The Lundquist Institute at Harbor UCLA Medical Center, Torrance, California; Lithuanian University of Health Sciences, Medical Academy, Department of Cardiology, Kaunas, Lithuania.
The Lundquist Institute at Harbor UCLA Medical Center, Torrance, California; Emory University School of Medicine, Division of Hospital Medicine, Atlanta, Georgia.
Am J Cardiol. 2021 Mar 1;142:52-58. doi: 10.1016/j.amjcard.2020.11.026. Epub 2020 Dec 3.
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.
目前的风险分层策略并不能完全解释心血管疾病(CVD)的风险。我们旨在评估低密度脂蛋白(LDL-P)和高密度脂蛋白(HDL-P)颗粒与冠状动脉钙进展和颈动脉壁损伤的关系。所有在多民族动脉粥样硬化研究(MESA)中通过离子迁移率测量 LDL-P 和 HDL-P、冠状动脉钙评分(CAC)、颈动脉内膜中层厚度(IMT)和颈动脉斑块数据在检查 1 和 5 时可用的参与者均包括在研究中。CAC 进展被按年计算,并被视为分类或连续变量。颈动脉 IMT 和斑块进展被视为连续变量。完全调整的回归模型包括已确立的 CVD 风险因素以及传统脂质。平均(±SD)随访时间为 9.6±0.6 年。所有 LDL-P 亚型以及基线时的大 HDL-P 均与 CAC 进展的年化率呈正相关且显著相关,但在调整已确立的风险因素和传统脂质后,仅与中、小 LDL-P 的相关性仍然显著(β -0.02,p=0.019 和β 0.01,p=0.003,每增加 1 nmol/L)。颈动脉斑块评分的进展与小和非常小的 LDL-P(所有 p<0.01)和非 HDL-P(p=0.013)呈正相关。只有与非常小的 LDL-P 的相关性在完全调整的模型中仍然显著(p=0.035)。平均 IMT 进展与任何脂质颗粒均无关。总之,在 MESA 队列中,通过离子迁移率测量的 LDL-P 与 CAC 进展以及颈动脉斑块进展显著相关,而传统脂质的影响则超出了这一范围。