Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial.
Effect of Eicosapentaenoic and Docosahexaenoic Acids Added to Statin Therapy on Coronary Artery Plaque in Patients With Coronary Artery Disease: A Randomized Clinical Trial.
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在他汀类动脉疾病患者中，在他汀类动脉菌斑中添加了他汀类动脉菌斑中的eicosapentaenoic和docosahecahexaenoic酸的影响：一项随机临床试验。
DOI：
10.1161/jaha.117.006981
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发表时间：
2017-12-15
影响因子：
5.4
通讯作者：
Welty FK
中科院分区：
文献类型：
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作者：
Alfaddagh A;Elajami TK;Ashfaque H;Saleh M;Bistrian BR;Welty FK
虽然他汀类药物减少心血管事件，但剩余风险仍然存在。因此，需要采取其他方式来降低风险。我们评估了在他汀类药物治疗中加入药理学剂量的二十碳五烯酸和二十二碳六烯酸对冠状动脉斑块体积的影响。共有285名稳定型冠状动脉疾病患者接受他汀类药物治疗，随机接受omega-3乙酯（每日1.86 g二十碳五烯酸和1.5 g二十二碳六烯酸）或不接受omega-3（对照）治疗30个月。冠状动脉斑块体积通过冠状动脉CT血管造影进行评估。平均（SD）年龄为63.0（7.7）岁;平均低密度脂蛋白胆固醇≤80 mg/dL。在意向治疗分析中，我们的主要终点，非钙化斑块体积，在组间无差异（P=0.14），但在符合方案分析中接近显著性（P=0.07）。当在意向治疗分析中按年龄分层时，年轻的omega-3受试者的主要终点、非钙化斑块（P=0.013）以及纤维、钙化和总斑块的进展显著较少。在斑块亚型分析中，对照组纤维斑块显著进展，而omega-3乙酯组无变化（中位数%变化[四分位距]分别为5.0% [-5.7，20.0] vs-0.1%[-12.3，14.5]; P=0.018）。在接受低强度他汀类药物治疗的受试者中，与对照组相比，omega-3乙酯受试者的纤维斑块进展减弱（中位%变化[四分位距]分别为0.3% [-12.8，9.0] vs 4.8% [-5.1，19.0]; P=0.032）。相比之下，两个治疗组中接受高强度他汀类药物治疗的受试者在斑块变化方面没有差异。在低密度脂蛋白胆固醇水平控制良好的依从性治疗受试者中，高剂量二十碳五烯酸和二十二碳六烯酸在预防纤维性冠状动脉斑块进展方面提供了他汀类药物的额外获益。低强度他汀类药物而非高强度他汀类药物的益处表明他汀类药物强度影响斑块体积。 URL：http://www.ClinicalTrials.gov。唯一标识符：NCT 01624727。
Although statins reduce cardiovascular events, residual risk remains. Therefore, additional modalities are needed to reduce risk. We evaluated the effect of eicosapentaenoic acid and docosahexaenoic acid in pharmacologic doses added to statin treatment on coronary artery plaque volume. A total of 285 subjects with stable coronary artery disease on statins were randomized to omega‐3 ethyl‐ester (1.86 g of eicosapentaenoic acid and 1.5 g of docosahexaenoic acid daily) or no omega‐3 (control) for 30 months. Coronary plaque volume was assessed by coronary computed tomographic angiography. Mean (SD) age was 63.0 (7.7) years; mean low‐density lipoprotein cholesterol ≤80 mg/dL. In the intention‐to‐treat analysis, our primary endpoint, noncalcified plaque volume, was not different between groups (P=0.14) but approached significance in the per protocol analysis (P=0.07). When stratified by age in the intention‐to‐treat analysis, younger omega‐3 subjects had significantly less progression of the primary endpoint, noncalcified plaque (P=0.013), and fibrous, calcified and total plaque. In plaque subtype analysis, controls had significant progression of fibrous plaque compared to no change in the omega‐3 ethyl‐ester group (median % change [interquartile range], 5.0% [−5.7, 20.0] versus −0.1% [−12.3, 14.5], respectively; P=0.018). Among those on low‐intensity statins, omega‐3 ethyl‐ester subjects had attenuation of fibrous plaque progression compared to controls (median % change [interquartile range], 0.3% [−12.8, 9.0] versus 4.8% [−5.1, 19.0], respectively; P=0.032). In contrast, those on high‐intensity statins had no difference in plaque change in either treatment arm. High‐dose eicosapentaenoic acid and docosahexaenoic acid provided additional benefit to statins in preventing progression of fibrous coronary plaque in subjects adherent to therapy with well‐controlled low‐density lipoprotein cholesterol levels. The benefit on low‐intensity statin, but not high‐intensity statin, suggests that statin intensity affects plaque volume. URL: http://www.ClinicalTrials.gov. Unique identifier: NCT01624727.