Gotto A M
Cornell University Medical College, New York, New York, USA.
Am J Cardiol. 1998 Nov 5;82(9A):22Q-25Q. doi: 10.1016/s0002-9149(98)00770-x.
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.
与低密度脂蛋白（LDL）胆固醇和高密度脂蛋白（HDL）胆固醇的数据不同，甘油三酯浓度与冠状动脉疾病（CAD）风险之间存在独立关联的数据并不明确，LDL胆固醇和HDL胆固醇的数据显示出与CAD风险有强烈、一致且相反的相关性。有一些证据表明，甘油三酯在某些亚组中是独立的风险因素，例如50 - 69岁的女性（弗雷明汉心脏研究）以及非胰岛素依赖型糖尿病患者。然而，甘油三酯作为CAD协同风险因素的证据更强。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，降脂治疗使事件减少的大部分归因于此。甘油三酯与CAD风险之间相关性的一个重要混杂因素是富含甘油三酯脂蛋白的异质性：较大的富含甘油三酯颗粒被认为与CAD风险无关，而较小（且密度较大）的颗粒被认为具有致动脉粥样硬化性。目前，测量空腹甘油三酯水平以及结合LDL胆固醇和HDL胆固醇浓度进行甘油三酯评估，是评估CAD风险中高甘油三酯血症最实用的方法，尽管餐后血脂可能是更好的动脉粥样硬化性指标。高甘油三酯血症的管理应首先侧重于非药物治疗（即饮食、运动、体重控制和减少饮酒）。对于糖尿病患者，严格控制血糖也很重要。然而，如果这种方法证明不足，有几种药物选择。贝特类药物可能有效降低甘油三酯并升高HDL胆固醇。烟酸已被证明可降低甘油三酯、升高HDL胆固醇、降低LDL胆固醇并降低脂蛋白(a)；它还可降低纤维蛋白原。他汀类药物似乎对降低高甘油三酯血症中的甘油三酯和LDL胆固醇有效；然而，它们不能使载脂蛋白B的代谢正常化，并且HDL胆固醇可能仍然较低。因此，与贝特类药物或烟酸联合使用可能是合适的。关注高甘油三酯血症与CAD风险增加的关系是评估CAD发生总体风险的重要一步。
