Chapman M John, Assmann Gerd, Fruchart Jean-Charles, Shepherd James, Sirtori Cesare
Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital de la Pitié, Paris, France.
Curr Med Res Opin. 2004 Aug;20(8):1253-68. doi: 10.1185/030079904125004402.
Reduction of low-density lipoprotein cholesterol (LDL-C) is presently the primary focus of lipid-lowering therapy for prevention and treatment of coronary heart disease (CHD). However, the high level of residual risk among statin-treated patients in recent coronary prevention studies indicates the need for modification of other major components of the atherogenic lipid profile. There is overwhelming evidence that a low plasma level of high-density lipoprotein cholesterol (HDL-C) is an important independent risk factor for CHD. Moreover, a substantial proportion of patients with or at risk of developing premature CHD typically exhibit distinct lipid abnormalities, including low HDL-C levels. Thus, therapeutic intervention aimed at raising HDL-C, within the context of reducing global cardiovascular risk, would benefit such patients, a viewpoint increasingly adopted by international treatment guidelines. Therapeutic options for patients with low HDL-C include treatment with statins, fibrates and nicotinic acid, either as monotherapy or in combination. Of these options, nicotinic acid is not only the most potent agent for raising HDL-C but is also effective in reducing key atherogenic lipid components including triglyceride-rich lipoproteins (mainly very low-density lipoproteins [VLDL] and VLDL remnants), LDL-C, and lipoprotein(a). The principal features of the atherogenic lipid profile in type 2 diabetes and the metabolic syndrome make them logical targets for nicotinic acid therapy, either alone or in combination with a statin. The lack of comprehensive European data on the prevalence of low HDL-C levels highlights a critical need for education on the importance of raising HDL-C in CHD prevention and treatment. The development of a reliable and accurate assay for HDL-C, as well as clarification of criteria for low and optimal levels of HDL-C in both men and women, constitute critical factors in the reliable identification and treatment of patients at elevated risk of CHD due to low HDL-C. Based on the available evidence, the European Consensus Panel recommends that the minimum target for HDL-C should be 40 mg/dL (1.03 mmol/L) in patients with CHD or with a high level of risk for CHD, including patients at high global risk with type 2 diabetes or the metabolic syndrome.
降低低密度脂蛋白胆固醇（LDL-C）是目前冠心病（CHD）防治中降脂治疗的主要重点。然而，近期冠心病预防研究中他汀类药物治疗患者的残余风险水平较高，这表明需要对致动脉粥样硬化血脂谱的其他主要成分进行调整。有压倒性的证据表明，血浆高密度脂蛋白胆固醇（HDL-C）水平低是冠心病的一个重要独立危险因素。此外，相当一部分患有早发性冠心病或有早发性冠心病风险的患者通常表现出明显的血脂异常，包括HDL-C水平低。因此，在降低整体心血管风险的背景下，旨在提高HDL-C的治疗干预将使这类患者受益，这一观点越来越多地被国际治疗指南所采纳。HDL-C低的患者的治疗选择包括使用他汀类药物、贝特类药物和烟酸进行治疗，可单一用药或联合用药。在这些选择中，烟酸不仅是提高HDL-C最有效的药物，而且在降低关键的致动脉粥样硬化血脂成分方面也有效，这些成分包括富含甘油三酯的脂蛋白（主要是极低密度脂蛋白[VLDL]和VLDL残粒）、LDL-C和脂蛋白(a)。2型糖尿病和代谢综合征中致动脉粥样硬化血脂谱的主要特征使其成为烟酸治疗的合理靶点，无论是单独使用还是与他汀类药物联合使用。欧洲缺乏关于HDL-C水平低的患病率的全面数据，这突出表明迫切需要开展教育，以说明提高HDL-C在冠心病防治中的重要性。开发一种可靠且准确的HDL-C检测方法，以及明确男性和女性HDL-C低水平和最佳水平的标准，是可靠识别和治疗因HDL-C低而患冠心病风险升高患者的关键因素。基于现有证据，欧洲共识小组建议，对于患有冠心病或冠心病风险高的患者，包括全球风险高的2型糖尿病或代谢综合征患者，HDL-C的最低目标应为40mg/dL（1.03mmol/L）。
