van den Bosch Sibbeliene E, Boer Lotte M de, Revers Alma, Schrauben Eric M, Ooij Pim van, Nederveen Aart J, Corpeleijn Willemijn E, Kastelein John J P, Wiegman Albert, Hutten Barbara A
Department of Pediatrics, Amsterdam University Medical Center, Location AMC, 1105 AZ Amsterdam, The Netherlands.
Department of Epidemiology and Data Science, Amsterdam University Medical Center, Location AMC, 1105 AZ Amsterdam, The Netherlands.
J Clin Med. 2025 Feb 27;14(5):1611. doi: 10.3390/jcm14051611.
: Elevated lipoprotein(a) [Lp(a)] and familial hypercholesterolemia (FH) are both inherited dyslipidemias that are independently associated with cardiovascular disease. Surrogate markers to assess signs of atherosclerosis, such as arterial stiffness, might be useful to evaluate the cardiovascular risk in young patients. The aim of this study is to evaluate the contribution of Lp(a) to arterial stiffness, as measured by carotid pulse wave velocity (cPWV) in young adults with FH. : For this cross-sectional study, 214 children with FH who participated in a randomized controlled trial between 1997 and 1999 on the efficacy and safety of pravastatin were eligible. After 20 years, these patients were invited for a hospital visit, including cPWV assessment (by 4D flow MRI) and Lp(a) measurement. Linear mixed-effects models were used to evaluate the association between Lp(a) and cPWV. : We included 143 patients (mean [standard deviation] age: 31.8 [3.2] years) from 108 families. Median (interquartile range) cPWV was 1.62 (1.31-2.06) m/s. Both the unadjusted (ß = -0.0014 m/s per 1 mg/dL increase in Lp(a), 95% CI: -0.0052 to 0.0023, = 0.455) and adjusted model (ß = -0.0005 m/s per 1 mg/dL increase in Lp(a), 95% CI: -0.0042 to 0.0032, = 0.785) showed no significant association between Lp(a) and cPWV. : Our findings indicate that Lp(a) levels are not associated with carotid arterial stiffness in young adults with FH. Possibly, High Lp(a) might cause atherosclerosis by mechanisms beyond arterial stiffness in young adults. Other surrogate markers of early signs of atherosclerosis may be more suitable to evaluate the Lp(a)-mediated contribution to atherosclerosis in young FH patients.
脂蛋白(a)[Lp(a)]升高和家族性高胆固醇血症(FH)都是遗传性血脂异常,均独立与心血管疾病相关。评估动脉粥样硬化迹象的替代标志物,如动脉僵硬度,可能有助于评估年轻患者的心血管风险。本研究的目的是评估在患有FH的年轻成年人中,Lp(a)对通过颈动脉脉搏波速度(cPWV)测量的动脉僵硬度的影响。
对于这项横断面研究,214名患有FH的儿童符合条件,他们在1997年至1999年期间参加了一项关于普伐他汀疗效和安全性的随机对照试验。20年后,邀请这些患者到医院就诊,包括进行cPWV评估(通过4D流动磁共振成像)和Lp(a)测量。使用线性混合效应模型评估Lp(a)与cPWV之间的关联。
我们纳入了来自108个家庭的143名患者(平均[标准差]年龄:31.8[3.2]岁)。cPWV的中位数(四分位间距)为1.62(1.31 - 2.06)m/s。未调整模型(每升高1mg/dL Lp(a),ß = -0.0014m/s,95%CI:-0.0052至0.0023,P = 0.455)和调整模型(每升高1mg/dL Lp(a),ß = -0.0005m/s,95%CI:-0.0042至0.0032,P = 0.785)均显示Lp(a)与cPWV之间无显著关联。
我们的研究结果表明,在患有FH的年轻成年人中,Lp(a)水平与颈动脉僵硬度无关。可能的是,高Lp(a)可能通过年轻成年人动脉僵硬度以外的机制导致动脉粥样硬化。动脉粥样硬化早期迹象的其他替代标志物可能更适合评估Lp(a)介导的对年轻FH患者动脉粥样硬化的影响。