Autonomic dysfunction and heart rate variability in depression

Depression occurs in people of all ages across all world regions; it is the second leading cause of disability and its global burden increased by 37.5% between 1990 and 2010. Autonomic changes are often found in altered mood states and appear to be a central biological substrate linking depression to a number of physical dysfunctions. Alterations of autonomic nervous system functioning that promotes vagal withdrawal are reflected in reductions of heart rate variability (HRV) indexes. Reduced HRV characterizes emotional dysregulation, decreased psychological flexibility and defective social engagement, which in turn are linked to prefrontal cortex hypoactivity. Altogether, these pieces of evidence support the idea that HRV might represent a useful endophenotype for psychological/physical comorbidities, and its routine application should be advised to assess the efficacy of prevention/intervention therapies in a number of psychosomatic and psychiatric dysfunctions. Further research, also making use of appropriate animal models, could provide a significant support to this point of view and possibly help to identify appropriate antidepressant therapies that do not interefere with physical health

Acute psychosocial challenge and cardiac autonomic response in women: the role of estrogens, corticosteroids, and behavioral coping styles.

Theoretical statements, as well as clinical and experimental data, suggest that the amplitude of cardiovascular reactivity to acute stressors can be a good predictor of preclinical and clinical cardiovascular states. The aim of the present study is to investigate the role of estrogens, the hypothalamic-pituitary-adrenocortical activity, and the behavioral profile in individual cardiac autonomic reactivity to brief laboratory stressors in women. Thirty-six adult, healthy women were exposed to a stress interview and a mental task test, each lasting 5 min. They were assigned to two experimental groups: D4, i.e. 4 days after menses beginning (follicular phase, n=18), and D14, i.e. 14 days after menses beginning (ovulatory phase, n=18). The cardiac measurements in the baseline, stress and recovery periods consisted in heart rate (average R-R interval) and parasympathetic tone (r-MSSD) quantification, while the HPA axis activity and stress reactivity were assessed via plasma cortisol and dehydroepiandrosterone concentrations. The ethological profile during the interview was drawn by means of non-verbal behavior analysis. The cardiac, adrenocortical and behavioral responses to the two stressors were similar in groups D4 and D14, despite significantly higher estradiol levels in the latter. Subjects with higher pre-stress cortisol levels had higher heart rate and lower vagal activity in the baseline, stress and recovery phases. Women showing higher level of submission were characterized by higher heart rate acceleration and vagal withdrawal during both the interview and the recovery phase. In addition, the subjects that exhibited greater displacement during the interview were also characterized by lower heart rate increments and less pronounced vagal suppression during post-stress recovery. In conclusion, the present results do not support a clear buffering role of estrogens in cardiovascular response to acute stressors. However, they confirm that baseline HPA axis activity can be predictive of cardiac autonomic activity and stress responsiveness. They also highlight the modulating role of the individual style of behavioral coping in cardiac sympathovagal stress reactivity. Therefore, the objective assessment of the individual behavioral profile via the analysis of non-verbal communication patterns might represent a powerful tool for identifying subjects with higher risk of cardiac events