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   <subfield code="a">Contribution of apolipoprotein A-I to the reduction in high-sensitivity C-reactive protein levels by different statins: comparative study of pitavastatin and atorvastatin</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Shigemasa Tani, Atsuhiko Takahashi, Ken Nagao, Atsushi Hirayama]</subfield>
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   <subfield code="a">Recently, investigation may have focused on modification of apolipoprotein A-I (apoA-I) associated with anti-inflammatory effect for the potential prevention of cardiovascular events. The purpose of this study was to evaluate the effects of atorvastatin and pitavastatin on serum apoA-I levels and to investigate the role of apoA-I in the anti-inflammatory effect of statin. We conducted a 6-month, prospective, randomized, open-label study in which we assigned hypercholesterolemic patients to a pitavastatin group (n=52; 2mg/day) or an atorvastatin group (n=52; 10mg/day) to investigate the effects of these two statins on the serum apoA-I levels and serum high-sensitivity C-reactive protein (hs-CRP) levels. There were no significant differences between the two groups in the changes in the low-density lipoprotein cholesterol, high-density lipoprotein cholesterol (HDL-C), or hs-CRP levels, but the change in apoA-I in the pitavastatin group was significantly greater than in the atorvastatin group (5.3 vs. 1.4%; p=0.0001). A stepwise regression analysis revealed that the percent change in (Δ) serum apoA-I level was an independent predictor of the Δ serum hs-CRP (standard correlation coefficient=−0.198; p=0.047). However, there was a significant negative correlation between the Δ apoA-I levels and Δ hs-CRP levels in the pitavastatin group (r=−0.283, p=0.042), but not the atorvastatin group (r=−0.133, p=0.356). The results suggest that the contribution of apoA-I to the reduction in serum hs-CRP levels by these two statins may be different. A decrease in hs-CRP level accompanied by an increase in apoA-I level may be involved in the pleiotropic effects of pitavastatin.</subfield>
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   <subfield code="a">Springer Japan, 2014</subfield>
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   <subfield code="a">Atherosclerosis</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Apolipoprotein A-I</subfield>
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   <subfield code="a">Tani</subfield>
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   <subfield code="u">Health Planning Center, Nihon University School of Medicine, 1-7-3 Kandasurugadai, Chiyoda-ku, 101-0062, Tokyo, Japan</subfield>
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   <subfield code="a">Takahashi</subfield>
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   <subfield code="a">Nagao</subfield>
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   <subfield code="u">Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan</subfield>
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   <subfield code="a">Hirayama</subfield>
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   <subfield code="t">Heart and Vessels</subfield>
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   <subfield code="g">30/6(2015-11-01), 762-770</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
   <subfield code="b">Springer special CC-BY-NC licence</subfield>
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