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Coenzyme Q10 and statins

Last reviewed dd mmm yyyy. Last edited dd mmm yyyy

Authoring team

  • statins mechanism of action is inhibition of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG CoA Reductase), the rate-limiting enzyme in the biosynthesis of cholesterol from acetyl-Coenzyme A via mevalonate and subsequent intermediates
    • inhibition of HMG CoA reductase also leads to a decrease the synthesis of nonsterol derivatives of mevalonate, including coenzyme Q10 (also known as ubiquinone)
    • studies have consistently shown that HMG CoA reductase inhibitors lower plasma coenzyme Q10 levels
  • coenzyme Q10
    • is an important redox component of the mitochondrial respiratory transport chain
      • role in the generation of high-energy products such as adenosine triphosphate (ATP)
      • ATP-bioavailability is a crucial factor regulating myocardial contractility
        • ATP-content correlating positively with systolic and diastolic left ventricular indices in diseased human myocardium
      • myocardial tissue levels of coenzyme Q10 are reduced in heart failure (1)
      • the reduced form of coenzyme Q10, is ubiquinol
        • ubiquinol is an antioxidant and free radical scavenger
      • vitamin E (a-tocopherol) and coenzyme Q10 are carried by LDL
  • coenzyme Q10 and statin treatment:
    • a study investigating the effect of treatment with simvastatin 20mg per day for a period of 6 months (2) showed
      • serum lipids showed the expected reductions.
      • plasma vitamin E and coenzyme Q10 levels were reduced by 17 ± 4% (P < 0·01) and 12 ± 4% (P < 0·03) at 6 months. However, the coenzyme Q10/LDL-cholesterol ratio and vitamin E/LDL-cholesterol ratio increased significantly
      • left ventricular ejection fraction (EF) decreased transiently after 1 month, while no significant change was observed at 3 and 6 months. Other markers of left ventricular function did not change significantly at any time point
      • the authors concluded that:
        • despite reduced plasma vitamin E and coenzyme Q10, 20 mg of simvastatin therapy is associated with a significantly increased coenzyme Q10/LDL-cholesterol ratio and vitamin E/LDL-cholesterol ratio
        • simvastatin treatment is not associated with impairment in left ventricular systolic or diastolic function in hypercholesterolaemic subjects after 6 months of treatment

Notes:

  • the transient reduction in a population with normal left ventricular ejection fraction was not associated with clinical evidence for reduced cardiac function (1)
  • in contrast to the findings of this single study statins have been shown to improve left ventricular function in several trials
    • atorvastatin therapy improved left ventricular ejection fraction in hypercholesteraemic patients with coronary artrey disease (CAD) by 13% after 2 years of treatment (3)
    • simvastatin has been shown to reduce the occurrence of heart failure in a cohort of CAD patients without previous evidence of congestive heart failure (4)
    • the improvement in cardiac function in heart failure in patients with CAD is perhaps not surpristing as it is most commonly owing to progression of coronary atherosclerosis and myocardial infarction – both of which are decreased by statin treatment

Reference:

  1. Folkers K et al. Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with coenzyme Q10. Proc Natl Acad Sci USA 1985;82: 901–4.
  2. Colquhoun DM et al. Effects of simvastatin on blood lipids, vitamin E, coenzyme Q10 levels and left ventricular function in humans. Eur J Clin Invest. 2005 Apr;35(4):251-8.
  3. Kontopoulos AG et al. Long-term treatment effect of atorvastatin on aortic stiffness in hypercholesterolemic patients. Curr Med Res Opin 2003;19: 22–7.
  4. Kjekshus J et al. The effects of simvastatin on the incidence of heart failure in patients with coronary heart Disease. J Card Fail 1997;3: 249–54.

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