Associations of LDL Cholesterol, Non-HDL Cholesterol, and Apolipoprotein B With Cardiovascular Disease Occurrence in Adults: Korean Genome and Epidemiology Study
2
조회
0
다운로드
1
인용
0
참고문헌
키워드
초록
Background: Despite the superiority of non-HDL cholesterol (non-HDL-C) and apolipoprotein B (ApoB) as lipid markers for atherosclerotic cardiovascular disease (ASCVD), these are only suitable as secondary markers. We compared LDL cholesterol (LDL-C), non-HDL-C, and ApoB concentrations with respect to the occurrence of cardiovascular disease in adults enrolled in the Korean Genome and Epidemiology Study (KoGES). Methods: We used information on age; sex; medical history; family history of ASCVD; current lipid-lowering therapy; current smoking status; and creatinine, total cholesterol, HDL-C, LDL-C, triglyceride, and ApoB concentrations from 5,872 KoGES participants without ASCVD. New ASCVD development was monitored during the 8-year follow-up period. Adjusted hazard ratios (aHRs) for ASCVD of LDL-C, non-HDL-C, and ApoB concentrations were calculated based on the multivariate Cox regression analyses. The participants were also grouped as low and high according to the median values for each lipid marker, and calculated aHRs of each group combined by two lipid makers. Results: ApoB showed the highest aHR per 1-SD for ASCVD (1.26; 95% confidence interval [CI], 1.11–1.43), followed by non-HDL-C (1.25; 95% CI, 1.11–1.41) and LDL-C (1.20; 95% CI, 1.06–1.37). The group with low LDL-C and high ApoB concentrations had a significantly higher aHR for ASCVD (1.61; 95% CI, 1.05–2.48) compared to the reference group values (low LDL-C and low ApoB concentrations). The aHR for the group with high LDL-C and low ApoB concentrations was not significant (1.30; 95% CI, 0.79–2.16). Conclusions: ApoB, non-HDL-C, and LDL-C are independent risk factors for ASCVD. Increases in the aHR per 1-SD for ASCVD were more strongly affected by ApoB, followed by non-HDL-C and LDL-C. Participants with low LDL-C and high ApoB concentrations showed increased ASCVD risk. For individuals with ASCVD risk factors, even those presenting normal LDL-C concentrations, measuring Apo
Abstract
Background: Despite the superiority of non-HDL cholesterol (non-HDL-C) and apolipoprotein B (ApoB) as lipid markers for atherosclerotic cardiovascular disease (ASCVD), these are only suitable as secondary markers. We compared LDL cholesterol (LDL-C), non-HDL-C, and ApoB concentrations with respect to the occurrence of cardiovascular disease in adults enrolled in the Korean Genome and Epidemiology Study (KoGES). Methods: We used information on age; sex; medical history; family history of ASCVD; current lipid-lowering therapy; current smoking status; and creatinine, total cholesterol, HDL-C, LDL-C, triglyceride, and ApoB concentrations from 5,872 KoGES participants without ASCVD. New ASCVD development was monitored during the 8-year follow-up period. Adjusted hazard ratios (aHRs) for ASCVD of LDL-C, non-HDL-C, and ApoB concentrations were calculated based on the multivariate Cox regression analyses. The participants were also grouped as low and high according to the median values for each lipid marker, and calculated aHRs of each group combined by two lipid makers. Results: ApoB showed the highest aHR per 1-SD for ASCVD (1.26; 95% confidence interval [CI], 1.11–1.43), followed by non-HDL-C (1.25; 95% CI, 1.11–1.41) and LDL-C (1.20; 95% CI, 1.06–1.37). The group with low LDL-C and high ApoB concentrations had a significantly higher aHR for ASCVD (1.61; 95% CI, 1.05–2.48) compared to the reference group values (low LDL-C and low ApoB concentrations). The aHR for the group with high LDL-C and low ApoB concentrations was not significant (1.30; 95% CI, 0.79–2.16). Conclusions: ApoB, non-HDL-C, and LDL-C are independent risk factors for ASCVD. Increases in the aHR per 1-SD for ASCVD were more strongly affected by ApoB, followed by non-HDL-C and LDL-C. Participants with low LDL-C and high ApoB concentrations showed increased ASCVD risk. For individuals with ASCVD risk factors, even those presenting normal LDL-C concentrations, measuring Apo
