医学
可欣
前蛋白转化酶
枯草杆菌素
心肌梗塞
普伐他汀
阿托伐他汀
PCSK9
心脏病学
内科学
胆固醇
脂蛋白
低密度脂蛋白受体
生物化学
酶
化学
作者
Yuichiro Kashima,Hiroshi Imamura,Atsushi Izawa,Uichi Ikeda
出处
期刊:Circulation
[Ovid Technologies (Wolters Kluwer)]
日期:2015-11-10
卷期号:132 (suppl_3)
标识
DOI:10.1161/circ.132.suppl_3.11981
摘要
Introduction: Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a key regulator of serum low-density lipoprotein levels and statins increase serum PCSK9 levels. Therefore, we investigated PCSK9 levels in ST-segment-elevation myocardial infarction (STEMI) patients who underwent PCI and were randomly allocated to atorvastatin or pravastatin therapy for 2 years. Hypothesis: Atorvastatin or pravastatin differentially influence long-term PCSK9 levels in STEMI patients. Methods: The present study is a subanalysis of the ALPS-AMI study and patients who were increased 10 to 20 mg of statin dose, and added ezetimibe during the study period were excluded from the ALPS-AMI study. PCSK9 levels were measured at 1 and 24 months in 225 STEMI patients who were randomly allocated to 10 mg/day of atorvastatin (n = 107) or pravastatin (n = 118) statin therapy. Results: No differences in 1-month PCSK9 levels between the atorvastatin and pravastatin groups were noted. However, the 24-month PCSK9 levels were significantly higher in pravastatin group (389.4 [interquartile range: 293.6-485.1] ng/mL than in atorvastatin group (314.5 [interquartile range: 235.4-375.8] ng/mL, P <0.001). Conclusions: This is the first clinical trial to compare the long-term effects of atorvastatin and pravastatin therapy on PCSK9 levels in patients with STEMI, and demonstrates that pravastatin therapy was more increased serum PCSK9 levels than atorvastatin therapy.
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