9 Markovitz et al showed a greater platelet secretory response to collagen in depressed patients than in healthy control subjects in baseline comparison measures. They then demonstrated a decrease in collagen-induced platelet secretion after treatment with sertraline for 6 weeks, most other platelet activation measures showing minimal change. These changes were, however, not related to improvement in the Beck Inhibitors,research,lifescience,medical Depression Inventory scores, but this finding

might be limited by the short treatment duration. Thus, the decreased platelet activation after SSRI treatment could diminish the risk of coronary heart disease among Inhibitors,research,lifescience,medical depressed subjects, but the authors underline the need for studies in a large number of patients, placebo controls, and a longer follow-up period.24 In a study by Musselman et al, after 6 weeks of open-label treatment with paroxetine, a normalization of platelet activation occurred in patients with depression. This was shown by a significant decrease in PF4 and of the platelet monoclonal antibodies anti ligand-induced platelet binding Inhibitors,research,lifescience,medical site (LIBS) and GA6 (anti P-selectin). Before treatment, these markers were higher among depressed patients compared with

the control group. The results of this study could be explained by recovery from depression. Thus, Inhibitors,research,lifescience,medical studies with placebo and/or psychotherapy are proposed by the authors as further investigation.25

A decrease in platelet response mediated by the 5-HT2A receptor following effective imipramine treatment was demonstrated by Gomez-Gil et al, shown by a significant decrease in 5-HT-amplified platelet aggregation to ADP, thus suggesting that desensitization Inhibitors,research,lifescience,medical or downregulation of platelet 5-HT2A receptor function could be linked to a therapeutic effect of some antidepressants.30 Comparing levels of plasma 5-HT and platelet 5-HT induced aggregation among depressed patients treated with either why fluoxetine or amitriptyline and nontreated patients, Menys et al demonstrated a statistically significant decrease in both plasma 5-HT levels and 5-HT induced platelet aggregation, only with fluoxetine. This suggests a higher inhibition of platelet activity by SSRIs than tricyclic antidepressants, and therefore a more suitable treatment for depressed patients with cardiovascular disease.26 Laine-Cessac et al this website failed to demonstrate a significant effect of a 1-month fluoxetine treatment in 8 depressed patients, on the following primary hemostasis and coagulation tests: PT, aPTT, TT, fibrinogen, platelet count, bleeding time, platelet aggregation induced by ADP, AA, ristocetin, and collagen.