참고문헌 (19)
- Sampson UK, "Residual cardiovascular risk despite optimal LDL cholesterol reduction with statins: the evidence, etiology, and therapeutic challenges", Curr Atheroscler Rep, 14, pp.1~10 (2012)
- Reith C, "Management of residual risk after statin therapy", Atherosclerosis, 245, pp.161~170 (2016)
- Shapiro MD, "From lipids to inflammation : new approaches to reducing atherosclerotic risk", Circ Res, 118, pp.732~749 (2016)
- Grundy SM, "2018 AHA", ACC, AAPA, pp.ABC, ACPM[DOI]
- Mach F, "2019 ESC", EAS Guidelines for the management of dyslipidaemias : lipid modification to reduce cardiovascular risk : the Task Force for the management of dyslipidaemias of the European Society of Cardiology(ESC)and European Atherosclerosis Society(EAS), 2020, pp.41, 111~188
- Verbeek R, "Non-high-density lipoprotein cholesterol : current status as cardiovascular marker", Curr Opin Lipidol, 26, pp.502~510 (2015)
- Sniderman AD, "Apolipoprotein B particles and cardiovascular disease : a narrative review", JAMA Cardiol, 4, pp.1287~1295 (2019)
- Cantey EP, "Discordance between lipoprotein particle number and cholesterol content : an update", Curr Opin Endocrinol Diabetes Obes, 25, pp.130~136 (2018)
- Mora S, "Advanced lipoprotein testing and subfractionation are not(yet)ready for routine clinical use", Circulation, 119, pp.2396~2404 (2009)
- Sniderman AD, "A meta-analysis of low-density lipoprotein cholesterol, non-high-density lipoprotein cholesterol, and apolipoprotein B as markers of cardiovascular risk", Circ Cardiovasc Qual Outcomes, 4, pp.337~345 (2011)
- Johannesen CDL, "Apolipoprotein B and non-HDL cholesterol better reflect residual risk than LDL cholesterol in statin-treated patients", J Am Coll Cardiol, 77, pp.1439~1450 (2021)
- Thanassoulis G, "Relations of change in plasma levels of LDL-C, non-HDL-C and apoB with risk reduction from statin therapy : a meta-analysis of randomized trials", J Am Heart Assoc, 3, pp.e000759~ (2014)
- Kim Y, "Cohort profile : the Korean Genome and Epidemiology Study(KoGES)consortium", Int J Epidemiol, 46, pp.e20~ (2017)
- Nance R, "Smoking intensity(pack", day)is a better measure than pack-years or smoking status for modeling cardiovascular disease outcomes, 2017, pp.81, 111~119
- Emerging Risk Factors Collaboration, "Major lipids, apolipoproteins, and risk of vascular disease", JAMA, 302, pp.1993~2000 (2009)
- Emerging Risk Factors Collaboration, "Lipid-related markers and cardiovascular disease prediction", JAMA, 307, pp.2499~2506 (2012)
- Marston NA, "Association of apolipoprotein B–containing lipoproteins and risk of myocardial infarction in individuals with and without atherosclerosis: distinguishing between particle concentration, type, and content", JAMA Cardiol, 7, pp.250~256 (2022)
- Langlois MR, "Quantifying atherogenic lipoproteins: current and future challenges in the era of personalized medicine and very low concentrations of LDL cholesterol. A consensus statement from EAS and EFLM", Clin Chem, 64, pp.1006~1033 (2018)
- Hong Jinyoung, "Intuitive Modification of the Friedewald Formula for Calculation of LDL-Cholesterol", Annals of Laboratory Medicine, 43(1), pp.29~37 (2023), 대한진단검사의학회[DOI]
