Gender differences in associations of depressive symptoms and anxiety with inflammatory markers in patients with non-obstructive coronary artery disease.

OBJECTIVE: The aim of this study was to examine gender differences of the associations between depressive symptoms and anxiety with inflammatory markers in patients with non-obstructive coronary artery disease (NOCAD). METHODS: Depressive symptoms and anxiety (Beck Depression Inventory BDI and Hospital Anxiety and Depression Scale HADS) were examined in 524 patients with NOCAD (52% women, mean age 64 ±â€¯9 years) as part of the TweeSteden Mild Stenosis (TWIST) observational cohort study. Blood samples were analyzed for neutrophil gelatinase-associated lipocalin (NGAL) levels, high-sensitive C-reactive protein (hsCRP), and leukocyte differentiation. Multivariate analysis for the inflammatory markers with main effects of depressive symptoms or anxiety, gender, and their interactions were observed. RESULTS: Women had elevated levels of hsCRP, and a lower monocyte and eosinophil count than men, with small to medium effect sizes (range η(p)2 = 0.019-0.047). After Holm-Bonferroni correction depressive symptoms according to the BDI were associated with an overall elevated hsCRP level explaining 2.4% of the hsCRP variance. A significant positive association between BDI cognitive symptoms with elevated hsCRP level was observed in men (R2 = 0.045), but not in women (R2 < 0.001). Adjustment for age, body mass index, smoking, and physical activity attenuated this finding. CONCLUSION: Small associations of inflammatory markers with depressive symptoms and anxiety were confounded by lifestyle factors, predominantly smoking. The interacting roles of gender, smoking, and psychological factors on inflammatory markers may point toward different behavioral and inflammatory pathways for women and men with NOCAD, which remains to be further explored. OBSERVATIONAL COHORT REGISTRATION: ClinicalTrials.gov identifier: NCT01788241.

Depression and markers of inflammation as predictors of all-cause mortality in heart failure.

BACKGROUND: In patients with heart failure (HF) depressive symptoms have been associated with mortality, as well as biological risk factors, including inflammation, nitric oxide (NO) regulation, and oxidative stress. We investigated the joint predictive value of depressive symptoms, inflammation and NO regulation on all-cause mortality in patients with HF, adjusted for covariates. METHODS: Serum levels of inflammation (TNFα, sTNFr1, sTNFr2, IL-6, hsCRP, NGAL), NO regulation (l-arginine, ADMA, and SDMA), and oxidative stress (isoprostane 8-Epi Prostaglandin F2 Alpha) were measured in 104 patients with HF (mean age 65.7±SD 8.4years, 28% women). Depressive symptoms (Beck Depression Inventory, BDI) were measured as continuous total, cognitive, and somatic symptoms, as well as categorized presence of mild/moderate depression (cut-off BDI ⩾10). In Cox proportional hazard models we adjusted for age, sex, poor exercise tolerance and comorbidity. RESULTS: After on average 6.1years follow-up (SD=2.9, range 0.4-9.2), 49 patients died. Total and somatic depressive symptoms, mild/moderate depression, higher NGAL, sTNFr2, IL-6, hsCRP and SDMA serum levels were significantly associated with a higher all-cause mortality rate, adjusted for covariates. The findings were most consistent for CRP level and somatic depressive symptoms. When combined, both depressive symptoms and markers of inflammation and NO regulation remained significantly associated with all-cause mortality. These associations were not confounded by age, sex, poor exercise tolerance and comorbidity. CONCLUSION: Depressive symptoms and markers of inflammation and NO regulation are codominant risk factors for all-cause mortality in heart failure.

The analytic impact of a reduced centrifugation step on chemistry and immunochemistry assays: an evaluation of the Modular Pre-Analytics.

BACKGROUND: The COBAS 6000 system can be completed by a Modular Pre-Analytics (MPA), an integrated laboratory automation system that streamlines preanalysis. For an optimal throughput, the MPA centrifuges blood collection tubes for 5 min at 1885 × g - a centrifugation time that is not in concordance with the World Health Organization guidelines which suggest centrifugation for 10/15 min at 2000-3000 × g. METHODS: In this study, the analytical outcome of 50 serum and 50 plasma samples centrifuged for 5 or 10 min at 1885 × g was investigated. The study included routine chemistry and immunochemistry assays on the COBAS 6000 and the Minicap capillary electrophoresis. RESULTS: Deming-fit and Bland-Altman plots of the 5-min and 10-min centrifugation steps indicated a significant correlation in serum samples. The lipaemia index in plasma samples centrifuged for 5 min displayed a statistically significant variation when compared with the 10-min centrifugation. CONCLUSIONS: Preanalytical centrifugation can be successfully down-scaled to a duration of 5 min for most routine chemistry and immunochemistry assays in serum and plasma samples. To prevent inaccurate results in plasma samples with an increased lipaemia index from being reported, the laboratory information system was programmed to withhold results above certain lipaemia indices. The presented data support the use of a 5-min centrifugation step to improve turnaround times, thereby meeting one of the desires of the requesting clinicians.