Elevated C-reactive protein levels associated with increased risk of fatal and nonfatal coronary artery disease events
Tuesday, November 19, 2013. An article published in the December 2013 issue of the journal Arteriosclerosis, Thrombosis, and Vascular Biology reports findings from the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk cohort of an association between high C-reactive protein (CRP) levels and a greater risk of fatal as well as nonfatal coronary artery disease (CAD) events, including heart attack and angina.
The study includes 18,450 men and women whose average Framingham Risk Score was 12.8, which indicates a 12.8% average risk for a coronary artery disease event over a ten year period. Blood samples collected upon enrollment in EPIC between 1993 and 1997 were analyzed for serum C-reactive protein levels. Through March, 2008, there were 2,915 coronary artery disease events, 361 strokes and 657 peripheral artery disease events.
Among participants whose C-reactive protein levels were among the top 25% of participants at more than 3.3 milligrams per liter (mg/L), the adjusted risk of nonfatal coronary artery disease events was 61% higher than those whose levels were among the lowest 25%, and for fatal events, the risk was double that of the lowest group. The adjusted risk of nonfatal peripheral artery disease events among those whose CRP levels were highest was also more than double in comparison with the lowest group.
"Our observation that CRP levels are more strongly associated with fatal CAD events compared with nonfatal CAD events is underlined by the observation that CRP adds more discriminative power to the fatal compared with the nonfatal predictive risk model as demonstrated by the comparative predictive risk analyses," the authors note.
"First, inflammation in general can promote more serious atherothrombotic reactions comprising thrombosis, endothelial dysfunction, and vasoconstriction, thereby increasing the likelihood of a fatal outcome following plaque rupture," they explain. "Second, our findings are also compatible with the hypothesis that in the case of an acute coronary syndrome, CRP contributes to a more severe outcome by aggravating myocardial cell death and contributing to a wider area of tissue loss."
"This study lends further support to investigate the efficacy and safety of targeting inflammation per se for the prevention of cardiovascular events," they conclude.
The results of a randomized trial reported on November 6, 2013 in Nutrition Journal found a reduction in inflammation and an increase in antioxidant enzyme activities in individuals with coronary artery disease who were supplemented with coenzyme Q10 (CoQ10).
Researchers in Taiwan divided 42 men and women who were being treated with statin drugs for coronary artery stenosis to receive 300 milligrams CoQ10 per day or a placebo for twelve weeks. Blood samples collected at the beginning and end of the trial were analyzed for CoQ10, vitamin E, inflammation markers including C-reactive protein, tumor necrosis factor-alpha (TNF-alpha) and interleukin 6, and the antioxidant enzymes superoxide dismutase (SOD), catalase and glutathione peroxidase.
Plasma coenzyme Q10 and vitamin E levels significantly increased among CoQ10-supplemented participants by the end of the trial. The authors remark that "Coenzyme Q10 not only protects vitamin E against superoxide-driven oxidation but also regenerates vitamin E during antioxidation processes."
Subjects who received CoQ10 experienced a reduction in interleukin-6 and TNF-alpha, indicating a decline in inflammation, as well as elevations in SOD, catalase and glutathione peroxidase that resulted in a significant increase in comparison with the placebo group. The authors conclude that "Coronary artery disease patients might benefit from using coenzyme Q10 supplements to increase their antioxidation and anti-inflammation capacity during statins therapy."
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