Lp(a) and LDL-C or apoB–Related Coronary Risk

Quick Takes

  • In this analysis, the correction of LDL-C for its Lp(a)-C content (assumed either as 30% or as 17.3% of total Lp(a) mass) did not substantially change LDL-C-associated CHD risk estimation at the population level.
  • LDL-C-related CHD risk estimates were higher in subjects with higher Lp(a) mass.

Study Questions:

How do low-density lipoprotein cholesterol (LDL-C) and lipoprotein(a) cholesterol [Lp(a)-C] levels compare in their association with incident coronary heart disease (CHD) in a general population?


Data from the BiomarCaRE (Biomarker for Cardiovascular Risk assessment across Europe consortium) were used for the present analysis, which included data from 10 cohorts with data on Lp(a). Participants with missing information on CHD or Lp(a) and those with CHD present at baseline were also excluded. 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. Lp(a) mass was stratified by ≥/<90th percentile. All study participants were followed up prospectively for an overall range of 2.5-25 years for incident CHD events, defined as fatal or nonfatal (definite or possible) myocardial infarction (MI), coronary death, unstable angina pectoris, cardiac revascularization, and unclassifiable death (i.e., death with insufficient evidence of coronary origin and no competing cause).


A total of 68,748 participants were included in the present study: Northern Sweden (n=8,774), FINRISK (n=6,048), SHHEC (Scottish Heart Health Extended Cohort) (n=12,585), MONICA/KORA Augsburg (Cooperative Health Research in the Region of Augsburg), (n=7,405), MATISS (Malattie ATerosclerotiche Istituto Superiore di Sanità) cohort (n=3,081), MONICA Brianza (n=4,303), Moli-Sani (n=21,640), and MONICA Catalonia (n=4,912). During a median follow-up of 9.72 years (interquartile range, 5.0-14.8 years), 3,536 subjects who were free of CHD at baseline developed a CHD event.

LDL-C, apolipoprotein B (apoB), and Lp(a) were all associated with incident CHD after multivariate adjustment. To account for the variability of Lp(a)-C in relation to Lp(a) mass, two different estimations were used, one calculating Lp(a)-C as 30%, the other as 17.3% of total Lp(a) mass. These corrections did not affect the relationship between corrected LDL-C and incident CHD meaningfully, demonstrating very comparable hazard ratios to those seen for uncorrected LDL-C. Lp(a) was also stratified into a low-moderate group (<90th percentile) and high group (≥90th percentile). A similar risk was observed for those in the low-moderate Lp(a) group compared to the total study sample. In contrast, those in the high Lp(a) group had a higher risk for CHD. When LDL-C values were corrected by 30% of Lp(a)-C content, attenuation of risk estimates was observed, such that participants with high Lp(a) had a similar risk to those with low-moderate Lp(a) mass. Analysis with apoB was similar in its association with CHD risk, as was observed for LDL-C when Lp(a) groups were examined.


The investigators conclude that 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.


Lp(a) levels may add information on CHD-related risk for some groups. However, data from this large cohort did not observe the added value of Lp(a) when examining LDL or apoB in association with CHD risk in a general population.

Clinical Topics: Dyslipidemia, Advanced Lipid Testing, Lipid Metabolism, Nonstatins, Prevention

Keywords: Cholesterol, LDL, Coronary Disease, Lipoprotein(a)

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