Irene Lopez-Vilchez1, Montserrat Serra-Millas2, Victor Navarro2, M Rosa Hernandez3, Jaume Villalta4, Maribel Diaz-Ricart3, Cristobal Gasto2, Gines Escolar3, Ana M Galan3. 1. Department of Hemotherapy and Hemostasis, Hospital Clinic, Biomedical Diagnosis Centre, Institute of Biomedical Research August Pi i Sunyer, University of Barcelona, Barcelona, Spain. Electronic address: ilopez1@clinic.ub.es. 2. Department of Psychiatry, Hospital Clinic, Institute Clinic of Neurosciences, Barcelona, Spain. 3. Department of Hemotherapy and Hemostasis, Hospital Clinic, Biomedical Diagnosis Centre, Institute of Biomedical Research August Pi i Sunyer, University of Barcelona, Barcelona, Spain. 4. Department of Internal Medicine, Hospital Clinic, Barcelona, Spain.
Abstract
BACKGROUND: Serotonergic mechanisms have been suggested as a link between major depression and cardiovascular risk. We investigated the existence of a prothrombotic condition in depressed patients and its possible modulation during treatment with a selective serotonin-reuptake inhibitor (SSRI). METHODS: Modifications in a series of biomarkers of platelet and coagulation activation were evaluated in blood from 19 patients with a major depression disorder (MDD) at the time of diagnosis, and at 8 and 24 weeks of treatment with escitalopram. Response of blood aliquots recirculated through a thrombogenic surface was assessed in a thrombosis model. Results were compared with those of 20 healthy-matched controls. RESULTS: In comparison with controls, platelets from MDD patients showed elevated volumes (p<0.01), significantly enhanced aggregating response to arachidonic acid and augmented expression of GPIb, fibrinogen, factor V, and anionic phospholipids by flow cytometry (p<0.05). Clot firmness and procoagulant activity of platelet-associated tissue factor were also significantly elevated (p<0.05). Studies with circulating blood revealed increased fibrin formation in early diagnosed patients (71.1±9.5% vs. 45.8±5.3%; p<0.05 vs. controls). After 24 weeks of treatment with escitalopram, the majority of the alterations observed were normalized, except for a residual increased expression of GPIIbIIIa (p<0.05) and persistent alterations in thromboelatometic parameters. LIMITATIONS: Despite the reduced number of followed-up patients our findings were consistent reaching statistical significance. CONCLUSIONS: Our results reveal a prothrombotic phenotype in MDD patients. While continuous treatment with an SSRI downregulated the majority of the biomarkers analyzed, alterations in viscoelastic parameters of clot formation remained unaffected by the antidepressant treatment.
BACKGROUND: Serotonergic mechanisms have been suggested as a link between major depression and cardiovascular risk. We investigated the existence of a prothrombotic condition in depressedpatients and its possible modulation during treatment with a selective serotonin-reuptake inhibitor (SSRI). METHODS: Modifications in a series of biomarkers of platelet and coagulation activation were evaluated in blood from 19 patients with a major depression disorder (MDD) at the time of diagnosis, and at 8 and 24 weeks of treatment with escitalopram. Response of blood aliquots recirculated through a thrombogenic surface was assessed in a thrombosis model. Results were compared with those of 20 healthy-matched controls. RESULTS: In comparison with controls, platelets from MDDpatients showed elevated volumes (p<0.01), significantly enhanced aggregating response to arachidonic acid and augmented expression of GPIb, fibrinogen, factor V, and anionic phospholipids by flow cytometry (p<0.05). Clot firmness and procoagulant activity of platelet-associated tissue factor were also significantly elevated (p<0.05). Studies with circulating blood revealed increased fibrin formation in early diagnosed patients (71.1±9.5% vs. 45.8±5.3%; p<0.05 vs. controls). After 24 weeks of treatment with escitalopram, the majority of the alterations observed were normalized, except for a residual increased expression of GPIIbIIIa (p<0.05) and persistent alterations in thromboelatometic parameters. LIMITATIONS: Despite the reduced number of followed-up patients our findings were consistent reaching statistical significance. CONCLUSIONS: Our results reveal a prothrombotic phenotype in MDDpatients. While continuous treatment with an SSRI downregulated the majority of the biomarkers analyzed, alterations in viscoelastic parameters of clot formation remained unaffected by the antidepressant treatment.
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: I Lopez-Vilchez; M Diaz-Ricart; V Navarro; S Torramade; J Zamorano-Leon; A Lopez-Farre; A M Galan; C Gasto; G Escolar Journal: Transl Psychiatry Date: 2016-09-06 Impact factor: 6.222
Authors: Christoph W Turck; Paul C Guest; Giuseppina Maccarrone; Marcus Ising; Stefan Kloiber; Susanne Lucae; Florian Holsboer; Daniel Martins-de-Souza Journal: Front Mol Neurosci Date: 2017-08-31 Impact factor: 5.639