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.
OBJECTIVE: This study investigated whether depressedpatients exhibit exaggerated platelet reactivity. METHOD: In vivo platelet activation, secretion, and dose-response aggregation were measured in 12 depressedpatients and eight normal comparison subjects after overnight bed rest and following orthostatic challenge. RESULTS: The depressedpatients 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 depressedpatients 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:Depressedpatients 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.
Authors: Helen Lavretsky; Ling Zheng; Michael W Weiner; Dan Mungas; Bruce Reed; Joel H Kramer; William Jagust; Helena Chui; Wendy J Mack Journal: Am J Psychiatry Date: 2010-02-16 Impact factor: 18.112
Authors: Nunzio Pomara; P Murali Doraiswamy; Lisa M Willoughby; Amy E Roth; Benoit H Mulsant; John J Sidtis; Pankaj D Mehta; Charles F Reynolds; Bruce G Pollock Journal: Neurochem Res Date: 2006-04-01 Impact factor: 3.996
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