Previous studies have identified a LDL cholesterol “disconnect” between LDL concentration and the number or size of LDL particles among patients with low levels of LDL cholesterol (Otvos, Jeyarajah, & Cromwell, 2002). The term disconnect suggests a differing risk profile depending on the type of LDL cholesterol measure that is used. Typically many individuals who are considered to have normal levels of LDL cholesterol will screen abnormal using phenotype designation. This difference, or disconnect, may help to explain why myocardial infarction can occur in some people who have normal cholesterol and/or LDL levels. Furthermore, since cholesterol is carried via lipoproteins within the blood in spherical particles, between any two individuals there can be tremendous differences in both the number, size and composition of these particles (Garvey 2003; Tulenko & Sumner, 2002). The implication of this disconnect is that CAD risk between two patients with identical LDL particle number and particle size would be the same, despite differing LDL concentration values (Garvey, 2003; Otvos et al., 2002; Tulenko & Sumner, 2002).

The ATP-III (NCEP) report establishes the following ranges for LDL cholesterol levels: optimal (<100mg/dL), near optimal/above optimal (100-129 mg/dL), borderline high (130-159 mg/dL), high (160-189 mg/dL), and very high (≥190 mg/dL) (NIH, 2002). When risk is very high (two or more additional risk factors of existing heart disease), an LDL goal of <70 mg/dL is a therapeutic option, but lifestyle changes should still be pursued. This therapeutic option extends also to patients at very high risk who have a baseline LDL <100 mg/dL (Grundy et al., 2004). The metabolic balance of lipoproteins which is both vital and dangerous also uses reverse cholesterol transport to lower cholesterol in the periphery (Trigatti, 2005). HDL is synthesized by intestinal mucosal cells and the liver. It contains a small amount of phospholipids and ApoA1 (Tulenko & Sumner, 2002). Research has consistently identified an inverse relationship between HDL levels and CAD incidence. The mechanism for this relationship is still unclear, leading some researchers to suggest that low HDL levels are simply a marker for other lipid abnormalities. While the role of decreased HDL levels in atherosclerosis is still vague, it is considered an independent risk factor for CAD (NIH, 2002). It also has been identified as the greatest predictor, along with ApoA1 as the most important risk factor in patients with existing CAD (Bolibar, von Eckardstein, Assman, &Thompson, 2000; Devroey, 2004). HDL absorbs cholesterol in peripheral cells which enter the core of the cell through the action of lecithin-cholesterol acyltransferase. Inclusion of HDL in risk assessment can greatly enhance risk stratification (Kannel & Wilson, 1992).