Abstract 4138473: Detailed Lipoprotein Profiling in Assessing Coronary Calcium Score Progression and Atherosclerotic Risk

Background: Coronary calcium scoring (CCS) evaluates atherosclerotic burden and cardiovascular risk, correlating with coronary artery disease (CAD) severity. Advances in Nuclear Magnetic Resonance ( 1 H-NMR) spectroscopy for lipoprotein fraction analysis highlight precise atherogenic lipid parameter estimation. Enhanced lipid testing, including sub-fractionation assays, improves risk assessment and identifies new biochemical markers for CAD burden. Hypothesis: Specific lipid fractions and subfractions are significantly associated with CCS progression, serving as biochemical markers of CAD progression. Aim: To evaluate the association between lipid fractions and subfractions with CCS progression, aiming to improve CAD risk stratification. Methods: This study used data from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil). CCS progression was any positive change in CCS values over 5 years. High-field 1 H-NMR spectroscopy assessed lipoprotein fractions and subfractions, including plasma concentration, particle size, cholesterol, and triglyceride content. Descriptive and inferential statistics compared baseline characteristics. Multivariable binary logistic regression models, both unadjusted and propensity score-adjusted, assessed associations between plasma levels of lipoprotein fractions and CCS progression. Statistical significance was set at p <0.05. Results/Data: In this study of 2,986 participants, 1,008 (33.8%) experienced CCS progression over 5 years. Significant associations were found between plasma lipoprotein fractions and CCS progression. Large, medium, and very small TRLP (89-37 and 29-24 nm) were linked to increased CCS risk, while small TRLP (36-30 nm) had an inverse association. Small cLDLP (20.4-19 nm) were directly associated with CCS progression, while medium and large cLDLP (23-20.5 nm) were inversely associated. Small cHDLP (7.4-8.0 nm) increased CCS risk, whereas medium to large cHDLP (8.1-13.0 nm) had an inverse association. Specific HDL subspecies (H7P to H3P, 12.0-8.7 nm) were inversely associated with CCS progression, while H2P and H1P (7.8-7.4 nm) increased CCS risk. TRLZ (30-100 nm) levels were positively associated with CCS progression, whereas LDLZ (19-22.5 nm) and HDLZ (7.1-13 nm) were inversely associated. Conclusion(s): Plasma levels of specific lipoprotein fractions and subfractions are associated with CCS progression, providing insights into the complexity of lipoprotein characteristics in CAD.