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Preliminary Findings with Venlafaxine Treatment
John E. Piletz1, Angelos Halaris1, Omer Iqbal2, Debra Hoppensteadt2, Jawed Fareed2, He Zhu2,
Departments of Psychiatry1, Pathology2, and Epidemiology3,
Loyola University Chicago, Stritch School of Medicine, 2160 South First Ave., Maywood, Il inois 60153;
Department of Psychiatry4, Medical University of South Carolina, 173 Ashley Ave., Charleston, South Carolina 29425-0742
soluble P-selectin was non-significantly lowered (p= 0.13).
Platelet membranous IRAS and CD61 levels were normal at
Disturbances in af ective state are known to cause platelet baseline but down-regulated after 4 and 8 weeks of treatment
activation, which may relate to evidence linking major depres- (p = 0.01 each).
sion and coronary artery disease. The platelet activation bio- Conclusion
marker, P-selectin, exists in various blood fractions that High levels of soluble P-selectin were identified in depression,
demarcate steps of platelet activation. If circulating platelets indicative of platelet activation. Venlafaxine treatment had
are more activated in depressed patients, the literature sug- minimal ef ect on soluble P-selectin but had clear ef ects on
gests that amongst antidepressant classes, the Serotonin- platelet IRAS and CD61. Therefore, platelet activation does
Selective Reuptake Inhibitors (SSRIs) are best able to normal- not readily normalize with mood correction after 8 weeks on
ize this abnormality. Serotonin/ Norepinephrine Reuptake venlafaxine, but other platelet ef ects seem to occur.
Inhibitors (SNRIs), like venlafaxine, have not been studied in
Keywords: P-selectin, IRAS, CD61, Platelets, Cardiovascular
To determine the status of activated P-selectin (platelet sur-
face-bound and/or released forms) in depressed patients be- INTRODUCTION
fore and after 8 weeks of treatment with the SNRI, venlafax- A large body of evidence indicates that major depressive dis-
order (MDD) imparts a substantial lifetime risk for developing
coronary artery disease (CAD).1 Prospective epidemiological
Baseline (untreated) subjects were major depressives (n= 23) studies have repeatedly produced relative risk values (RRs)
and age/sex-matched healthy controls (n= 17) with no evi- associated with depression in the 1.3 - 4.5 range for future car-
dence of coronary artery disease. A subgroup of the diac disease, stroke, and/or death.2 The greatest RRs are
depressed cohort (n= 15) was restudied after 4 and 8 weeks found in patients exhibiting clinical depression within 6 months
on venlafaxine. P-selectin levels were compared to two bio- post-myocardial infarction.3, 4 No exact mechanism has been
markers not known to change during platelet activation: the established linking depression to CAD, but there are findings
membranous fibronectin-signaling protein, IRAS, and the anti- of sympathoadrenal activation and hypothalamic-pituitary-
gen of the GPI b/I Ia receptor, CD61.
adrenal axis dysregulation in depressed patients.5 Another
finding is that platelets are more activated (sticky) in depres-
sion 6-8, which is thought to predispose to atherosclerosis.
At baseline, both activated forms of P-Selectin were high in
Unfortunately, not al studies agree that platelets are more
the depressives, but only the soluble form showed statistical
activated in depression.9-12 Part of the discrepancy may owe to
significance (p= 0.03) versus healthy controls. Venlafaxine dif erent methods for assessing platelet activation. To clarify
treatment led to mood normalization based on reduced
Hamilton Depression scores (p< 0.0001), while the level of this, we have focused on the most frequently studied biomark-
er of platelet activation, P-selectin, and have analyzed its three
activated forms: the soluble form in unperturbed plasma (sP-
Angelos Halaris, MD, Ph.D.
selectin), the unstimulated form detected by flow cytometry
(platelet basal P-selectin), and the agonist-stimulated form
detected by flow cytometry (platelet stimulated P-selectin). To
anchor these measurements, we have added two unrelated
platelet biomarkers: the integrin beta-3 protein antigen (CD61)
and the integrin alpha-5 accessory protein, IRAS, on unper-
turbed platelets. These biomarkers are not associated with
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