Relationship between plasma coenzyme Q₁₀, asymmetric dimethylarginine and arterial stiffness in patients with phenotypic or genotypic familial hypercholesterolemia on long-term statin therapy

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• 作者：Joanna M. Young^a ; ^b ; ^{joanna.young@cdhb.govt.nz} ; Sarah L. Molyneux^c ; Annette M. Reinheimer^a ; Christopher M. Florkowski^a ; ^c ; Christopher M. Frampton^b ; Russell S. Scott^a ; ^b ; Peter M. George^c
• 关键词：Coenzyme Q10 ; Statin therapy ; Familial hypercholesterolemia ; Arterial stiffness ; Augmentation index ; Asymmetric dimethylarginine
• 刊名：Atherosclerosis
• 出版年：2011
• 出版时间：September, 2011
• 年：2011
• 卷：218
• 期：1
• 页码：188-193
• 全文大小：1K

文摘

Objective

We investigated whether statin-treated heterozygous familial hypercholesterolemic (FH) patients have lower plasma coenzyme Q₁₀ (CoQ₁₀) levels than low-density lipoprotein receptor (LDLR) mutation negative FH patients on equivalent statin doses, and whether lower CoQ₁₀ concentrations are associated with increased arterial stiffness.

Methods

Thirty LDLR mutation negative patients with clinical FH and 30 mutation positive FH patients matched for gender, statin duration and dose, and a further 30 controls were studied. Plasma CoQ₁₀ and asymmetric dimethylarginine (ADMA) levels were measured by HPLC and the augmentation index by pulse wave analysis.

Results

Plasma CoQ₁₀ levels, and the ratios of CoQ₁₀ to total cholesterol and LDL-cholesterol were similar in treated FH patients with identified LDLR mutations to mutation negative patients on equivalent doses of statin therapy (m>pm> > 0.05). CoQ₁₀ and lipid levels were also comparable to controls not using any lipid modifying treatment. Arterial stiffness was higher in mutation negative patients (m>pm> = 0.04) and there was a trend for an increase in mutation positive patients (m>pm> = 0.09). ADMA was higher in the mutation positive group (m>pm> < 0.01). The augmentation index corrected for age, blood pressure, and heart rate, was negatively correlated with plasma CoQ₁₀ within FH patients (m>pm> < 0.05).

Conclusion

Long-term, high-dose statin therapy does not lead to subnormal CoQ₁₀ concentrations in patients with phenotypic or genotypic FH. Arterial stiffness is elevated in FH patients compared to untreated controls, and low CoQ₁₀ levels are associated with increased arterial stiffness. CoQ₁₀ supplementation trials are warranted in FH patients.