Abstract

A low intake of selenium is associated with increased cardiovascular mortality. This could be reduced by supplementation with selenium and coenzyme Q10. D-dimer, a fragment of fibrin mirroring fibrinolysis, is a biomarker of thromboembolism, increased inflammation, endothelial dysfunction and is associated with cardiovascular mortality in ischemic heart disease. The objective was to examine the impact of selenium and coenzyme Q10 on the level of D-dimer, and its relationship to cardiovascular mortality. D-dimer was measured in 213 individuals at the start and after 48 months of a randomised double-blind placebo-controlled trial with selenium yeast (200 µg/day) and coenzyme Q10 (200 mg/day) (n = 106) or placebo (n = 107). The follow-up time was 4.9 years. All included individuals were low in selenium (mean 67 μg/L, SD 16.8). The differences in D-dimer concentration were evaluated by the use of T-tests, repeated measures of variance and ANCOVA analyses. At the end, a significantly lower D-dimer concentration was observed in the active treatment group in comparison with those on placebo (p = 0.006). Although D-dimer values at baseline were weakly associated with high-sensitive CRP, while being more strongly associated with soluble tumour necrosis factor receptor 1 and sP-selectin, controlling for these in the analysis there was an independent effect on D-dimer. In participants with a D-dimer level above median at baseline, the supplementation resulted in significantly lower cardiovascular mortality compared to those on placebo (p = 0.014). All results were validated with a persisting significant difference between the two groups. Therefore, supplementation with selenium and coenzyme Q10 in a group of elderly low in selenium and coenzyme Q10 prevented an increase in D-dimer and reduced the risk of cardiovascular mortality in comparison with the placebo group. The obtained results also illustrate important associations between inflammation, endothelial function and cardiovascular risk.

Highlights

  • We found a significantly lower concentration of D-dimer (p = 0.002) in those supplemented with selenium and coenzyme Q10, after adjusting for co-variates that might influence the concentration of D-dimer, like the C-reactive protein (CRP), sP-selectin, tumour necrosis factor (TNF)-r1, TNf-r2, endostatin and Growth differentiation factor 15 (GDF-15), all of which being biomarkers of inflammation

  • Q10 on the level of D-dimer in an elderly community-living population in Sweden has has shown that this treatment prevented an increase in D-dimer levels, as compared with shown that this treatment prevented an increase in D-dimer levels, as compared with the the placebo group in which the levels appeared to increase

  • D-dimer, a fragment of cleaved fibrin, reflects the fibrinolytic process, which is why it is used in clinical routines to rule out a possible thromboembolic process

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Summary

Introduction

D-dimer is a fragment of degraded fibrin and reflects the activation of fibrinolysis and thrombosis, and the activity of peripheral artery disease [1]. It is an indicator of the fibrin turnover [2]. The most common indications for use of D-dimer are in the diagnosis of venous thromboembolism [3,4,5,6,7], for the exclusion of pulmonary embolism [8] and in the evaluation of recanalisation of pulmonary emboli after anticoagulation [9]. The assay is mainly based on antibodies against D-dimer [11], and as different antibodies are used in commercial kits, there is some variability in the obtained measurements [12]

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