Combining Lp(a) with CT-quantified pericoronary fat inflammation sharpens MACE prediction in non-obstructive coronary disease, 1,052-patient study finds (Int J Cardiol 2026)

Original title: CCTA-quantified pericornary inflammation and lipoprotein (a): Combined predictive value in non-obstructive CAD

Int J Cardiol · 8 September 2025 · 7

Yang X, Li B, Chen H, Ding R, Chang N, Ji C, Gu H, Wang X

This study followed 1,052 patients with non-obstructive coronary artery disease over a median 6.8 (5.6-7.9) years, testing whether combining Lp(a) with CCTA-quantified pericoronary adipose tissue attenuation (PCATa), a marker of coronary inflammation, improves prediction of major adverse cardiovascular events (MACE). MACE occurred in 183 patients (17.4%); those with events had higher Lp(a) (26.20 [17.63-45.08] vs. 12.00 [4.58-26.00], P < 0.001) and higher PCATa (-72.6 ± 8.4 vs. -79.7 ± 9.5 HU, P < 0.001), and Lp(a) itself correlated with PCATa (P < 0.001). In multivariate Cox regression, both Lp(a) (HR 1.26, P < 0.001) and PCATa (HR 1.44, P < 0.001) independently predicted MACE alongside age, hypertension, triglycerides and plaque markers, and patients with Lp(a) 30 mg/dL or above plus PCATa above -78 HU had the highest event incidence (P < 0.001), with the combined marker achieving the highest discriminative AUC. Elevated Lp(a) tracks with greater pericoronary inflammation, and pairing the two markers refines risk stratification in patients who would otherwise appear low-risk on stenosis severity alone.

Original abstract

Objective: This study aimed to enhance major adverse cardiovascular events (MACEs) prediction by pericoronary adipose tissue attenuation (PCATa) in non-obstructive coronary artery disease (CAD) patients when combined with lipoprotein (a) (Lp(a)).

Methods: A total of 1052 patients with non-obstructive CAD were included. Detailed clinical data and CCTA features were analyzed. The MACEs in this study was defined as a composite of non-fatal myocardial infarction, new-onset heart failure requiring hospitalization, stroke, all-cause mortality, and coronary revascularization.

Results: During a median follow-up of 6.8 (5.6-7.9) years, 183 (17.4 %) patients suffered from MACEs. Patients experiencing MACEs demonstrated elevated Lp(a) levels and PCATa values (26.20 (17.63-45.08) vs. 12.00 (4.58-26.00), P < 0.001; -72.6 ± 8.4 HU vs. -79.7 ± 9.5 HU, P < 0.001). Lp(a) was associated with PCATa (P < 0.001). Elevated PCATa was associated with quantitatively greater atherosclerotic burden (P < 0.001). Multivariate Cox regression showed that age (HR = 1.03, P = 0.001), hypertension (HR = 1.39, P = 0.036), triglyceride (HR = 1.23, P = 0.003), high-risk plaque (HR = 2.30, P < 0.001), LAPV% (HR = 2.66, P < 0.001), Lp(a) (HR = 1.26, P < 0.001) and PCATa (HR = 1.44, P < 0.001) were independently associated with increased risk of MACEs. Kaplan-Meier analysis demonstrated that patients with Lp(a) ≥30 mg/dL and PCATa > - 78 HU had the highest incidence of MACEs (P < 0.001). Additionally, combination Lp(a) and PCATa showed the highest AUC (P < 0.001).

Conclusion: Incorporating Lp(a) and PCATa significantly improves MACEs prediction in non-obstructive CAD patients, where higher Lp(a) levels are linked to elevated PCATa.

Summary written by lp-a.org from the published abstract; figures as published. Page updated 17 August 2026. Methods.