Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management.

Triglyceride-rich lipoproteins and high-density lipoprotein cholesterol in patients at high risk of cardiovascular disease: evidence and guidance for management.
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DOI:
10.1093/eurheartj/ehr112
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发表时间:
2011-06
影响因子:
39.3
通讯作者:
European Atherosclerosis Society Consensus Panel
European Atherosclerosis Society Consensus Panel
中科院分区:
医学1区
文献类型:
--
作者:
Chapman MJ;Ginsberg HN;Amarenco P;Andreotti F;Borén J;Catapano AL;Descamps OS;Fisher E;Kovanen PT;Kuivenhoven JA;Lesnik P;Masana L;Nordestgaard BG;Ray KK;Reiner Z;Taskinen MR;Tokgözoglu L;Tybjærg-Hansen A;Watts GF;European Atherosclerosis Society Consensus Panel

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即使低密度脂蛋白胆固醇(LDL - C)达到目标值,伴有心脏代谢异常的患者仍处于心血管事件的高风险中。本文旨在(i)审慎评估富含甘油三酯的脂蛋白(TRLs)水平升高和高密度脂蛋白胆固醇(HDL - C)水平降低作为心血管危险因素的证据,以及(ii)就治疗策略提供建议。目前的证据支持升高的TRL及其残粒、低HDL - C与心血管风险之间存在因果关联。这一解读基于对TRL和残粒的机制及遗传学研究,以及提示循环甘油三酯与心血管疾病相关的流行病学数据。对于HDL,流行病学、机制和临床干预数据都支持低HDL - C会增加心血管风险这一观点;然而遗传学证据尚不明确,这可能反映了HDL代谢的复杂性。专家组认为,针对甘油三酯升高(≥1.7 mmol/L或150 mg/dL,这是TRL及其残粒的一个标志物)和/或低HDL - C(<1.0 mmol/L或40 mg/dL)进行治疗可能会带来进一步的益处。第一步应该是生活方式干预,同时考虑药物治疗的依从性以及血脂异常的继发原因。如果纠正不充分,可以考虑添加烟酸或贝特类药物,或者强化降低LDL - C的治疗。关于他汀类药物联合治疗的决策应考虑相关的安全性问题,即烟酸导致血糖、尿酸或肝酶升高的风险,以及贝特类药物导致肌病、血清肌酐升高和胆石症的风险。这些建议将有助于降低在LDL - C达标的心脏代谢异常患者中仍然存在的显著心血管风险。
Even at low-density lipoprotein cholesterol (LDL-C) goal, patients with cardiometabolic abnormalities remain at high risk of cardiovascular events. This paper aims (i) to critically appraise evidence for elevated levels of triglyceride-rich lipoproteins (TRLs) and low levels of high-density lipoprotein cholesterol (HDL-C) as cardiovascular risk factors, and (ii) to advise on therapeutic strategies for management. Current evidence supports a causal association between elevated TRL and their remnants, low HDL-C, and cardiovascular risk. This interpretation is based on mechanistic and genetic studies for TRL and remnants, together with the epidemiological data suggestive of the association for circulating triglycerides and cardiovascular disease. For HDL, epidemiological, mechanistic, and clinical intervention data are consistent with the view that low HDL-C contributes to elevated cardiovascular risk; genetic evidence is unclear however, potentially reflecting the complexity of HDL metabolism. The Panel believes that therapeutic targeting of elevated triglycerides (≥1.7 mmol/L or 150 mg/dL), a marker of TRL and their remnants, and/or low HDL-C (<1.0 mmol/L or 40 mg/dL) may provide further benefit. The first step should be lifestyle interventions together with consideration of compliance with pharmacotherapy and secondary causes of dyslipidaemia. If inadequately corrected, adding niacin or a fibrate, or intensifying LDL-C lowering therapy may be considered. Treatment decisions regarding statin combination therapy should take into account relevant safety concerns, i.e. the risk of elevation of blood glucose, uric acid or liver enzymes with niacin, and myopathy, increased serum creatinine and cholelithiasis with fibrates. These recommendations will facilitate reduction in the substantial cardiovascular risk that persists in patients with cardiometabolic abnormalities at LDL-C goal.
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期刊: BMJ (Clinical research ed.)
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