Brachial FMD is an adequate non-invasive measure of endothelial function and reduced brachial FMD reflects endothelial dysfunction. It has been found to impair the parameters of endothelial health, reducing flow-mediated dilatation (FMD). Acute mental stress may induce myocardial infarction or sudden cardiac death. Mental stress has been shown to be a risk factor for atherosclerosis. The development of endothelial dysfunction may be one possible mechanism linking slow cardiac recovery and atherosclerosis via autonomic nervous system mediated effect. 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. ConclusionsĬardiac recovery plays a role in atherosclerosis development in persons with high and low FMD. No significant interactions of FMD and cardiac reactivity for IMT were found. Among individuals with high FMD, slow RSA recovery predicted higher IMT. Among participants with low FMD, slower PEP recovery was related to higher IMT. 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). We also measured heart rate, respiratory sinus arrhythmia (RSA), and pre-ejection period (PEP) in response to the mental arithmetic and speech tasks. Preclinical atherosclerosis was assessed by carotid intima-media thickness (IMT) and endothelial function was measured as flow-mediated dilatation (FMD) using ultrasound techniques. Participants were 81 healthy young adults aged 24-39 years. 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. The joint effects of stress-induced sympathetic or parasympathetic activity and endothelial function on atherosclerosis development have not been investigated. Acute mental stress may contribute to the cardiovascular disease progression via autonomic nervous system controlled negative effects on the endothelium.
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