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Association between serum lipoprotein(a) levels and aortic vulnerable plaques assessed by non-obstructive general
Keisuke Kojima1, Yudai Tanaka1, Katsunori Fukumoto1
1Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Background And Aims:
Elevated lipoprotein(a) [Lp(a)] levels are recognized as a genetic risk factor for atherosclerotic cardiovascular disease. Previous coronary imaging studies have linked elevated Lp(a) levels to vulnerable coronary plaque characteristics. However, the relationship between elevated Lp(a) levels and vulnerable aortic plaque characteristics remains unclear. We investigated the association between serum Lp(a) levels and vulnerable aortic plaque characteristics assessed by non-obstructive general angioscopy (NOGA).
Methods:
We analyzed 276 consecutive patients with coronary artery disease who underwent NOGA between December 2014 and March 2023. Patients were divided according to serum Lp(a) levels using a 30 mg/dL cutoff. Vulnerable aortic plaque characteristics, including plaque rupture, thrombus, yellow plaque, ulceration, and fissure, were assessed by NOGA.
Results:
Elevated Lp(a) levels (>30 mg/dL) were observed in 27% of patients, whereas markedly elevated Lp(a) levels (>50 mg/dL) were observed in 14%. Patients with elevated Lp(a) levels showed a significantly higher prevalence of plaque rupture (84% vs. 62%, p < 0.001), thrombus, and fissure than those with lower Lp(a) levels. In contrast, the prevalence of yellow plaque did not differ significantly between groups. The prevalence of plaque rupture progressively increased according to Lp(a) strata. In multivariate logistic regression analysis, elevated Lp(a) levels remained independently associated with plaque rupture after adjustment for traditional cardiovascular risk factors.
Conclusions:
Elevated serum Lp(a) levels were independently associated with aortic plaque rupture assessed by NOGA. These findings suggest that elevated Lp(a) levels may be associated with persistent aortic plaque vulnerability despite intensive LDL-C lowering.