The relationship between depression and the metabolic syndrome is unclear, and whether metabolic syndrome explains the association between depression and cardiovascular disease (CVD) risk is unknown.
We studied 652 women who received coronary angiography as part of the Women's Ischemia Syndrome Evaluation (WISE) study and completed the Beck Depression Inventory (BDI). Women who had both elevated depressive symptoms (BDI ≥10) and a previous diagnosis of depression were considered at highest risk, whereas those with one of the two conditions represented an intermediate group. The metabolic syndrome was defined according to the ATP-III criteria. The main outcome was incidence of adverse CVD events (hospitalizations for myocardial infarction, stroke, congestive heart failure, and CVD-related mortality) over a median follow-up of 5.9 years.
After adjusting for demographic factors, lifestyle and functional status, both depression categories were associated with about 60% increased odds for metabolic syndrome compared with no depression (p = .03). The number of metabolic syndrome risk factors increased gradually across the three depression categories (p = .003). During follow-up, 104 women (15.9%) experienced CVD events. In multivariable analysis, women with both elevated symptoms and a previous diagnosis of depression had 2.6 times higher risk of CVD. When metabolic syndrome was added to the model, the risk associated with depression only decreased by 7%, and both depression and metabolic syndrome remained significant predictors of CVD.
In women with suspected coronary artery disease, the metabolic syndrome is independently associated with depression but explains only a small portion of the association between depression and incident CVD.
BDI = Beck Depression Inventory; CAD = coronary artery disease; CVD = cardiovascular disease; DASI = Duke Activity Status Inventory; HDL = high-density lipoprotein; LDL = low-density lipoprotein; WISE = Women's Ischemia Syndrome Evaluation; NHLBI = National Heart, Lung, and Blood Institute.
From the Division of Cardiology (V.V., L.J.S.), and the Division of General Medicine (S.P.), Department of Medicine, Emory University School of Medicine, Atlanta, Georgia; the Department of Epidemiology, University of Pittsburgh, Pittsburgh, Pennsylvania (B.D.J., C.M.C., M.B.O.); the Cardiovascular Institute, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania (O.C.M.); the Division of Cardiovascular Medicine, Department of Medicine, University of Florida, Gainesville, Florida (D.S.S.); the Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama (V.B.); the Department of Psychiatry, University of California, San Diego, California (T.R.); the National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland (G.S.); the Department of Medical and Clinical Psychology, Uniformed Services University of Health Sciences, Bethesda, Maryland (D.S.K.); and the Division of Cardiology, Department of Medicine, Cedars-Sinai Research Institute, Cedars-Sinai Medical Center, Los Angeles, California (C.N.B.M.).
Address correspondence and reprint requests to Viola Vaccarino, MD, PhD, Division of Cardiology, Department of Medicine, Emory University School of Medicine, 1256 Briarcliff Road NE, Suite-1 North, Atlanta, GA 30306. E-mail: firstname.lastname@example.org
Received for publication April 18, 2007; revision received July 30, 2007.
This work was supported by contracts from the National Heart, Lung, and Blood Institutes, nos. N01-HV-68161, N01-HV-68162, N01-HV-68163, N01-HV-68164; Grants K24HL077506, R01-HL68630, and R01 AG026255 (to V.V.); a GCRC Grant M01-RR00425 from the National Center for Research Resources; and Grants from the Gustavus and Louis Pfeiffer Research Foundation, The Women's Guild, Cedars-Sinai Medical Center and the Ladies Hospital Aid Society of Western Pennsylvania, and QMED, Inc.