Abstract

Hypertriglyceridemia is made up of a complex array of dyslipidemias. Difficulties in establishing the independent predictive value of elevated triglycerides in coronary artery disease arise because the triglyceride-rich lipoprotein particles that accumulate are diverse, with differential atherogenic potential, and because hypertriglyceridemia states are typically associated with low high-density lipoprotein cholesterol. When high-density lipoprotein cholesterol is considered in multivariate analysis of the role of hypertriglyceridemia in coronary artery disease, the importance of elevated triglycerides pales, emerging as a statistical second fiddle. However, recent data have affirmed the primary role of triglycerides in the genesis of atherosclerosis. This process involves the overabundance of triglyceride-rich lipoprotein particles, which, paradoxically, can be enriched with cholesterol through the action of cholesterol ester transfer protein. These particles appear to be especially atherogenic. Also, low-density lipoproteins become smaller and denser-small, dense phenotype or pattern B-in hypertriglyceridemia states. This profile is associated with a threefold increase in coronary artery disease risk and is not evident on routine lipid testing. Aggressive management of hypertriglyceridemia requires more detailed lipid analyses to identify patients at risk. In treating hypertriglyceridemia, a risk factor beyond low-density lipoprotein would allow a broader definition of patients at risk for coronary artery disease so that more people would benefit from lipid-lowering initiatives.