The evidence that depressive and anxiety disorders confer a high relative risk (RR) for cardiovascular disease (CVD) development is clear and compelling. A cadre of inflammation, platelet activation and other biomarkers of endothelial dysfunction strongly suggest multiple and possibly interrelated mechanisms underlying this co-morbidity. Early detection of the vulnerability to develop CVD has become an urgent health issue. However, detection alone of vulnerability without proper therapeutic intervention aimed at reversing it, is merely of scientific interest. The evidence to date that antidepressant drugs, while highly efficacious in restoring euthymia, may not normalize the biomarkers of CVD vulnerability. Hence, there is a need to identify other pharmacologic interventions for depression. Quetiapine, due to its unique molecular structure and unique pharmacological profile, belongs to none of the known classes of antidepressants. However, quetiapine clearly has antidepressant and anti-anxiety efficacies. Now, we propose to explore whether quetiapine can reverse those pathophysiological changes occurring in mixed depression/anxiety that have been linked causally to the development of CVD. Accordingly, the primary purpose of this study is to compare C-Reactive Protein between the treatment and healthy control groups at 12 weeks post treatment.