High Lp(a) marks vulnerable, lipid-rich coronary plaques in acute coronary syndrome, an imaging study of 500 angiographic and 51 OCT patients (Atherosclerosis 2016)

Original title: Lipoprotein (a) is related to coronary atherosclerotic burden and a vulnerable plaque phenotype in angiographically obstructive coronary artery disease

Atherosclerosis · 14 January 2016 · 7

Niccoli G, Cin D, Scalone G, Panebianco M, Abbolito S, Cosentino N, Jacoangeli F, Refaat H, Gallo G, Salerno G, Volpe M, Crea F et al.

This multicenter study examined Lp(a) levels in relation to coronary atherosclerotic burden by angiography and plaque vulnerability by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS) and obstructive coronary artery disease, enrolling 500 patients (370 men, average age 66) for the angiographic cohort and 51 patients (29 men, average age 65) for the OCT cohort. In the angiographic cohort, Lp(a) was a weak independent predictor of Sullivan score, stenosis score, and extent index (all P<0.0001). In the OCT cohort, patients with Lp(a) at or above 30 mg/dL, compared with those below, had a higher prevalence of lipidic plaque at the culprit stenosis (67% vs 27%, P=0.02), a wider lipid arc (135 vs 59, P=0.03), and a higher prevalence of thin-cap fibroatheroma (38% vs 10%, P=0.04). The findings show elevated Lp(a) in ACS patients is associated with greater atherosclerotic burden and identifies a subset with high-risk, vulnerable coronary plaque features.

Original abstract

Background: Lipoprotein Lp(a) has been shown to be an independent risk factor for coronary artery disease (CAD). However, its association with CAD burden in patients with ACS is largely unknown, as well as the association of Lp(a) with lipid rich plaques prone to rupture.

Aim: We aim at assessing CAD burden by coronary angiography and plaque features including thin cap fibroatheroma (TCFA) by optical coherence tomography (OCT) in consecutive patients presenting with acute coronary syndrome (ACS) and obstructive CAD along with serum Lp(a) levels.

Methods: This study comprises an angiographic and an OCT cohort. A total of 500 ACS patients (370 men, average age 66 ± 11) were enrolled for the angiographic cohort and 51 ACS patients (29 males, average age 65 ± 11) were enrolled for the OCT cohort. Angiographic CAD severity was assessed by Sullivan score and by Bogaty score including stenosis score and extent index. OCT plaque features were evaluated at the site of the minimal lumen area and along the culprit segment.

Results: In the angiographic cohort, at multivariate analysis, Lp(a) was a weak independent predictor of Sullivan score (p < 0.0001), stenosis score (p < 0.0001) and extent index (p < 0.0001). In the OCT cohort, patients with higher Lp(a) levels (≥ 30 md/dl) compared to patients with lower Lp(a) levels (<30 md/dl) exhibited a higher prevalence of lipidic plaque at the site of the culprit stenosis (67% vs. 27%; P = 0.02), a wider lipid arc (135 ± 114 vs 59 ± 111; P = 0.03) and a higher prevalence of TCFA (38% vs. 10%; P = 0.04).

Conclusions: Among patients with ACS, raised Lp(a) levels are associated with an increased atherosclerotic burden and it identifies a subset of patients with features of high risk coronary atherosclerosis.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.