Abstract 18288: The Total-to-high Density Lipoprotein-cholesterol Ratio Associates With Coronary Atheroma Progression Rates and Reclassifies Disease Progression Across Populations With Varying Metabolic Risk
Introduction: Total to high-density lipoprotein cholesterol (TC/HDL-C), routinely available from the standard lipid profile, is postulated to characterize atherogenic lipids beyond low density lipoprotein cholesterol (LDL-C) and non-HDL-C
Hypothesis: On-treatment TC/HDL-C significantly associates with coronary atheroma progression rates at variable levels of LDL-C, non-HDL-C, apolipoprotein B (apoB), triglycerides (TG), C-reactive protein (CRP), and irrespective of diabetes status, obesity or intensity of statin therapy
Methods: We analyzed data from 9 trials involving 4957 patients with coronary disease undergoing serial intravascular ultrasonography and assessed the effect of on-treatment levels of TC/HDL-C [</≥ median: 3.3] on changes in percent atheroma volume (ΔPAV, annualized and controlled for baseline PAV and clinical trial) at variable levels of LDL-C, non-HDL-C, apoB [</≥ median: 80, 107, and 76 mg/dL, respectively], CRP [</≥ 2mg/L] and TG [</≥150 mg/dL], and in patients with/without diabetes or obesity, and in those receiving high-intensity statin therapy (HIST) or not
Results: Discordance, defined by median cut points, between TC/HDL-C vs. LDL-C, non-HDL-C and apoB was sizeable at 26, 20 and 27%, respectively. Lower (< median) on-treatment TC/HDL-C associated with PAV regression (ΔPAV <0) while higher (≥median) TC/HDL-C associated with PAV progression across all levels of LDL-C, non-HDL-C, apoB, TG as well as the presence/absence of obesity or HIST. Lower (<median) TC/HDL-C associated with lower PAV progression irrespective of CRP levels or the presence/absence of diabetes
Conclusion: TC/HDL-C, available at no extra cost, correlates significantly with coronary atheroma progression rates when discordant with other lipid-metabolic parameters and in clinical scenarios such as diabetes, obesity and in patients receiving HIST. Future studies are needed to determine the implications of applying TC/HDL-C for reducing residual risk
Author Disclosures: M.B. Elshazly: None. S.J. Nicholls: Research Grant; Significant; AstraZeneca, Novartis, Eli Lilly, Anthera, LipoScience, Roche, and Resverlogix. Honoraria; Significant; AstraZeneca, Roche, Esperion, Abbott, Pfizer, Merck, Takeda, LipoScience, Omthera, Novo-Nordisk, sanofi-aventis,, Atheronova, Anthera, CSL Behring, and Boehringer Ingelheim. S.E. Nissen: Research Grant; Modest; Amgen, AstraZeneca, 12 Eli Lilly, Orexigen, Vivus, Novo Nordisk, Resverlogix, Novartis, Pfizer, Takeda, Sankyo, and sanofi-aventis. Consultant/Advisory Board; Modest; serving as a consultant for a number of pharmaceutical companies without financial compensation because all honoraria, consulting fees, or any other payments from any for-profit entity are paid, directly to charity so that neither income nor any tax deduction is received. J. St. John: None. S.S. Martin: None. S.R. Jones: Consultant/Advisory Board; Significant; medical advisory board for Atherotech Diagnostic Lab and as an advisor to Sanofi and Regeneron. B. Stegman: None. S.R. Kapadia: None. E. Tuzcu: None. R. Puri: None.
- © 2015 by American Heart Association, Inc.