Triglyceride as a risk factor for coronary artery disease.
Triglyceride as a risk factor for coronary artery disease.
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DOI：
10.1016/s0002-9149(98)00770-x
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发表时间：
1998-11
期刊：
影响因子：
--
通讯作者：
A. Gotto
中科院分区：
文献类型：
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作者：
A. Gotto
甘油三酯浓度与冠状动脉疾病（CAD）风险之间的独立关联数据是模棱两可的，不像低密度脂蛋白（LDL）胆固醇和高密度脂蛋白（HDL）胆固醇的数据，它们与CAD风险显示出强烈的、一致的和相反的相关性。有一些证据表明，甘油三酯在某些亚组中是一个独立的危险因素，例如50-69岁的女性（弗雷明汉心脏研究）和非胰岛素依赖型糖尿病患者。然而，甘油三酯作为一种协同CAD危险因素的证据更强。例如，在赫尔辛基心脏研究中，具有高LDL胆固醇、低HDL胆固醇和高甘油三酯“脂质三联征”的患者在接受降脂治疗后减少了大部分事件。甘油三酯与冠心病风险之间相关性的一个重要混杂因素是富含甘油三酯的脂蛋白的异质性：较大的富含甘油三酯的颗粒被认为与冠心病风险无关，而较小（且密度较大）的颗粒被认为具有动脉粥样硬化性。目前，测量空腹甘油三酯水平和甘油三酯评估结合LDL胆固醇和HDL胆固醇浓度是评估高甘油三酯血症在冠心病风险中最实用的方法，尽管餐后血脂可能被证明是一个更好的动脉粥样硬化指标。高甘油三酯血症的治疗最初应侧重于非药物治疗（即饮食、运动、控制体重和减少酒精）。对于糖尿病患者，严格控制血糖也很重要。然而，如果这种方法被证明是不够的，还有几种药理学选择。贝特类可能对降低甘油三酯和增加高密度脂蛋白胆固醇有效。烟酸（烟酸）已被证明可以降低甘油三酯，增加高密度脂蛋白胆固醇，降低低密度脂蛋白胆固醇，并降低脂蛋白(a)；它还能降低纤维蛋白原。他汀类药物似乎对降低高甘油三酯血症患者的甘油三酯和LDL胆固醇有效；然而，它们不能使载脂蛋白B的代谢正常化，高密度脂蛋白胆固醇可能保持在低水平。因此，与贝特或烟酸联合使用可能是合适的。关注高甘油三酯血症与冠心病风险增加有关，是评估全球冠心病发展风险的重要一步。
The data for an independent association between triglyceride concentrations and risk for coronary artery disease (CAD) are equivocal, unlike the data for low-density lipoprotein (LDL) cholesterol and high-density lipoprotein (HDL) cholesterol, which show strong, consistent, and opposing correlations with CAD risk. There is some evidence for triglyceride as an independent risk factor in certain subgroups, for example, women 50–69 years of age (Framingham Heart Study) and in patients with noninsulin-dependent diabetes. However, the evidence is stronger for triglyceride as a synergistic CAD risk factor. For example, patients with the “lipid triad” of high LDL cholesterol, low HDL cholesterol, and high triglyceride accounted for most of the event reduction with lipid-lowering therapy in the Helsinki Heart Study. An important confounder of the correlation between triglyceride and CAD risk is the heterogeneity of triglyceride-rich lipoproteins: the larger triglyceride-rich particles are thought not to be associated with CAD risk, whereas the smaller (and denser) particles are believed to be atherogenic. At present, measurement of fasting triglyceride levels and triglyceride assessment in conjunction with LDL cholesterol and HDL cholesterol concentrations are the most practical methods of evaluating hypertriglyceridemia in CAD risk, although postprandial lipemia may prove a better indicator of atherogenicity. Management of hypertriglyceridemia should initially focus on nonpharmacologic therapy (i.e., diet, exercise, weight control, and alcohol reduction). In diabetic patients, meticulous glycemic control is also important. However, if this approach proves inadequate, there are several pharmacologic options. Fibrates may be effective in decreasing triglyceride and increasing HDL cholesterol. Nicotinic acid (niacin) has been shown to decrease triglyceride, increase HDL cholesterol, lower LDL cholesterol, and decrease lipoprotein(a); it also decreases fibrinogen. The statins appear to be effective in decreasing triglyceride and LDL cholesterol in hypertriglyceridemia; however, they do not normalize metabolism of apolipoprotein B, and HDL cholesterol may remain low. Therefore, combination with a fibrate or niacin may be appropriate. Attention to hypertriglyceridemia with respect to increased CAD risk represents an important step in assessing global risk for CAD development.