Key result
Elevated Lp(a) linked to ~46% higher prevalence of culprit TCFA in ACS.
Why the study?
Does elevated Lp(a) increase the presence of thin-cap fibroatheroma and plaque vulnerability in patients with acute coronary syndrome?
Cohort (n=1,292)
Does elevated Lp(a) increase the presence of thin-cap fibroatheroma and plaque vulnerability in patients with acute coronary syndrome?
Odds Ratio: 1.46 (95% CI 1.01–2.12)
Absolute Event Rate: 59.8% vs 49.9%
p-value: p=0.045
Elevated Lp(a) levels (≥75 nmol/L) are independently associated with increased pancoronary plaque vulnerability, including culprit and nonculprit thin-cap fibroatheroma, in patients with acute coronary syndrome.
Background Elevated lipoprotein(a) [Lp(a)] levels contribute to cardiovascular disease. However, there is insufficient evidence for pancoronary plaque vulnerability in patients with different Lp(a) levels. Purpose This study aimed to investigate the correlation between elevated Lp(a) levels and pancoronary plaque vulnerability in patients with acute coronary syndrome (ACS) by using three-vessel optical coherence tomography (OCT). Methods In this retrospective study, a total of 1,292 ACS patients who underwent three-vessel OCT imaging after successful intervention were included between January 2017 to December 2021. Baseline serum samples were obtained and stored at -80°C. Analyses of Lp(a) concentrations were performed using a rapid latex particle-enhanced turbidimetric immunoassay. Lp(a) levels of 75 nmol/L or higher were considered elevated. The primary endpoint was the presence of thin-cap fibroatheroma (TCFA). The relationship between Lp(a) levels and TCFA was identified by using logistic regression models, including baseline characteristics and laboratory tests. Results The average age of patients was 57.2 ± 11.1 years, and 948 (73.4%) were male. Lp(a) was elevated ≥ 75 nmol/L in 15.4% (199/1292) of all enrolled patients. In culprit lesions, patients with elevated Lp(a) had a higher prevalence of TCFA (59.8% vs. 49.9%, P=0.010) and macrophage accumulation (P=0.046), and a thinner minimal fibrous cap thickness (53.3[40.7-76.7] μm vs. 60.0[43.3-86.7] μm, P=0.007) than patients with Lp(a) <75 nmol/L. In nonculprit lesions, patients with elevated Lp(a) had a higher prevalence of plaque rupture, TCFA (38.7% vs. 29.8%, P=0.013), macrophage accumulation, and microvessels (75.2% vs. 81.9%, P=0.041). The lesion-level analyses also showed a higher prevalence of nonculprit TCFA (14.5% vs. 11.4%, P=0.032) and macrophage accumulation, smaller minimal lumen area (3.9[2.5-5.4] mm2 vs. 4.0[2.5-5.9] mm2, P=0.033), and thinner minimal fibrous cap thickness (90.0[63.3-120.0] μm vs. 96.7[70.0-130.0] μm, P=0.039) in the elevated Lp(a) group. After adjusting for covariates, elevated Lp(a) levels independently predicted culprit TCFA (odds ratio [OR]: 1.46, 95% confidence interval [CI]: 1.01-2.12, P=0.045) and nonculprit TCFA (OR:1.71, 95% CI: 1.18-2.48, P=0.005). Conclusion ACS patients with elevated Lp(a) had increased levels of pancoronary plaque vulnerabilities. Lp(a) ≥75 nmol/L was independently associated with culprit and nonculprit TCFA. Lp(a) might become a potential target for treating coronary vulnerable plaques.Figure
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Fang et al. (2025) conducted a cohort in acute coronary syndrome (n=1,292). Elevated lipoprotein(a) (≥75 nmol/L) vs. Lipoprotein(a) <75 nmol/L was evaluated on presence of thin-cap fibroatheroma (TCFA) (OR 1.46, 95% CI 1.01-2.12, p=0.045). Elevated lipoprotein(a) levels ≥75 nmol/L were independently associated with a higher prevalence of culprit thin-cap fibroatheroma (OR 1.46; 95% CI 1.01-2.12; P=0.045) in patients with ACS.
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