European Atherosclerosis Society, INSERM UMR-S939, Pitié-Salpetriere University Hospital, Paris 75651, France.
Eur Heart J. 2011 Jun;32(11):1345-61. doi: 10.1093/eurheartj/ehr112. Epub 2011 Apr 29.
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.
即使在低密度脂蛋白胆固醇（LDL-C）目标水平，患有心脏代谢异常的患者仍然存在发生心血管事件的高风险。本文旨在（i）批判性评估甘油三酯丰富的脂蛋白（TRL）升高和高密度脂蛋白胆固醇（HDL-C）降低作为心血管风险因素的证据，以及（ii）为管理提供治疗策略建议。目前的证据支持 TRL 及其残基升高、HDL-C 降低与心血管风险之间存在因果关系。这种解释基于 TRL 和残基的机制和遗传研究，以及提示循环甘油三酯与心血管疾病之间存在关联的流行病学数据。对于 HDL，流行病学、机制和临床干预数据一致认为，HDL-C 降低与心血管风险增加有关；然而，遗传证据尚不清楚，这可能反映了 HDL 代谢的复杂性。专家组认为，针对升高的甘油三酯（≥1.7mmol/L 或 150mg/dL）、TRL 及其残基的标志物和/或低 HDL-C（<1.0mmol/L 或 40mg/dL）进行治疗可能会带来进一步的益处。第一步应该是进行生活方式干预，同时考虑药物治疗的依从性和血脂异常的继发原因。如果治疗效果不理想，可以考虑添加烟酸或贝特类药物，或加强 LDL-C 降低治疗。在决定他汀类药物联合治疗时应考虑到相关的安全性问题，即烟酸可能导致血糖、尿酸或肝酶升高，贝特类药物可能导致肌病、血清肌酐升高和胆石症。这些建议将有助于降低心脏代谢异常患者在 LDL-C 目标水平下仍然存在的大量心血管风险。
