A Randomized , Double-Blind , Placebo-Controlled Crossover Study of Coenzyme Q 10 Therapy in Hypertensive Patients With the Metabolic Syndrome

Control of blood pressure (BP) in hypertensive patients often requires multiple drug therapy but poor adherence is frequently due, in part, to undesirable side effects. Accordingly, adjunctive therapy with agents such as coenzyme Q10 supposedly with few side effects, have become increasingly popular. Coenzyme Q10 is an antioxidant and integral component of the mitochondrial electron transport chain.1 There is evidence that plasma coenzyme Q10 concentrations are reduced in patients with essential hypertension.2 Furthermore, increased oxidative stress has been observed in hypertensive states.3 It has been proposed that coenzyme Q10 supplementation has an antihypertensive action resulting from vasodilatation via a direct effect on the endothelium and underlying vascular smooth muscle.4–6 A number of clinical studies have described the potential of coenzyme Q10 to lower BP in hypertensive patients. 2,7–17 Rosenfeldt et al. conducted a meta-analysis, comprising three randomized trials,7–9 one randomized crossover study,10 and eight open-label studies2,11–17 in 362 hypertensive patients, most of whom had essential hypertension or isolated systolic hypertension.4 They reported that coenzyme Q10 therapy had the potential to reduce BP by up to 17/10 mm Hg.4 The metaanalysis was however, limited by the inclusion of studies which were open-labeled and not placebo-controlled. Furthermore, there were considerable differences in patient populations with respect to age, underlying disease and comorbidities, coenzyme Q10 dose and duration, and use of concomitant antihypertensive therapy between the trials. Finally, the metaanalysis did not make use of individual patient data from the component studies, which would have provided a more robust assessment of any effect of coenzyme Q10 on arterial pressure. 1Lipid and Diabetes Research Group, Diabetes Research Institute, Christchurch Hospital Campus, Christchurch, New Zealand; 2Department of Medicine, University of Otago, Christchurch, New Zealand; 3Clinical Biochemistry Unit, Department of Biochemistry, Canterbury Health Laboratories, Christchurch, New Zealand. Correspondence: Joanna M. young (joanna.young@cdhb.govt.nz)