, Issue 22, Pages 1840-1846Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacc.2010.03.107
Keywords
endothelium; stress-induced cardiomyopathy; Tako-Tsubo cardiomyopathy; vasculature; women
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Funding
- Department of Defense [W74V8H-05-1-0001]
- National Institutes of Health [1R01-HL092954-01A1]
- Mayo Foundation
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Objectives The aim of the current study was to test the hypothesis that vascular and endothelial functional responses to acute mental stress are abnormal in patients with apical ballooning syndrome (ABS). Background Apical ballooning syndrome is a transient cardiomyopathy that occurs predominantly in post-menopausal women and may be triggered by acute mental stress. The mechanism for ABS is unknown. Methods Reactive hyperemia as a parameter of endothelial function and vascular responses to acute mental stress were measured using peripheral arterial tonometry (PAT) at baseline and following 3 acute mental stress tests in female patients with ABS (n = 12, at least 6 months after being hospitalized or diagnosed with ABS), postmenopausal female controls (n = 12), and female patients with myocardial infarction (MI) (n = 4). Plasma catecholamine levels were measured at baseline and following the 3 mental stress tests. Results Reactive hyperemia PAT scores following mental stress were significantly lower in patients with ABS compared with post-menopausal controls (p < 0.05). The PAT scores during mental stress were significantly lower in patients with ABS compared with patients with MI and post-menopausal controls (p < 0.05). There were no differences in PAT scores during acute mental stress in patients with MI versus post-menopausal controls. Furthermore, catecholamine levels were significantly increased in patients with ABS, compared with post-menopausal controls, following acute mental stress testing (p < 0.05). Conclusions There is increased vascular reactivity and decreased endothelial function in response to acute mental stress in patients with a prior episode of ABS. The findings implicate vasomotor dysfunction as a potential mechanism involved in the pathogenesis of this unique cardiomyopathy. (J Am Coll Cardiol 2010;56:1840-6) (C) 2010 by the American College of Cardiology Foundation
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