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20th World Congress on Heart Disease



Daniela Jezova, M.D., Slovak Academy of Sciences, Bratislava, Slovakia


An optimal cardiovascular response to threatening challenges is indispensable for coping with the situation. Anxiety disorders and high anxiety as a personality trait have been expected to be associated with autonomic lability and hyperreactivity during stress. Data published on this topic are rather variable. We have performed a series of studies in healthy humans and patients to clarify the relationship between anxiety and cardiovascular activation under stress conditions. In a group of healthy volunteers with high trait anxiety, we have observed an exaggerated hear rate (HR) response during psychosocial stress compared to non-anxious individuals. However, in contrast to general expectations, plasma epinephrine and norepinephrine responses were lower in anxious subjects. Treatment of anxious subjects with a mixture of aminoacids lysine and arginine (10 days) was able to normalize stress-induced catecholamine responses. We have revealed that the influence of trait anxiety on cardiovascular activation is gender dependent. Anxious women in the follicular phase of the menstrual cycle exhibited a greater stress-induced rise in systolic blood pressure compared to anxious women in the luteal phase and to non-anxious women in both phases. Accordingly, we have brought evidence for a reduced neuroendocrine response to stressors in patients with an anxiety disorder or with immune dysfunction accompanied by anxiety. Patients with different types of allergy showed increased trait anxiety and attenuated heart rate response during psychosocial stress. Similarly, the activity of alpha-amylase, an enzyme activated by the sympathetic nervous system, was reduced in patients compared to controls. In conclusion, high trait anxiety appears to be associated with impaired coordination of the stress response, rather than global hypo- or hyper-responsiveness.
Supported by APVV-0496-12.



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