Atorvastatin-Induced Changes in Plasma Coenzyme Q10 and Brain Natriuretic Peptide in Patients With Coronary Artery Disease

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  • Suzuki Takayuki
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama
  • Nozawa Takashi
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama
  • Sobajima Mitsuo
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama
  • Igarashi Norio
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama
  • Matsuki Akira
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama
  • Fujii Nozomu
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama
  • Inoue Hiroshi
    Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama

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Abstract

The beneficial effects of statins in patients with coronary artery disease (CAD) may be balanced by concerns that statins can depress production of ubiquinone (CoQ10), which serves as a component of mitochondrial energy production and an antioxidant. Accordingly, the effects of atorvastatin (ATO)-induced changes in plasma CoQ10 on BNP and oxidative stress were investigated. In 29 patients with CAD, the plasma levels of CoQ10 and BNP and urinary excretion of 8-iso-prostaglandin F2α (8-iso-PGF) were determined before and after 3-month treatment with ATO. Ten patients had received pravastatin and 10 patients fluvastatin, while 9 patients had not received any statin before ATO. There was a linear correlation between ATO-induced changes in total cholesterol and CoQ10 (r = 0.632, P < 0.01), and an inverse correlation between ATO-induced changes in CoQ10 and BNP (r = -0.497, P < 0.01). There was no significant correlation between ATO-induced changes in CoQ10 and 8-iso-PGF. Multivariate analysis revealed that ATO-induced decreases in plasma CoQ10 were significantly associated with increasing BNP levels. In conclusion, long-term treatment with ATO might increase plasma levels of BNP in patients with CAD when it is accompanied by a greater reduction in plasma CoQ10. However, ATO-induced decreases in CoQ10 might not increase oxidative stress. <br>

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