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
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