Publication
Association of Coronary Calcium, Carotid Wall Thickness, and Carotid Plaque Progression With Low-Density Lipoprotein and High-Density Lipoprotein Particle Concentration Measured by Ion Mobility (From Multiethnic Study of Atherosclerosis [MESA])
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- Last modified
- 09/04/2025
- Type of Material
- Authors
- Language
- English
- Date
- 2021-02-09
- Publisher
- EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC
- Publication Version
- Copyright Statement
- © 2020 Elsevier Inc. All rights reserved.
- License
- Final Published Version (URL)
- Title of Journal or Parent Work
- Volume
- 142
- Start Page
- 52
- End Page
- 58
- Grant/Funding Information
- This research was supported by R01 HL071739 and a grant from Quest Diagnostics, and MESA was supported by contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168 and N01-HC-95169 from the National Heart, Lung, and Blood Institute, and by grants UL1-TR-000040, UL1 TR 001079, and UL1-RR-025005 from National Center for Research Resources. The authors thank the other investigators, the staff, and the participants of the MESA study for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org
- Abstract
- Current risk stratification strategies do not fully explain cardiovascular disease (CVD) risk. We aimed to evaluate the association of low-density lipoprotein (LDL-P) and high-density lipoprotein (HDL-P) particles with progression of coronary artery calcium and carotid wall injury. All participants in the Multi-Ethnic Study Atherosclerosis (MESA) with LDL-P and HDL-P measured by ion mobility, coronary artery calcium score (CAC), carotid intima-media thickness (IMT), and carotid plaque data available at Exam 1 and 5 were included in the study. CAC progression was annualized and treated as a categorical or continuous variable. Carotid IMT and plaque progression were treated as continuous variables. Fully adjusted regression models included established CVD risk factors, as well as traditional lipids. Mean (±SD) follow-up duration was 9.6 ± 0.6 years. All LDL-P subclasses as well as large HDL-P at baseline were positively and significantly associated with annualized CAC progression, however, after adjustment for established risk factors and traditional lipids, only the association with medium and very small LDL-P remained significant (β -0.02, p = 0.019 and β 0.01, p = 0.003, per 1 nmol/l increase, respectively). Carotid plaque score progression was positively associated with small and very small LDL-P (p <0.01 for all) and non-HDL-P (p = 0.013). Only the association with very small LDL-P remained significant in a fully adjusted model (p = 0.035). Mean IMT progression was not associated with any of the lipid particles. In conclusion, in the MESA cohort, LDL-P measured by ion mobility was significantly associated with CAC progression as well as carotid plaque progression beyond the effect of traditional lipids.
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