PURPOSE OF REVIEW To review the recent evidence from observational/genetic/interventional studies addressing triglycerides and residual cardiovascular risk (CVRisk). RECENT FINDINGS Large population-based and secondary prevention studies consistently show an association of higher triglycerides with increased CVRisk. This is compounded by genetic studies demonstrating an independent relationship between triglyceride raising or lowering genetic variants affecting triglyceride-rich lipoproteins (TRL) metabolism and CVRisk. Mendelian randomization analysis suggests the benefit of genetic lowering of triglycerides and LDL-cholesterol is similar per unit change in apolipoprotein-B. Among cholesterol-lowering trials, more intensive statin therapy produced greater CVRisk reductions in patients with higher TRL-cholesterol or triglycerides; proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibition led to similar triglycerides reduction but greater non-HDL-C or apolipoprotein-B reductions than fibrates or fish oils. Regarding n-3 fatty acids, A Study of Cardiovascular Events in Diabetes (ASCEND) and Vitamin D and Omega-3 Trial (VITAL) primary prevention trials with eicosapentaenoic acid (EPA) and docosahexaenoic acid failed to demonstrate cardiovascular benefits, Conversely, Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial (REDUCE-IT) using high-dose icosapent-ethyl (purified EPA) in primary (diabetes) and secondary prevention with hypertriglyceridemia showed significant cardiovascular events reductions (greater than expected by the observed triglycerides or apolipoprotein-B reductions, suggesting potential benefits through non-lipid pathways). SUMMARY Evidence suggests higher triglycerides are a marker of CVRisk and may help identify patients who benefit from intensification of therapy. Moreover, genetic studies support a causal link between TRL/triglycerides and cardiovascular disease. Treatment with high-dose EPA may be of benefit in high-risk patients with hypertriglyceridemia to reduce CVRisk.

中文翻译：

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甘油三酸酯和残留风险。

综述的目的回顾来自观察/遗传/介入研究的最新证据，这些研究涉及甘油三酸酯和残余心血管风险（CVRisk）。最新发现大量基于人群和二级预防的研究始终显示，甘油三酸酯含量较高与CVRisk升高相关。基因研究证实了甘油三酸酯升高或降低影响富含甘油三酸酯的脂蛋白（TRL）代谢和CVRisk的遗传变异之间的独立关系，这使情况更加复杂。孟德尔随机化分析表明，降低载脂蛋白B的单位变化可以降低甘油三酸酯和LDL-胆固醇的遗传性。在降低胆固醇的试验中，对于TRL-胆固醇或甘油三酯较高的患者，更严格的他汀类药物治疗可产生更大的CVRisk降低。前蛋白转化酶枯草杆菌蛋白酶/ kexin型9（PCSK9）抑制导致类似的甘油三酸酯减少，但非高密度脂蛋白C或载脂蛋白B的减少比贝特类或鱼油更大。关于n-3脂肪酸，使用二十碳五烯酸（EPA）和二十二碳六烯酸进行的糖尿病心血管事件（ASCEND）和维生素D和Omega-3试验（VITAL）一级预防试验的研究未能证明具有心血管益处，相反，高糖甘油三酯血症的初次（糖尿病）和二级预防中使用高剂量二十碳五烯（纯化的EPA）的二十碳五烯酸乙酯干预试验（REDUCE-IT）的心血管事件显示心血管事件明显减少（大于观察到的甘油三酸酯或载脂蛋白- B减少，表明通过非脂质途径的潜在益处）。总结证据表明，较高的甘油三酸酯是CVRisk的标志，可能有助于确定受益于强化治疗的患者。此外，遗传研究支持TRL /甘油三酸酯与心血管疾病之间的因果关系。高剂量EPA治疗可能对高甘油三酯血症高危患者降低CVRisk有益。