Association between postprandial lipoprotein subclasses and Framingham cardiovascular disease risk stratification.

ABSTRACT

OBJECTIVE: To determine the ability of postprandial lipoprotein subclass concentrations to stratify patients with respect to their risk for cardiovascular disease (CVD). METHODS: Using the Framingham cardiovascular disease risk score (FRS) algorithm, a total of 112 consecutive patients referred for community health screening were stratified into two groups (a) low-risk (FRS < 10%) and (b) intermediate/high-risk (FRS ≥ 10%). Serum lipoprotein subclass concentrations were determined by Vertical Auto Profile (VAP-II). RESULTS: Fasting and postprandial levels of LDL4, HDL2, VLDL1 + 2, VLDL3, and RLP, as well as fasting levels of ApoB and postprandial levels of LDL3 and IDL1, were significantly different in the intermediate/high risk FRS group vs. the low-risk group (P < 0.05). Correlations between Framingham CVD risk and LDL3, LDL4, IDL1, VLDL1 + 2, VLDL3, RLP, and ApoB were positive while negative for HDL2 in both the fasting and postprandial states. Intermediate/high risk for CVD was shown to be significantly associated with both fasting and postprandial levels of VLDL1 + 2 and RLP, as well as with postprandial LDL4 and VLDL3, as determined using forward conditional logistic regression analysis. Postprandial levels of VLDL1 + 2 were better at identifying patients in the intermediate/high-risk FRS group than fasting levels, although the differences were not significant due to overlapping reference intervals. In addition, the association between RLP and VLDL subclasses relative to Framingham CVD risk increased significantly in the postprandial state (ΔR2 = 0.023; ΔF = 7.178; ΔP = 0.025) but not in the fasting state. CONCLUSIONS: The use of postprandial lipoprotein subclass concentrations is not inferior to the use of fasting levels in identifying intermediate/high-risk FRS individuals. In addition, changes in RLP and VLDL subclass concentrations in fasting vs. postprandial states may reveal lipid metabolic mechanisms associated with CVD.