Sung Da-Eun, Rhee Eun-Jung, Lee Jong-Young, Lee Mi-Yeon, Sung Ki-Chul
Department of Internal Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Division of Endocrinology and Metabolism, Department of Internal Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Eur J Prev Cardiol. 2025 Apr 3. doi: 10.1093/eurjpc/zwaf088.
Lipoprotein(a) [Lp(a)] is a genetically determined, independent risk factor for atherosclerotic cardiovascular disease. However, its role in coronary artery calcification (CAC) remains unclear. We aimed to determine whether Lp(a) levels are associated with the incidence and progression of CAC.
We conducted a longitudinal cohort study (2015-22) of 41 929 adults (aged ≥30 years) who underwent baseline Lp(a) measurement and CAC assessment via multi-detector computed tomography. Participants were stratified into those with baseline CAC = 0 (n = 32 338) and CAC > 0 (n = 9591). Outcomes were analysed according to Lp(a) quintiles and clinically relevant categories (<30, 30-50, 50-100, ≥ 100 mg/dL). Cox proportional hazards models estimated hazard ratios (HRs) for incident CAC (CAC > 0) among those with CAC = 0 (median follow-up, 4.04 years). Linear mixed-effects models evaluated CAC progression among those with CAC > 0 (median follow-up, 3.78 years). All models were adjusted for cardiovascular risk factors. Among participants with CAC = 0 (mean age, 40.94 ± 5.81 years; 85.69% men), neither Lp(a) quintiles nor clinical categories were significantly associated with incident CAC [HR for highest vs. second quintile: 0.998 (95% confidence interval, CI, 0.90-1.10); HR for ≥100 vs. <30 mg/dL: 0.83 (95% CI, 0.57-1.23)]. Among those with CAC > 0 (mean age, 45.99 ± 7.20 years; 94.90% men), CAC progression did not differ materially across Lp(a) quintiles or clinical thresholds.
Elevated Lp(a) levels were not associated with new-onset CAC or progression of existing CAC in this large longitudinal cohort.
脂蛋白(a)[Lp(a)]是动脉粥样硬化性心血管疾病的一个由基因决定的独立危险因素。然而，其在冠状动脉钙化（CAC）中的作用仍不清楚。我们旨在确定Lp(a)水平是否与CAC的发生和进展相关。
我们对41929名成年人（年龄≥30岁）进行了一项纵向队列研究（2015 - 2022年），这些成年人通过多排螺旋计算机断层扫描进行了基线Lp(a)测量和CAC评估。参与者被分为基线CAC = 0（n = 32338）和CAC > 0（n = 9591）两组。根据Lp(a)五分位数和临床相关类别（<30、30 - 50、50 - 100、≥100mg/dL）分析结果。Cox比例风险模型估计了CAC = 0者（中位随访时间4.04年）发生CAC（CAC > 0）的风险比（HR）。线性混合效应模型评估了CAC > 0者（中位随访时间3.78年）的CAC进展情况。所有模型均对心血管危险因素进行了校正。在CAC = 0的参与者中（平均年龄40.94±5.81岁；85.69%为男性），Lp(a)五分位数和临床类别均与发生CAC无显著相关性[最高五分位数与第二五分位数的HR：0.998（95%置信区间，CI，0.90 - 1.10）；≥100mg/dL与<30mg/dL的HR：0.83（95%CI，0.57 - 1.23）]。在CAC > 0的参与者中（平均年龄45.99±7.20岁；94.90%为男性），Lp(a)五分位数或临床阈值之间的CAC进展没有实质性差异。
在这个大型纵向队列中，Lp(a)水平升高与新发CAC或现有CAC的进展无关。
