Brian T Steffen1, Weihua Guan2, Alan T Remaley3, James H Stein4, Mathew C Tattersall4, Joel Kaufman5, Michael Y Tsai6. 1. Department of Laboratory Medicine & Pathology, University of Minnesota, Minneapolis, MN, USA. 2. Division of Biostatistics, School of Public Health, University of Minnesota, Minneapolis, MN, USA. 3. Lipoprotein Metabolism Section, Cardiovascular and Pulmonary Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. 4. Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, Madison, WI, USA. 5. Department of Epidemiology, School of Public Health, University of Washington, Seattle, WA, USA. 6. Department of Laboratory Medicine & Pathology, University of Minnesota, Minneapolis, MN, USA. Electronic address: tsaix001@umn.edu.
Abstract
BACKGROUND: High blood cholesterol contributes to atherosclerosis, yet reliance on the lipid panel alone may mischaracterize individuals with elevated lipoprotein particle numbers. OBJECTIVE: The aim of the article was to determine whether elevated lipoprotein or apolipoprotein measures are associated with carotid atherosclerosis and plaque progression independent of cardiovascular (CV) risk factors including standard lipids in a subcohort of 2228 Multi-Ethnic Study of Atherosclerosis participants. METHODS: Ultrasonography assessed carotid artery plaque and common carotid intima-media thickness (cIMT) at baseline and after a median period of 9.4 years. Nuclear magnetic resonance spectroscopy estimated lipoprotein particle concentrations. Apolipoprotein B (ApoB) and apolipoprotein A-I were measured using an automated immunoassay. Regression analysis determined associations of apolipoprotein and lipoprotein measurements with cIMT and relative risk regression determined associations with carotid plaque progression. RESULTS: After adjustment for typical CV risk factors, individuals in top quartiles of ApoB, ApoB/apolipoprotein A-I, low-density lipoprotein particles (LDL-P), small LDL-P, and total LDL-P/high-density lipoprotein (HDL) particles showed similar risks of carotid plaque and cIMT progression as LDL-C, non-HDL cholesterol (HDL-C), total cholesterol (TC), and TC/HDL-C. A significant association with plaque progression remained in the top ApoB quartile after further adjustment for LDL-C (P = .02) or TC + HDL-C (P = .04), but was nonsignificant when adjusted for all lipid covariates (P = .086). Those in the top quartile of small LDL-P concentrations showed greater cIMT progression than those in the referent after adjustment for LDL-C, but this was nonsignificant after adjustment for TC + HDL-C. CONCLUSION: When coupled with evidence that apolipoprotein testing identifies lipid-lipoprotein discordance, these findings suggest that ApoB and small LDL-P provide atherosclerosis risk information that is not revealed by typical CV risk factors.
BACKGROUND: High blood cholesterol contributes to atherosclerosis, yet reliance on the lipid panel alone may mischaracterize individuals with elevated lipoprotein particle numbers. OBJECTIVE: The aim of the article was to determine whether elevated lipoprotein or apolipoprotein measures are associated with carotid atherosclerosis and plaque progression independent of cardiovascular (CV) risk factors including standard lipids in a subcohort of 2228 Multi-Ethnic Study of Atherosclerosisparticipants. METHODS: Ultrasonography assessed carotid artery plaque and common carotid intima-media thickness (cIMT) at baseline and after a median period of 9.4 years. Nuclear magnetic resonance spectroscopy estimated lipoprotein particle concentrations. Apolipoprotein B (ApoB) and apolipoprotein A-I were measured using an automated immunoassay. Regression analysis determined associations of apolipoprotein and lipoprotein measurements with cIMT and relative risk regression determined associations with carotid plaque progression. RESULTS: After adjustment for typical CV risk factors, individuals in top quartiles of ApoB, ApoB/apolipoprotein A-I, low-density lipoprotein particles (LDL-P), small LDL-P, and total LDL-P/high-density lipoprotein (HDL) particles showed similar risks of carotid plaque and cIMT progression as LDL-C, non-HDL cholesterol (HDL-C), total cholesterol (TC), and TC/HDL-C. A significant association with plaque progression remained in the top ApoB quartile after further adjustment for LDL-C (P = .02) or TC + HDL-C (P = .04), but was nonsignificant when adjusted for all lipid covariates (P = .086). Those in the top quartile of small LDL-P concentrations showed greater cIMT progression than those in the referent after adjustment for LDL-C, but this was nonsignificant after adjustment for TC + HDL-C. CONCLUSION: When coupled with evidence that apolipoprotein testing identifies lipid-lipoprotein discordance, these findings suggest that ApoB and small LDL-P provide atherosclerosis risk information that is not revealed by typical CV risk factors.
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