BACKGROUND: Depression is associated with an increased risk of cardiovascular disease (CVD). Although the mechanism is uncertain, prothrombotic and inflammatory factors may play a role. OBJECTIVES: As platelets play a key role in CVD, we determined first, whether depressed individuals had more activated platelets than non-depressed individuals and second, whether treatment of depression reduced platelet activation levels. PATIENTS/ METHODS: We recruited 108 depressed outpatients and 45 control subjects all without a history of CVD. After psychological assessment, the depressed patients were offered treatment with medication and/or psychotherapy. Flow cytometric markers of platelet activation and level of depression were assessed at baseline and at 4 weeks and 6 months after treatment. RESULTS: Depression was associated with increased platelet activation with a higher number of circulating CD62p (0.76x10(9) L(-1) vs. 0.46, P=0.019) and CD63 (P=0.05) positive platelets compared with controls. Patients with depression also had more circulating platelet-leukocyte aggregates than controls (P<0.001). There was a positive correlation between the severity of depression and the level of platelet activation. Platelets from depressed patients were also hyperreactive to adenosine 5 -diphosphate (ADP) stimulation with increased CD62p and CD63 exposure (P=0.003 and 0.019, respectively). Six months of treatment resulted in a reduced number of circulating CD62p and CD63 positive platelets (29.84% and 53.38% decrease) and a 20.9% reduction in CD63 exposure after ADP activation. CONCLUSIONS: Depression is associated with increased in vivo platelet activation and resolution of depression using psychotherapy and/or medication reduces platelet activation. These findings provide insights into the link between depression and cardiovascular risk.
BACKGROUND:Depression is associated with an increased risk of cardiovascular disease (CVD). Although the mechanism is uncertain, prothrombotic and inflammatory factors may play a role. OBJECTIVES: As platelets play a key role in CVD, we determined first, whether depressed individuals had more activated platelets than non-depressed individuals and second, whether treatment of depression reduced platelet activation levels. PATIENTS/ METHODS: We recruited 108 depressed outpatients and 45 control subjects all without a history of CVD. After psychological assessment, the depressedpatients were offered treatment with medication and/or psychotherapy. Flow cytometric markers of platelet activation and level of depression were assessed at baseline and at 4 weeks and 6 months after treatment. RESULTS:Depression was associated with increased platelet activation with a higher number of circulating CD62p (0.76x10(9) L(-1) vs. 0.46, P=0.019) and CD63 (P=0.05) positive platelets compared with controls. Patients with depression also had more circulating platelet-leukocyte aggregates than controls (P<0.001). There was a positive correlation between the severity of depression and the level of platelet activation. Platelets from depressedpatients were also hyperreactive to adenosine 5 -diphosphate (ADP) stimulation with increased CD62p and CD63 exposure (P=0.003 and 0.019, respectively). Six months of treatment resulted in a reduced number of circulating CD62p and CD63 positive platelets (29.84% and 53.38% decrease) and a 20.9% reduction in CD63 exposure after ADP activation. CONCLUSIONS:Depression is associated with increased in vivo platelet activation and resolution of depression using psychotherapy and/or medication reduces platelet activation. These findings provide insights into the link between depression and cardiovascular risk.
Authors: Andrew A Rebel; Siri A Urquhart; Kendra L Puig; Atreyi Ghatak; Stephen A Brose; Mikhail Y Golovko; Colin K Combs Journal: J Neurosci Res Date: 2015-02-22 Impact factor: 4.164
Authors: Patrizia Amadio; Gualtiero I Colombo; Eva Tarantino; Sara Gianellini; Alessandro Ieraci; Maura Brioschi; Cristina Banfi; José P Werba; Alessandro Parolari; Francis S Lee; Elena Tremoli; Silvia S Barbieri Journal: Eur Heart J Date: 2017-05-07 Impact factor: 29.983
Authors: M Krivosova; M Grendar; I Hrtanek; I Ondrejka; I Tonhajzerova; N Sekaninova; L Bona Olexova; D Mokra; J Mokry Journal: Physiol Res Date: 2020-12-31 Impact factor: 1.881