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Correlations between peripheral vascular function, inflammation and depression in human subjects
Author(s) -
Stapleton Phoebe A.,
d'Audiffret Alexandre C.,
Frisbee Stephanie J.,
Goodwill Adam G.,
James Milinda E.,
Frisbee Jefferson C.
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.795.3
Subject(s) - reactive hyperemia , depression (economics) , medicine , peripheral , brachial artery , inflammation , vascular disease , endothelial dysfunction , cardiology , tumor necrosis factor alpha , blood flow , blood pressure , economics , macroeconomics
In addition to traditional risk factors for peripheral vasculopathy, including altered lipid profiles and chronic inflammation, ongoing study has suggested that psychological health, and specifically personal depression, may represent a profound contributor to poor vascular outcomes. The present study interrogated relationships between established risk factors for peripheral vascular disease, indices of personal depression, and vascular/endothelial function in human subjects recruited through a vascular surgery clinic at WVU HSC. During clinic visits, patients completed a depression screener, received baseline evaluations of health, provided venous blood samples and had brachial artery hyperemia evaluated following alleviation of 2 and 5 minute occlusions via ultrasound imaging. Results indicated that reactive hyperemia was reduced in patients in proportion to plasma TNF‐α and IL‐1β, (IL‐1β > TNF‐α). Additionally, depression severity was correlated both inflammation markers, as well as with impairments to reactive hyperemia. However, there was no evidence that self‐reported depression was an exacerbating influence on RH independent from that for inflammation. These results suggest that depression may not represent a causative factor contributing to poor vascular outcome, but may reflect a pathology arising from establishment of vascular dysfunction. (NIH R01 DK64668, AHA EIA 0740129N)