Depression emerges as a risk factor for cardiovascular disease, and it is thought that successful antidepressant treatment may reduce such a risk. Therefore, antidepressant treatment embodies a potential preventive measure to reduce cardiovascular events in patients with depression. Accumulating evidence indicates that antidepressants have off-target effects on vascular dysfunction and in the early stages of atherosclerosis, which form the basis for cardiovascular disease (CVD) pathogenesis. In this context, we performed a thorough review of the evidence pertaining to the effects of different classes of antidepressant medications on hemodynamic and early atherosclerosis markers. The preclinical and clinical evidence reviewed revealed a preponderance of studies assessing selective serotonin reuptake inhibitors (SSRI), whereas other classes of antidepressants are less well-studied. Sufficient evidence supports a beneficial effect of SSRIs on vascular inflammation, endothelial function, arterial stiffening, and possibly delaying carotid atherosclerosis. In clinical studies, dissecting the hypothesized direct beneficial antidepressant effect of SSRIs on endothelial health from the global improvement upon remission of depression has proven to be difficult. However, preclinical studies armed with appropriate control groups provide evidence of molecular mechanisms linked to endothelial function that are indeed modulated by antidepressants. This suggests at least a partial direct action on vascular integrity. Further research on endothelial markers should focus on the effect of antidepressants on treatment responders versus non-responders in order to better ascertain the possible beneficial vascular effects of antidepressants, irrespective of the underlying course of depression.

Background Anti-Müllerian hormone (AMH) constitutes a marker of ovarian reserve and appears to have a predictive role regarding the time of menopause. Moreover, AMH is associated with adverse cardiac events. History of premature menopause and early onset of menopause have been associated with increased risk of cardiovascular (CV) disease. In addition, menopausal transition and duration of menopause have been associated with increased burden of subclinical atherosclerosis. However, the association between AMH as a marker of female reproductive age with atherosclerosis in premenopausal women is currently unknown. Purpose To investigate whether AMH concentrations are associated with markers of early atherosclerosis in healthy, normally menstruating women. Methods In a cross-sectional study, vascular structure and function were assessed by measurement of carotid and femoral intima-media thickness (IMT), lipid profile and serum AMH concentrations were assessed. Exclusion criteria were clinically overt CV disease, abnormal ovulatory cycles, polycystic ovarian syndrome, acute infection or chronic inflammatory disease, risk factors for CV disease and any medication Results Seventy premenopausal women, aged 32.7±6.5 years, were included. Mean AMH levels were lower in smokers than in non-smokers and negatively associated with total cholesterol (TC) levels. An inverse association between mean AMH concentrations and IMT in all segments was observed. No correlation with other markers of subclinical atherosclerosis or traditional CV risk factors was found. After multi-variable adjustment for traditional CV risk factors, the association between AMH concentrations combined IMT and carotid bulb IMT, remained significant. Conclusions In healthy, normally ovulating women, low AMH concentrations are associated with an adverse lipid profile and subclinical atherosclerosis, independently of traditional CV risk factors. This finding suggest a role of decreased follicular reserve with atherosclerotic disease. Funding Acknowledgement Type of funding source: None