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Impact of Lipoprotein(a) Level on Low-Density Lipoprotein Cholesterol- or Apolipoprotein B-Related Risk of Coronary
Natalie Arnold1, Christopher Blaum2, Alina Goßling2
1Department of Cardiology, University Heart & Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; German Center for Cardiovascular Research (DZHK), partner site Hamburg/Kiel/Luebeck, Hamburg, Germany; Center for Population Health Innovation (POINT), University Heart and Vascular Center Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Insights
Correcting low-density lipoprotein cholesterol (LDL-C) for lipoprotein(a) cholesterol (Lp(a)-C) did not improve coronary heart disease (CHD) risk prediction in the general population. Lp(a) levels influenced the association between LDL-C, apolipoprotein B, and CHD events.
Area of Science:
- Cardiovascular Medicine
- Clinical Chemistry
- Epidemiology
Background:
- Conventional low-density lipoprotein cholesterol (LDL-C) measurements include cholesterol from lipoprotein(a) (Lp(a)-C) due to overlapping densities.
- Accurate assessment of cardiovascular risk requires understanding the independent contributions of LDL-C and Lp(a).
Purpose of the Study:
- To compare the association of LDL-C and Lp(a)-corrected LDL-C (LDLLp(a)corr) with incident coronary heart disease (CHD).
- To investigate if Lp(a) levels modify the association between LDL-C or apolipoprotein B (apoB) and coronary events.
Main Methods:
- LDLLp(a)corr was calculated by subtracting Lp(a)-C from LDL-C in 68,748 CHD-free individuals.
- Fine and Gray competing risk models assessed associations between LDL-C, LDLLp(a)corr, and incident CHD.
- Analyses stratified by Lp(a) mass (≥/<90th percentile) examined interactions with LDL-C and apoB.
Main Results:
- LDL-C and LDLLp(a)corr showed similar risk estimates for incident CHD.
- Higher Lp(a) mass (≥90th percentile) was associated with higher risk estimates for uncorrected LDL-C and incident CHD.
- ApoB risk estimates were lower in individuals with higher Lp(a) mass compared to those with lower Lp(a) mass.
Conclusions:
- Correcting LDL-C for Lp(a)-C provided no significant additional information for CHD risk estimation at the population level.
- Lp(a) mass categorization influenced the association between LDL-C or apoB and future CHD, particularly at higher Lp(a) levels.
Background:
Conventional low-density lipoprotein cholesterol (LDL-C) quantification includes cholesterol attributable to lipoprotein(a) (Lp(a)-C) due to their overlapping densities.
Objectives:
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.
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