Endothelial function and vascular response to mental stress are impaired in patients with apical ballooning syndrome
- PMID: 21087714
- PMCID: PMC3786427
- DOI: 10.1016/j.jacc.2010.03.107
Endothelial function and vascular response to mental stress are impaired in patients with apical ballooning syndrome
Abstract
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), post-menopausal 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.
Copyright © 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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