Plasma coenzyme Q10 predicts lipid-lowering response to high-dose atorvastatin

Background

Coenzyme Q10 (CoQ10) is a provitamin synthesized via the 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase pathway, and thus may serve as a potential marker of intrinsic HMG-CoA reductase activity. HMG-CoA reductase inhibitors (statins) decrease CoQ10, although it is unclear whether this is due to reductions in lipoproteins, which transport CoQ10.

Objective

We evaluated whether baseline plasma CoQ10 concentrations predict lipid-lowering response to high-dose atorvastatin, and to what extent CoQ10 changes after atorvastatin therapy depend on lipoprotein changes.

Methods

Individuals without dyslipidemia or known cardiovascular disease (n = 84) received atorvastatin 80 mg/day for 16 weeks. Blood samples collected at baseline and after 4, 8, and 16 weeks of treatment were assayed for CoQ10.

Results

Individuals with higher baseline CoQ10/low-density lipoprotein cholesterol (LDL-C) ratios displayed diminished absolute and percent LDL-C reductions at 8 and 16 weeks of atorvastatin treatment (P < 0.001 to P = 0.01). After 16 weeks of atorvastatin, plasma CoQ10 decreased 45% from 762 ± 301 to 374 ± 150 ng/mL (P < 0.001). CoQ10 changes were correlated with LDL-C and apolipoprotein B changes (r = 0.27 − 0.38; P = 0.001 to P = 0.02), but remained significant when normalized to all lipoproteins. CoQ10 changes were not associated with adverse drug reactions.

Conclusion

Baseline CoQ10/LDL-C ratio was associated with the degree of LDL-C response to atorvastatin. Atorvastatin decreased CoQ10 concentrations in a manner that was not completely dependent on lipoprotein changes. The utility of CoQ10 as a predictor of atorvastatin response should be further explored in patients with dyslipidemia.

Keywords: Biomarkers, Coenzyme Q10, HMG CoA-reductase inhibitors, Lipids, Pharmacology