Comparing Type D personality and older age as correlates of tumor necrosis factor-alpha dysregulation in chronic heart failure.
Tumor necrosis factor-alpha (TNF-alpha) and its soluble receptors 1 (sTNFR1) and 2 (sTNFR2) have been shown to be implicated in the pathogenesis of chronic heart failure (CHF). Ageing is accompanied by increased plasma levels of pro-inflammatory cytokines. We hypothesized that Type D personality (joint tendency to experience negative emotions and to inhibit self-expression) and age may have similar pro-inflammatory effects in the context of CHF. Participants in this study were 130 consecutive outpatients with CHF (76% men); there were 70 relatively younger (<or=59 years) and 60 relatively older (>or=60 years) patients. They all completed the 14-item Type D Scale (DS14); 43 patients (33%) had a Type D personality. A multivariate model of cytokine levels indicated an independent overall effect of both older age [F(1,128)=9.11, p=.003] and Type D personality [F(1,128)=8.28, p=.005]. Stratifying patients in age/personality subgroups showed that younger non-Type D patients had the lowest and older Type D patients the highest sTNFR1 and sTNFR2 levels (986+/-318 vs 1661+/-1128 pg/ml and 1838+/-777 vs 2823+/-1439 pg/ml, p<.0001). Importantly, the mean sTNFR1 level in younger Type D patients (1359+/-660 pg/ml) was equivalent to that in older non-Type D patients (1360+/-440 pg/ml, p=.99) who were on average 18 years older. Younger Type D and older non-Type D patients also had similar sTNFR2 levels (2406+/-1329 vs 2448+/-812 pg/ml, p=.88). Only older Type D patients had a higher mean TNF-alpha level as compared to patients who were younger or who were not Type D (5.4+/-2.9 vs 3.9+/-2.4 pg/ml, p=.008). A logistic regression model including sex, severity of CHF, systolic heart failure and ischemic etiology indicated that the combined risk category of older age or Type D was independently associated with substantially increased sTNFR1 and sTNFR2 levels. Hence, Type D personality was associated with increased TNF-alpha activity. This disease-promoting effect of Type D matched the pro-inflammatory effect of ageing.
Denollet
Johan
J
CoRPS-Centre of Research on Psychology in Somatic diseases, Department of Medical Psychology, Tilburg University, Tilburg, The Netherlands. denollet@uvt.nl
Vrints
Christiaan J
CJ
Conraads
Viviane M
VM
D000328:Adult; D000367:Age Factors; D000368:Aged; D002908:Chronic Disease; D016207:Cytokines / Q000097:blood / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006333:Heart Failure / Q000097:blood / Q000473:pathology* / Q000523:psychology; D006801:Humans; D008297:Male; D008875:Middle Aged; D010551:Personality / Q000145:classification / Q000502:physiology*; D010552:Personality Assessment / Q000592:standards / Q000706:statistics & numerical data; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000097:blood* / Q000378:metabolism; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000097:blood* / Q000378:metabolism; D012044:Regression Analysis; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood* / Q000378:metabolism
D016207:Cytokines; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha