title: Neither plasma coenzyme Q10 concentration, nor its decline during pravastatin therapy, is linked to recurrent cardiovascular disease events: a prospective case-control study from the LIPID study.
abstract: Statins decrease LDL cholesterol and the risk of atherosclerotic cardiovascular disease (CVD). They also decrease coenzyme Q10 (CoQ10), an effect that may negate some of the statin benefit on CVD. We examined the relationship between plasma CoQ10 concentration and CVD in a prospective case-control study of the effect of pravastatin. Plasma samples from 250 LIPID trial patients who over 6 years suffered a recurrent CVD event (CVD death, nonfatal MI or stroke) and 250 matched controls who remained event-free for the same duration of follow-up were assayed for CoQ10 and lipids (cholesterol and cholesterylesters). Mean plasma CoQ10 concentrations were significantly lower in pravastatin-treated patients than in those assigned placebo (0.51 versus 0.60 micromol/L, P = 0.006), and there was a moderate correlation between CoQ10 and common cholesterylesters (Pearson correlation coefficients in patients randomised to placebo, range r = 0.42-0.63). Univariate conditional logistic regression did not suggest any relationship between plasma CoQ10 and the risk of future CVD events (odds ratio 1.18; 95% CI 0.74-1.87; P = 0.49). Instead, we observed a reduction in the rate of recurrent CVD events with increasing ratio of plasma cholesterylarachidonate to cholesteryllinoleate. This study confirms that pravastatin lowers plasma CoQ10 concentrations, but this does not appear to predict the risk of recurrent CVD events.
authors.affiliation: Centre for Vascular Research, School of Medical Sciences, University of New South Wales, UNSW, Sydney, NSW 2052, Australia. r.stocker@usw.edu.au
authors.forename: Roland
authors.initials: R
authors.lastname: Stocker
authors.forename: Christine
authors.initials: C
authors.lastname: Pollicino
authors.forename: Craig A
authors.initials: CA
authors.lastname: Gay
authors.forename: Paul
authors.initials: P
authors.lastname: Nestel
authors.forename: David
authors.initials: D
authors.lastname: Colquhoun
authors.forename: Malcolm
authors.initials: M
authors.lastname: Whiting
authors.forename: Andrew
authors.initials: A
authors.lastname: Tonkin
authors.forename: David
authors.initials: D
authors.lastname: Sullivan
authors.forename: John
authors.initials: J
authors.lastname: Simes
mesh_terms: D002318:Cardiovascular Diseases / Q000097:blood* / Q000473:pathology; D016022:Case-Control Studies; D003067:Coenzymes; D004305:Dose-Response Relationship, Drug; D005231:Fatty Acids, Unsaturated / Q000378:metabolism; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D008055:Lipids / Q000737:chemistry; D010919:Placebos; D017035:Pravastatin / Q000494:pharmacology*; D011446:Prospective Studies; D012008:Recurrence; D012044:Regression Analysis; D012306:Risk; D014451:Ubiquinone / Q000031:analogs & derivatives* / Q000097:blood
chemical_list: D003067:Coenzymes; D005231:Fatty Acids, Unsaturated; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008055:Lipids; D010919:Placebos; D014451:Ubiquinone; C024989:coenzyme Q10; D017035:Pravastatin