Platelet Thromboxane A₂ Secretion in Patients With Major Depression Responsive to Electroconvulsive Therapy

Address correspondence and reprint requests to: Dominique L. Musselman, MD, E-mail: dmussel{at}emory.edu.

	Abstract

Objective: To determine a) whether clinical response to electroconvulsive therapy (ECT) is associated with decreased platelet activation in patients with major depressive disorder (MDD) and b) if any medical/demographic characteristics predict response to ECT or changes in platelet activation. Increased platelet activation may underlie the increased risk of coronary artery disease (CAD) in patients with MDD. Methods: Before their first and sixth ECT treatments, study patients (n = 44) completed the Beck Depression Inventory (BDI) to assess the severity of depressive symptoms. Activity of the platelet thromboxane (TBX) A₂ pathway was assessed by measuring the morning spot urinary concentrations of 11-dehydroxy-thromboxane B₂ (11-D-TBX B₂), a major metabolite of platelet-derived TBX A₂. Results: Multivariate logistic regression analyses revealed that improvement on the BDI was significantly more likely in patients without a history of hypertension (p = .02) and in patients who were prescribed a greater number of "platelet-altering" medications (p = .03). During a course of ECT, a decrease in urinary 11-D-TBX B₂ was significantly more likely to occur in ECT nonresponders (p = .01) and younger patients (p = .02). Conclusions: Clinical response to ECT coadministered may not be associated with decreases in platelet-derived TBX. Future studies will confirm which somatic "antidepression" treatments offer optimal thrombovascular benefits for depressed patients with multiple risk factors for, or clinically evident, cerebral disease or CAD.

Key Words: electroconvulsive therapy, platelet function, thromboxane, major depressive disorder, antidepressants, autocrine pathways