The Effect of Lipoprotein(a) Levels on Non-Culprit Atherosclerosis in Patients With Acute Coronary Syndrome Who Underwent Percutaneous Coronary Intervention: An Optical Coherence Tomography Study.

BACKGROUND

The association between lipoprotein(a) [Lp(a)] levels and progression of non-culprit atherosclerosis (NSA) in patients with acute coronary syndrome (ACS) who underwent percutaneous coronary intervention (PCI) is unknown.

METHODS

This study enrolled 177 patients with ACS who underwent OCT-guided PCI and follow-up OCT examinations of non-culprit lesions between 2013 and 2018. Lesion characteristics including fibrous tissue, calcium, lipid, and macrophage content were assessed using quantitative plaque analysis. High Lp(a) levels were defined as Lp(a) ≥ 30 mg/dL. The association between Lp(a) levels and NSA progression was investigated using linear effect models adjusted for clinical risk factors. A discordance analysis was also performed.

RESULTS

At 1-year follow-up, individuals with Lp(a) levels ≥ 30 mg/dL had increased total atheroma volume and lipid component, and higher incidence of thin-cap fibroatheroma (TCFA) (p = 0.021; p = 0.006; p = 0.025, respectively). After adjusted, multivariable linear regression model revealed an association between Lp(a) and plaque progression in NSA (7.22 for each 1 SD increase, 95% CI: 0.96-13.48; p = 0.025) and increased lipid component (3.60 for each 1 SD increase, 95% CI: 0.63-6.56; p = 0.019). Discordance analyses showed that individuals with discordantly low Lp(a) levels had the lightest plaque progression and increase in lipid plaque burden (17.34 [10.22, 28.21] vs. 28.73 [14.88, 45.88] versus 25.73 [13.85, 45.70], p = 0.017).

CONCLUSION

Among patients with ACS, elevated Lp(a) levels were related to the progression of coronary plaques in non-culprit lesions, including increased total atheroma volume and lipid component, and a higher prevalence of TCFA at follow-up.