Abstract：
BACKGROUND: Conventional low-density lipoprotein cholesterol (LDL-C) quantification includes cholesterol attributable to lipoprotein(a) (Lp(a)-C) due to their overlapping densities.
OBJECTIVE: The purposes of this study were to compare the association between LDL-C and LDL-C corrected for Lp(a)-C (LDLLp(a)corr) with incident coronary heart disease (CHD) in the general population and to investigate whether concomitant Lp(a) values influence the association of LDL-C or apolipoprotein B (apoB) with coronary events.
METHODS: Among 68,748 CHD-free subjects at baseline LDLLp(a)corr was calculated as \"LDL-C-Lp(a)-C,\" where Lp(a)-C was 30% or 17.3% of total Lp(a) mass. Fine and Gray competing risk-adjusted models were applied for the association between the outcome incident CHD and: 1) LDL-C and LDLLp(a)corr in the total sample; and 2) LDL-C and apoB after stratification by Lp(a) mass (≥/<90th percentile).
RESULTS: Similar risk estimates for incident CHD were found for LDL-C and LDL-CLp(a)corr30 or LDL-CLp(a)corr17.3 (subdistribution HR with 95% CI) were 2.73 (95% CI: 2.34-3.20) vs 2.51 (95% CI: 2.15-2.93) vs 2.64 (95% CI: 2.26-3.10), respectively (top vs bottom fifth; fully adjusted models). Categorization by Lp(a) mass resulted in higher subdistribution HRs for uncorrected LDL-C and incident CHD at Lp(a) ≥90th percentile (4.38 [95% CI: 2.08-9.22]) vs 2.60 [95% CI: 2.21-3.07]) at Lp(a) <90th percentile (top vs bottom fifth; Pinteraction0.39). In contrast, apoB risk estimates were lower in subjects with higher Lp(a) mass (2.43 [95% CI: 1.34-4.40]) than in Lp(a) <90th percentile (3.34 [95% CI: 2.78-4.01]) (Pinteraction0.49).
CONCLUSIONS: Correction of LDL-C for its Lp(a)-C content provided no meaningful information on CHD-risk estimation at the population level. Simple categorization of Lp(a) mass (≥/<90th percentile) influenced the association between LDL-C or apoB with future CHD mostly at higher Lp(a) levels.
OBJECTIVE: The purposes of this study were to compare the association between LDL-C and LDL-C corrected for Lp(a)-C (LDLLp(a)corr) with incident coronary heart disease (CHD) in the general population and to investigate whether concomitant Lp(a) values influence the association of LDL-C or apolipoprotein B (apoB) with coronary events.
METHODS: Among 68,748 CHD-free subjects at baseline LDLLp(a)corr was calculated as \"LDL-C-Lp(a)-C,\" where Lp(a)-C was 30% or 17.3% of total Lp(a) mass. Fine and Gray competing risk-adjusted models were applied for the association between the outcome incident CHD and: 1) LDL-C and LDLLp(a)corr in the total sample; and 2) LDL-C and apoB after stratification by Lp(a) mass (≥/<90th percentile).
RESULTS: Similar risk estimates for incident CHD were found for LDL-C and LDL-CLp(a)corr30 or LDL-CLp(a)corr17.3 (subdistribution HR with 95% CI) were 2.73 (95% CI: 2.34-3.20) vs 2.51 (95% CI: 2.15-2.93) vs 2.64 (95% CI: 2.26-3.10), respectively (top vs bottom fifth; fully adjusted models). Categorization by Lp(a) mass resulted in higher subdistribution HRs for uncorrected LDL-C and incident CHD at Lp(a) ≥90th percentile (4.38 [95% CI: 2.08-9.22]) vs 2.60 [95% CI: 2.21-3.07]) at Lp(a) <90th percentile (top vs bottom fifth; Pinteraction0.39). In contrast, apoB risk estimates were lower in subjects with higher Lp(a) mass (2.43 [95% CI: 1.34-4.40]) than in Lp(a) <90th percentile (3.34 [95% CI: 2.78-4.01]) (Pinteraction0.49).
