Comparing Type D personality and older age as correlates of tumor necrosis factor-α dysregulation in chronic heart failure

Tumor necrosis factor-α (TNF-α) 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 (⩽59 years) and 60 relatively older (⩾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-α 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-α activity. This disease-promoting effect of Type D matched the pro-inflammatory effect of ageing.