Triglycerides are a primary source of energy and their levels in the periphery vary significantly. Historically, it has been understood that high VLDL and triglyceride levels were the result of elevated total cholesterol and lower levels of HDL cholesterol (Ginsberg, 1999; Tulenk & Sumner, 2002), but recent studies have shifted elevated triglyceride levels from an association with CAD to an independent predictor of the disease (Cullen 2000; Ginsberg, 1999; NIH, 2002; Malloy & Kane, 2001;). Furthermore, this independent relationship suggests some triglyceride-rich lipoproteins are atherogenic (Cullen 2000; NIH, 2002), meaning VLDL levels may prove to be a significant risk factor in the future. With hypertriglyceridemia, triglycerides are transferred from VLDL and chylomicrons (cholesterol molecules formed from dietary substrates) to LDL, leading primarily to small dense LDL particles and more CAD (Tulenko & Sumner, 2002).

Triglycerides should be measured after fasting as non-fasting triglyceride and other postprandial measurements are difficult to homogenize and arduous to perform (Sullivan, 2002). Finally, the authors of the ATP-III report set the classification of triglyceride in the following categories: Normal (<150 mg/dL), borderline high (150-199 mg/dL), high (200-499mg/dL), and very high (≥500mg/dL). Chylomicrons are very similar in their structure to VLDL, but are released by the intestinal mucosa cells directly after consuming fat (Tulenka & Sumner, 2002). They are less dense due to their large size (100-500nm) and the amount of triglyceride that is transported in them. Chylomicrons are found in the blood and lymphatic fluid where they serve to transport fat from its port of entry in the intestine to the liver and to adipose tissue. They travel via the lymphatic system and their large size renders penetration of the endothelium improbable. Though chylomicrons are large and rich in triglyceride, they contain only a relatively small amount of protein (Hertz, 1999; Schumaker &, Lambertas, 1992). Once chylomicrons enter the blood. they acquire ApoE and ApoC-II. They gradually reduce in size by lipoprotein lipase which removes free-fatty acids from the triglyceride pool in the cell. Chylomicron remnants are reassembled with endogenous triglyceride and cholesterol esters to form VLDLs (Tulenka & Sumner, 2002). Partially degraded chylomicrons, called chylomicron remnants, probably carry some atherogenic potential (NIH, 2002). The ATP-III does not report guidelines for chylomicron levels. Recently, investigators from the INTERHEART study have demonstrated abnormal lipid levels, when combined with smoking, provide over 90% of the risk associated with CAD (Yusef et al., 2004) and can be generalized globally. The authors of the study suggest that the ApoB/ApoA1 ratio was the most important risk factor for CAD. Previous research suggests that ApoB/ApoA1 has not warranted as much attention of other subfractions of cholesterol and therefore needs further study (Sullivan, 2002). The relative lack of familiarity among professionals regarding the importance of ApoB and ApoA1 levels has been a primary cause of ApoB measurement not prevailing over cholesterol levels as the basis for treatment guidelines. Finally, Sullivan (2002) suggests the stage has not been reached where ApoA1 levels can supersede HDL levels as the basis for treatment guidelines (Sullivan, 2002). INTERHEART is a landmark study that will likely reveal a greater role of the ApoB/ApoA1 ratio in the progression of CAD.