CONCLUSIONS: Correction of LDL-C for its Lp(a)-C content provided no meaningful information on CHD-risk estimation at the population level. Simple categorization of Lp(a) mass (≥/<90th percentile) influenced the association between LDL-C or apoB with future CHD mostly at higher Lp(a) levels.
摘要：
背景:常规的低密度脂蛋白胆固醇(LDL-C)定量包括归因于脂蛋白(a)(Lp(a)-C)的胆固醇,这归因于它们的重叠密度。
目的：本研究的目的是比较LDL-C和LDL-C校正后的Lp（a）-C（LDLLp（a）corr）与冠心病（CHD）的相关性，并研究伴随的Lp（a）值是否影响LDL-C或载脂蛋白B（apoB）与冠状动脉事件的相关性。
方法：在68,748名无冠心病的受试者中，基线LDLLp（a）corr被计算为“LDL-C-Lp（a）-C，其中Lp(a)-C为总Lp(a)质量的30%或17.3%。应用精细和灰色竞争风险调整模型来分析结果事件CHD与：1）总样本中LDL-C和LDLLp（a）corr之间的关联；2）按Lp（a）质量（≥/<90百分位数）分层后的LDL-C和apoB之间的关联。
结果：LDL-C和LDL-CLp（a）corr30或LDL-CLp（a）corr17.3（具有95％CI的亚分布HR）为2.73（95％CI：2.34-3.20）vs2.51（95％CI：2.15-2.93）vs2.64（95％CI：2.26-3.10），分别（顶部和底部第五；完全调整的模型）。按Lp（a）质量分类导致Lp（a）≥90百分位数（4.38[95％CI：2.08-9.22]）对2.60[95％CI：2.21-3.07]）的未校正LDL-C和先入期CHD的亚分布HR较高，在Lp（a）<90百分位数（顶部对底部；Pinteraction0.39）。相比之下,Lp(a)质量较高(2.43[95%CI:1.34-4.40])的受试者apoB风险估计值低于Lp(a)<90百分位数(3.34[95%CI:2.78-4.01])(Pinteraction0.49)。
结论：LDL-C对其Lp（a）-C含量的校正没有提供关于人群水平的CHD风险估计的有意义的信息。Lp（a）质量的简单分类（≥/<90百分位数）影响LDL-C或apoB与未来冠心病之间的关联，主要是在较高的Lp（a）水平。
目的：本研究的目的是比较LDL-C和LDL-C校正后的Lp（a）-C（LDLLp（a）corr）与冠心病（CHD）的相关性，并研究伴随的Lp（a）值是否影响LDL-C或载脂蛋白B（apoB）与冠状动脉事件的相关性。
方法：在68,748名无冠心病的受试者中，基线LDLLp（a）corr被计算为“LDL-C-Lp（a）-C，其中Lp(a)-C为总Lp(a)质量的30%或17.3%。应用精细和灰色竞争风险调整模型来分析结果事件CHD与：1）总样本中LDL-C和LDLLp（a）corr之间的关联；2）按Lp（a）质量（≥/<90百分位数）分层后的LDL-C和apoB之间的关联。
结果：LDL-C和LDL-CLp（a）corr30或LDL-CLp（a）corr17.3（具有95％CI的亚分布HR）为2.73（95％CI：2.34-3.20）vs2.51（95％CI：2.15-2.93）vs2.64（95％CI：2.26-3.10），分别（顶部和底部第五；完全调整的模型）。按Lp（a）质量分类导致Lp（a）≥90百分位数（4.38[95％CI：2.08-9.22]）对2.60[95％CI：2.21-3.07]）的未校正LDL-C和先入期CHD的亚分布HR较高，在Lp（a）<90百分位数（顶部对底部；Pinteraction0.39）。相比之下,Lp(a)质量较高(2.43[95%CI:1.34-4.40])的受试者apoB风险估计值低于Lp(a)<90百分位数(3.34[95%CI:2.78-4.01])(Pinteraction0.49)。
结论：LDL-C对其Lp（a）-C含量的校正没有提供关于人群水平的CHD风险估计的有意义的信息。Lp（a）质量的简单分类（≥/<90百分位数）影响LDL-C或apoB与未来冠心病之间的关联，主要是在较高的Lp（a）水平。
