Plain language summary
Cardiovascular disease is the leading cause of death worldwide. Systemic inflammation and oxidative stress significantly contribute to the narrowing of the blood supply to the heart leading to coronary artery disease (CAD). Increased levels of several markers of inflammation, such as C-reactive protein (CRP), tumour necrosis factor-α (TNF- α), and interleukin-6 (IL-6), appear to be indicative of heart attack risk. Coenzyme Q10 (CoQ10) is a naturally occurring nutrient made in the body but can also be found in some foods or taken via supplements. It is an antioxidant that protects cell membranes and mitochondria against oxidative damage and also does so in the heart by preventing endothelial damage and the associated narrowing of blood vessels. Several trials investigated the effects of CoQ10 on inflammation and oxidative stress, with some noteworthy results and yet also some conflicting evidence. Hence this systematic review and meta-analysis aimed to shed some light on the controversial findings regarding coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress amongst patients with CAD. The authors included 13 clinical randomised controlled trials, amounting to 364 cardiac patients in the intervention groups. The treatment duration ranged from 4 to 48 weeks, and the dosage of CoQ10 varied between 60 to 300 mg/day. In conclusion, the meta-analysis showed that CoQ10 supplementation increased antioxidant markers of superoxide dismutase (SOD) and catalase (CAT), and decreased the oxidative stress marker malondialdehyde (MDA) and its derivative forms. There was no consistent effect on inflammatory markers of CRP, TNF-α, IL-6 or the levels of the antioxidant glutathione peroxidase. The discrepancies amongst the different studies may be a result of the divergent study designs, different population characteristics, the dosage of CoQ10 used and the duration of intervention.
Abstract
OBJECTIVE Systemic inflammation and oxidative stress significantly contribute in developing coronary artery disease (CAD). This systematic review and meta-analysis was aimed to determine the effects of coenzyme Q10 (CoQ10) supplementation on biomarkers of inflammation and oxidative stress among patients with CAD. METHODS The electronic databases including MEDLINE, EMBASE, Scopus, Web of Science, and Cochrane Library databases were systematically searched until Oct 2018. The quality assessment and heterogeneity of the selected randomized clinical Trials (RCTs) were examined using the Cochrane Collaboration risk of bias tool, and Q and I2 tests, respectively. Given the presence of heterogeneity, random-effects model or fixed-effect model were used to pool standardized mean differences (SMDs) as summary effect sizes. RESULTS A total of 13 clinical RCTs of 912 potential citations were found to be eligible for the current meta-analysis. The pooled findings for biomarkers of inflammation and oxidative stress demonstrated that CoQ10 supplementation significantly increased superoxide dismutase (SOD) (SMD 2.63; 95% CI, 1.17, 4.09, P < 0.001; I2 = 94.5%) and catalase (CAT) levels (SMD 1.00; 95% CI, 0.57, 1.43, P < 0.001; I2 = 24.5%), and significantly reduced malondialdehyde (MDA) (SMD - 4.29; 95% CI - 6.72, - 1.86, P = 0.001; I2 = 97.6%) and diene levels (SMD - 2.40; 95% CI - 3.11, - 1.68, P < 0.001; I2 = 72.6%). We did not observe any significant effect of CoQ10 supplementation on C-reactive protein (CRP) (SMD - 0.62; 95% CI - 1.31, 0.08, P = 0.08; I2 = 87.9%), tumor necrosis factor alpha (TNF-α) (SMD 0.22; 95% CI - 1.07, 1.51, P = 0.73; I2 = 89.7%), interleukin-6 (IL-6) (SMD - 1.63; 95% CI - 3.43, 0.17, P = 0.07; I2 = 95.2%), and glutathione peroxidase (GPx) levels (SMD 0.14; 95% CI - 0.77, 1.04, P = 0.76; I2 = 78.7%). CONCLUSIONS Overall, this meta-analysis demonstrated CoQ10 supplementation increased SOD and CAT, and decreased MDA and diene levels, but did not affect CRP, TNF-α, IL-6, and GPx levels among patients with CAD.
Methodological quality
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