Highlighted Articles - Atherosclerosis March 2015 Issue
27 March 2015
Volume 239 | Issue 1 | March 2015
By Elvira Mambetisaeva, Sarah Leigh and Steve Humphries (Editor–in-Chief)
In an attempt to establish whether or not Coenzyme Q10 (CoQ10) supplementation is effective in reducing statin myalgia, Taylor et al performed a randomized trial of simvastatin combined with CoQ10 or placebo, for 8 weeks in 41 patients with confirmed muscle myalgia. From their results Taylor et al conclude that CoQ10 does not reduce statin myalgia in these subjects. Kenneth Feingold emphasizes the challenges presented in studying statin induced myalgia in his invited commentary. He highlights that only 36% of Taylor et al’s original population were actually confirmed to have statin induced myalgia; clearly this poses problems not only for the diagnosis of statin induced muscle symptoms, but also for the investigation of potential therapies. Kenneth Feingold commends the design of Taylor et al’s study over that of previous reports and comments that two major issues remain; firstly, how statin induced myalgia can be reliably diagnosed and secondly, how to effective therapies can be found to deal with it. Both issues are critical if affected patients are to be encouraged to continue taking their statins!
Breast arterial calcification (BAC) observed on screening mammography is a type of medial calcification. Several studies suggest that BAC is associated with traditional cardiovascular risk factors. The systematic review of 116 articles by Hendriks et al illustrates the association of BAC with increased cardiovascular disease events, while only being associated with some of the known cardiovascular risk factors. The authors conclude that medial arterial calcification might contribute to cardiovascular disease through a pathway distinct from the intimal atherosclerotic process.
Unconjugated bilirubin was shown in recent studies to be a potent antioxidant and to have anti-mutagenic, immune-modulatory, platelet inhibitory and possibly lipid-lowering effects. Gilbert’s syndrome is associated with mild and benign hyperbilirubinemia and a significantly reduced risk of mortality from cardiovascular disease. The review article by Kundur et al summarises the relationship between Gilbert’s syndrome, unconjugated bilirubin and the cardiovascular risk factors that can result in increased platelet activation.
Non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of the metabolic syndrome. It is strongly associated with insulin and other metabolic risk factors such as diabetes mellitus, central abdominal obesity and dyslipidaemia. NAFLD is an independent risk factor for cardiovascular disease (CVD) and predicts future events, independently of other risk factors. The review by Than & Newsome discusses the pathogenesis of NAFLD and the development of new approaches for the management and treatment of this disease.
Papers in this issue include: