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Association between lipoprotein(a) and obstructive coronary artery disease and high-risk plaque
Insights from the PROMISE trial
O'Toole, T., Shah, N. P., Giamberardino, S. N., Kwee, L. C., Voora, D., McGarrah, R. W., Ferencik, M., Lu, M. T., Kraus, W. E., Foldyna, B., Douglas, P. S., Shah, S. H., & Pagidipati, N. J. (2024). Association between lipoprotein(a) and obstructive coronary artery disease and high-risk plaque: Insights from the PROMISE trial. American Journal of Cardiology. Advance online publication. https://doi.org/10.1016/j.amjcard.2024.09.006
BACKGROUND: The role of lipoprotein (a), or Lp(a), in the development of obstructive coronary artery disease (CAD) and high-risk plaque (HRP) among primary prevention patients with stable chest pain is unknown. We sought to evaluate the relationship of Lp(a), independent of low-density lipoprotein cholesterol (LDL-C), with the presence of obstructive CAD and HRP in an attempt to improve understanding of the residual risk imparted by Lp(a) on CAD.
METHODS: We performed a secondary analysis among PROMISE (Prospective Multicenter Imaging Study for Evaluation of Chest Pain) Trial participants who had coronary computed tomographic angiography (CTA) performed and Lp(a) data available. Lp(a) concentration was analyzed as a binary variable with elevated Lp(a) defined as ≥50 mg/dL. "Stenosis ≥ 50%" was defined as ≥50% coronary artery stenosis in any epicardial vessel, and "Stenosis ≥ 70%" was defined as ≥70% coronary artery stenosis in any epicardial vessel and/or ≥50% left main coronary artery stenosis. HRP was defined as presence of plaque on CTA imaging with evidence of positive remodeling, low CT attenuation, or napkin ring sign. Multivariate logistic regression models were constructed to evaluate the association between Lp(a) and the outcomes of obstructive CAD and HRP stratified by LDL-C ≥100 mg/dL vs. <100 mg/dL.
RESULTS: Of the 1,815 patients who underwent CTA and had Lp(a) data available, those with elevated Lp(a) were more commonly female and Black than those with lower Lp(a). Elevated Lp(a) was associated with both Stenosis ≥ 50% (OR 1.57, 95% CI 1.14-2.15, p=0.005) and Stenosis ≥ 70% (OR 2.05, 95% CI 1.34-3.11, p=0.0008) in multivariate models, and this relationship was not modified by LDL-C ≥100 mg/dL vs. <100 mg/dL (interaction p>0.4). Elevated Lp(a) was not associated with HRP when adjusted for obstructive CAD.
CONCLUSIONS: This study of patients without known CAD found that elevated Lp(a) ≥50 mg/dL was independently associated with the presence of obstructive CAD regardless of controlled vs. uncontrolled LDL-C, but was not independently associated with HRP when Stenosis ≥ 50% or ≥ 70% was accounted for. Further research is warranted to delineate the role of Lp(a) in the residual risk for ASCVD that patients may have despite optimal LDL-C lowering.