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Open Access Highly Accessed Research article

Early atherosclerosis and cardiac autonomic responses to mental stress: a population-based study of the moderating influence of impaired endothelial function

Nadja Chumaeva12, Mirka Hintsanen1, Taina Hintsa1, Niklas Ravaja3, Markus Juonala4, Olli T Raitakari45 and Liisa Keltikangas-Järvinen1*

Author Affiliations

1 Institute of Behavioural Sciences, University of Helsinki, P.O. Box 9, FIN-00014 Helsinki, Finland

2 Division of Medical Problems of Cell Biology, Institute of Cell Biophysics, Institutional Street 3, Pushchino, Moscow region, 142290 Russia

3 Center for Knowledge and Innovation Research, Helsinki School of Economics, P.O. Box 1210, 00101 Helsinki, Finland

4 Research Centre of Applied and Preventive Cardiovascular Medicine, University of Turku, Kiinanmyllynkatu 10, 20520 Turku, Finland

5 Department of Clinical Physiology, University of Turku and Turku University Hospital, P.O. Box 52, 20521 Turku, Finland

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BMC Cardiovascular Disorders 2010, 10:16  doi:10.1186/1471-2261-10-16

Published: 29 March 2010

Abstract

Background

Acute mental stress may contribute to the cardiovascular disease progression via autonomic nervous system controlled negative effects on the endothelium. The joint effects of stress-induced sympathetic or parasympathetic activity and endothelial function on atherosclerosis development have not been investigated. The present study aims to examine the interactive effect of acute mental stress-induced cardiac reactivity/recovery and endothelial function on the prevalence of carotid atherosclerosis.

Methods

Participants were 81 healthy young adults aged 24-39 years. Preclinical atherosclerosis was assessed by carotid intima-media thickness (IMT) and endothelial function was measured as flow-mediated dilatation (FMD) using ultrasound techniques. We also measured heart rate, respiratory sinus arrhythmia (RSA), and pre-ejection period (PEP) in response to the mental arithmetic and speech tasks.

Results

We found a significant interaction of FMD and cardiac RSA recovery for IMT (p = 0.037), and a significant interaction of FMD and PEP recovery for IMT (p = 0.006). Among participants with low FMD, slower PEP recovery was related to higher IMT. Among individuals with high FMD, slow RSA recovery predicted higher IMT. No significant interactions of FMD and cardiac reactivity for IMT were found.

Conclusions

Cardiac recovery plays a role in atherosclerosis development in persons with high and low FMD. The role of sympathetically mediated cardiac activity seems to be more important in those with impaired FMD, and parasympathetically mediated in those with relatively high FMD. The development of endothelial dysfunction may be one possible mechanism linking slow cardiac recovery and atherosclerosis via autonomic nervous system mediated effect.