Antidepressants: bleeding or thrombosis?

• Published in: Thrombosis research Vol. 181; pp. S23 - S28
• Main Authors: Hoirisch-Clapauch, Silvia, Nardi, Antonio E
• Format: Journal Article
• Language: English
• Published: United States Elsevier Ltd 01.09.2019
• Subjects: Antidepressants; Antidepressive Agents - adverse effects; Antidepressive Agents - pharmacology; Bleeding; Cardiovascular diseases; Hematology, Oncology, and Palliative Medicine; Hemorrhage - chemically induced; Humans; inhibitors; Selective serotonin reuptake inhibitors; Serotonin and noradrenaline reuptake; Thrombosis; Thrombosis - chemically induced; Tricyclic antidepressants; inhibitors; Antidepressants; Tricyclic antidepressants; Selective serotonin reuptake inhibitors; Cardiovascular diseases; Serotonin and noradrenaline reuptake; Thrombosis; Bleeding
• ISSN: 0049-3848; 1879-2472
• DOI: 10.1016/S0049-3848(19)30362-7

ABSTRACTThe contribution of depression to the pathogenesis of cardiovascular disease includes autonomic disturbances, endothelial dysfunction, inflammation, smoking, sedentary lifestyle, carbohydrate craving, and impaired fibrinolysis. There is evidence that serotonergic antidepressants (selective serotonin reuptake inhibitors and serotonin and noradrenaline reuptake inhibitors) restore the fibrinolytic profile. Contrary to common belief, such antidepressants do not affect platelet aggregation induced by adenosine diphosphate or adrenaline but reduce platelet adhesion to collagen. Since platelet collagen receptor glycoprotein VI binds to fibrin, it is possible that fibrinolytic properties of serotonergic antidepressants could impair platelet adhesion to collagen. The profibrinolytic and antiplatelet properties of serotonergic antidepressants help explain the increased risk of gastrointestinal, intracranial, and surgical bleeding in patients using these medications. Studies evaluating the impact of antidepressants on thrombotic and cardiovascular risk have yielded contradictory results. Corroborating the hypothesis that serotonergic antidepressants have profibrinolytic and antiplatelet properties, some authors showed that these medications prevent both cardiovascular and thromboembolic events. Others showed an increased risk of ischemic stroke, cardiac events and thromboembolic disease. Silent brain infarction may present in some elders with depressive symptoms, so it is presumed that antidepressants are prescribed for subclinical stroke patients. Another explanation for the increased risk of cardiovascular and thromboembolic events reported by some authors in individuals taking antidepressants includes antidepressant side effects such as sedation and weight gain and depression comorbidities such as anxiety, obesity and hyperhomocysteinemia. In conclusion, we suggest that serotonergic antidepressants be considered weak anticoagulants. We also suggest that depressed patients with comorbidities increasing the risk of cardiovascular and thromboembolic disease be recommended to follow a balanced diet and engage in physical activity, such as daily walking.