Depressed patients exhibited enhanced baseline platelet activation and responsiveness to orthostatic challenge compared with normal subjects, suggesting a mechanism for increased cardiovascular risk.
Case-Control (n=20)
OBJECTIVE: This study investigated whether depressed patients exhibit exaggerated platelet reactivity. METHOD: In vivo platelet activation, secretion, and dose-response aggregation were measured in 12 depressed patients and eight normal comparison subjects after overnight bed rest and following orthostatic challenge. RESULTS: The depressed patients exhibited increased platelet activation at baseline, demonstrated by increased binding of monoclonal antibody (moAb) annexin V protein reacting with prothrombinase complex binding sites. Following orthostatic challenge, the depressed patients exhibited increases in binding of moAbs PAC1 and anti-LIBS1 against activated glycoprotein IIb/IIIa and GE12 against P-selectin expressed upon secretion. The normal comparison subjects exhibited increases in platelet activation only with GE12. CONCLUSIONS: Depressed patients exhibit enhanced baseline platelet activation and responsiveness in comparison with normal subjects. Heightened susceptibility to platelet activation may be a mechanism by which depression is a significant risk factor for ischemic heart and cerebrovascular disease and/or mortality after myocardial infarction.
Musselman et al. (Tue,) conducted a case-control in Major depression (n=20). Orthostatic challenge vs. Normal comparison subjects was evaluated on In vivo platelet activation, secretion, and dose-response aggregation. Depressed patients exhibited enhanced baseline platelet activation and responsiveness to orthostatic challenge compared with normal subjects, suggesting a mechanism for increased cardiovascular risk.
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