Abstract

BackgroundDepressive patients show a state dependent platelet activation that may heighten their cardiovascular risk, specially when comorbid with Coronary Artery Disease (CAD). We still have little information however on the possibility that residual symptoms that often persist after recovery from a major depressive episode may contribute to drive forward platelet activation, thus extending the exposure to the associated cardiovascular risk. MethodsNineteen major depressed inpatients treated with electroconvulsive therapy (ECT) were enrolled and tested for platelet aggregation by measuring platelet factor-4 (PF4) and β-thromboglobulin (β-TG) plasma levels, and for psychometric evaluation by using the 20-item Hamilton Depression Rating Scale (HDRS) and the Symptom Checklist 90 Revised (SCL-90R). Subjects were tested at the beginning of treatment (baseline) and after clinical remission (endpoint). ResultsAt baseline the patients showed high HDRS (31±6) and total SCL-90R (200±38) scores, followed by a significant decrease at endpoint. However, even if all patients showed full syndromal recovery, SCL-90R “Hostility” and “Psychoticism” subscores showed no significant reduction from baseline, indicating the persistence of subtle residual symptoms. Baseline PF4 and β-TG plasma levels were found remarkably higher and no significant reduction was observed at the endpoint. LimitationsSmall study population. No follow-up evaluation. ConclusionsDespite of clinical remission obtained with ECT in patients with major depression, persistence of subsyndromal residual symptoms may contribute to maintain a condition of platelet hyperactivation at the endpoint, increasing their cardiovascular risk and making them more vulnerable to develop cardiovascular disease.

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