Selective Serotonin Reuptake Inhibitors Influence Agonist‐Induced Platelet Aggregation. Preliminary Results from Co‐morbidity of Depression and Cardiovascular Disease Study

Abstract

Selective serotonin reuptake inhibitors (SSRI) are a first‐line treatment option for mood disorders such as depression (D). They inhibit neuronal reuptake of serotonin and result in depleted serotonin stores in the dense bodies of platelets. It is hypothesized that depressive illnesses cause platelet activation and endothelial dysfunction, which could be modulated by the use of SSRIs. To validate this hypothesis an institutional‐based co‐morbidity of D and cardiovascular (CV) study was undertaken. 25 healthy control subjects and 25 patients meeting the DSM‐IV criteria for major depressive disorder were recruited in this study. Blood samples were collected at baseline and then 4 and 8 weeks following treatment with Escitalopram. Agonist‐induced platelet aggregation showed varying degrees of inhibition of collagen, ADP, arachidonic acid and epinephrine‐induced platelet aggregation. Agonist Induced Percent Platelet Aggregation BL 4 weeks 8 weeks Collagen 71.5±22.4 63.4±35.1 74.7±21.3 AA 64.1±35.1 67.1±25.1 55.7±36.1 ADP 48.2±30.9 33.0±26.7 52.4±31.0 EPI 55.6±29.2 37.4±25.8 50.4±32.3 Saline 6.9±4.5 9.4±7.8 5.0±3.9 These results indicate that treatment with SSRIs may inhibit platelet aggregation by some agonists, which may have an impact in the prevention of atherothrombotic and CV disease. SSRIs might alter hemostasis in some patients by inhibiting platelet function.