Lipoprotein(a) and plaque progression: insights from serial coronary computed tomography angiography and quantitative plaque assessment

脂蛋白(a)与斑块进展:来自连续冠状动脉计算机断层扫描血管造影和定量斑块评估的启示

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Abstract

BACKGROUND: Lipoprotein(a) [Lp(a)] is a well-established independent risk factor for cardiovascular disease. However, the long-term effects of Lp(a) on coronary plaque phenotype remain unclear. OBJECTIVE: To explore the potential association between Lp(a) levels and coronary plaque volume, composition, and progression using coronary computed tomography angiography (CCTA). METHODS: Patients with available data for Lp(a) and underwent baseline CCTA examinations between January 2009 to December 2015 and subsequently underwent a follow-up coronary CTA were retrospectively enrolled. Quantitative CCTA analyses measured plaque length, total plaque volume and composition volume. Patients were categorized into an elevated Lp(a) group (≥30 mg/dL) and a normal Lp(a) group (<30 mg/dL). The association between Lp(a) and baseline plaque characteristic and progression were investigated in linear mixed-effects models adjusted for clinical factors. Subgroup analyses were also conducted. RESULTS: Among 453 patients (mean age 64.7 years, 77.7% male) with a median follow-up of 6.15 years. elevated Lp(a) was linked to higher baseline plaque burden (all p < 0.001) and accelerated LAP volume progression (β = 0.55 mm(3)/year, 95% CI: 0.04-1.06; p = 0.036) after adjusting for confounders. In addition, patients with diabetes, female gender, family history of CAD, or aged <60 years and with normal lipid profiles showed higher progression in total plaque volume and LAP, fibro-fatty, and fibrous components. Increased calcification volume progression was also seen in those with diabetes, female gender, smoking, drinking, or normal LDL-C levels. The association between Lp(a) and calcification progression was more pronounced in statin users. CONCLUSIONS: Elevated Lp (a) level was associated with high coronary artery plaque burden at baseline and rapid progression of LAP at follow-up. Lp(a) may serve as a significant residual risk factor in seemingly "low-risk" populations.

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