Objective: To examine whether markers of oxidative stress differ as a function of Type D personality, depression, and chronic heart failure (CHF) etiology. Type D (distressed) personality and depression are related to poor cardiac prognosis. Because patients with CHF are characterized by increased oxidative stress, this may be a candidate mechanism responsible for the adverse prognosis in emotionally distressed patients with CHF.
Methods: Serum levels of xanthine oxidase (XO), inducible heat shock protein (Hsp)70, and deoxyribonucleic acid damage marker 8-OHdG were measured in 122 patients, and effects of Type D, depression, and etiology were assessed.
Results: CHF patients with Type D personality had lower levels of Hsp70 than non-Type D patients (6.48 ng/mL versus 7.85 ng/mL, p = .04, d = 0.26), and in case of an ischemic etiology, higher levels of XO (13.57 ng/mL versus 9.84 ng/mL, p = .01, d = 0.98). There were no significant univariate differences for depression. When adding depression as an additional independent variable in the Type D analysis, the effect of Type D personality remained significant (F = 5.460, p = .02) and was independent of depression (F = 0.942, p = .33). The ratio of XO to Hsp70 was significantly higher in Type D patients with CHF as compared with non-Type D patients (6.14 versus 2.83, p = .03, d = 0.39), independent of etiology class.
Conclusion: CHF patients with Type D personality are characterized by an increased oxidative stress burden, apparent in the decreased antioxidant levels and an increased oxidative stress ratio.
8-OHdG = 8-hydroxy-2-deoxyguanosine; ACE = angiotensin-converting enzyme; CHF = chronic heart failure; ELISA = enzyme-linked immunosorbent assay; HF = heart failure; Hsp70 = heat shock protein 70; LVEF = left ventricular ejection fraction; MANOVA = multivariate analysis of variance; MDD = major depressive disorder; MI = myocardial infarction; NA = negative affectivity; ROS = reactive oxygen species; SI = social inhibition; TNF = tumor necrosis factor; XO = xanthine oxidase.
From the CoRPS-Center of Research on Psychology in Somatic diseases (N.K., J.D.), Tilburg University, Tilburg, Netherlands; School of Health Sciences and Social Care (Y.G.), Brunel University, Uxbridge, Middlesex, UK; and the Department of Cardiology (J.W.), TweeSteden Hospital, Tilburg, Netherlands.
Address correspondence and reprint requests to Nina Kupper, Department of Medical Psychology, Tilburg University, Center of Research on Psychology in Somatic diseases, Warandelaan 2, PO box 90153, 5000 LE Tilburg, Netherlands. E-mail: email@example.com
Received for publication September 5, 2008; revision received May 20, 2009.
The present research was supported, in part by VICI Grant 453-04-004 from the Netherlands Organization for Scientific Research (NWO, The Hague, Netherlands) (J.D.) and Grant NHS 2003B038 from The Netherlands Heart Foundation (J.D.).