Affiliation:
1. Department of Clinical Pharmacology and Propaedeutics of Internal Diseases, I.M. Sechenov First Moscow State Medical University
(Sechenov University), Moscow, Russian Federation
2. Federal State Budgetary Institution "Scientific Centre for Expert Evaluation
of Medicinal Products" of the Ministry of Health of the Russian Federation, Moscow, Russian Federation
3. A.P. Arzamastsev Department
of Pharmaceutical and Toxicological Chemistry, I.M. Sechenov First Moscow State Medical University (Sechenov University),
Moscow, Russian Federation
Abstract
Background:
Coenzyme Q10 is a key component of the mitochondrial respiratory chain and a fat-soluble
endogenous antioxidant performing many vital functions in the human body. Many researchers studied the plasma
concentrations of ubiquinol, ubiquinone, total CoQ10 and the redox state (ubiquinol/ubiquinone ratio) of CoQ10 in
healthy volunteers. However, these parameters in the plasma of patients with chronic heart failure (CHF) remain
almost uninvestigated.
Objective:
The aim of this case-control study was to investigate the effect of atorvastatin, amlodipine and ethoxidol
on endogenous plasma concentrations of ubiquinol, ubiquinone, total CoQ10 and its redox state in patients with CHF.
Methods:
The study included 62 patients with CHF divided into four groups depending on the prescribed therapy.
For the quantitative determination of ubiquinol, ubiquinone, and total CoQ10 in the plasma of patients, HPLCMS/
MS was used.
Results:
It was established that the endogenous plasma concentration of total CoQ10 in patients with CHF is significantly
lower than in healthy volunteers, and the ratio of reduced and oxidized forms of CoQ10 is shifted towards
ubiquinone. It was a statistically significant effect of drugs with different physicochemical structures and pharmacological
action on the plasma concentrations of ubiquinol, ubiquinone and total CoQ10: atorvastatin administration led
to a decrease in the concentration of ubiquinol (-33.3Δ%), and total CoQ10 (-15Δ%), administration of amlodipine
contributed to an increase in the levels of ubiquinol (+27.7Δ%) and total CoQ10 (+18.2Δ%), and the administration
of ethoxidol caused an increase in the concentration of ubiquinol (+25Δ%), ubiquinone (+17.7Δ%) and total CoQ10
(+20.2Δ%).
Conclusion:
Amlodipine is able to neutralize the negative effect of atorvastin on the redox balance of CoQ10 in
patients with CHF. An additional prescription of the antioxidant ethoxidol to standard therapy for patients with CHF
was substantiated. Determination of the redox state of CoQ10 in plasma can be used to diagnose and assess the degree
of oxidative stress in patients with cardiovascular diseases, as well as to assess the efficacy and safety of ongoing
pharmacotherapy.
Publisher
Bentham Science Publishers Ltd.
Subject
Clinical Biochemistry,Pharmacology