脂蛋白 (a) 和累积低密度脂蛋白胆固醇暴露对异型家族性高胆固醇血症患者冠状动脉疾病的临床影响。

IF 3 2区 医学 Q2 PERIPHERAL VASCULAR DISEASE Journal of atherosclerosis and thrombosis Pub Date : 2024-08-06 DOI:10.5551/jat.65009
Daisuke Shishikura, Mariko Harada-Shiba, Masahito Michikura, Shimpei Fujioka, Tomohiro Fujisaka, Hideaki Morita, Yumiko Kanzaki, Masaaki Hoshiga
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引用次数: 0

摘要

目的:主要由遗传变异决定的脂蛋白(a)(Lp[a])升高会导致动脉粥样硬化性心血管疾病(ASCVD),尤其是在家族性高胆固醇血症(FH)患者中。我们的目的是阐明脂蛋白(a)和低密度脂蛋白胆固醇(LDL-C)累积暴露对 FH 患者的 CAD 的临床影响:对 147 名临床诊断为杂合性家族性高胆固醇血症(HeFH)的患者进行了回顾性研究。根据是否存在 CAD 将患者分为两组。对他们的临床特征和血脂谱进行了评估:两组患者未经治疗的 LDL-C 水平无明显差异(P=0.4),而 CAD 患者的 LDL-C 累积暴露量和 Lp(a) 浓度明显更高(分别为 11956 对 8824 毫克/年/分升,P<0.01;40 对 14 毫克/分升,P<0.001)。接收器操作特征曲线(ROC)分析表明,预测FH患者CAD的脂蛋白(a)和累积LDL-C暴露的临界值分别为28 mg/dL(AUC 0.71)和10600 mg/年/dL(AUC 0.77)。多变量分析显示,累积低密度脂蛋白胆固醇暴露量≥ 10600 毫克/年/分升(p<0.0001)和脂蛋白(a)水平≥ 28 毫克/分升(p<0.001)是预测 CAD 的独立因素。值得注意的是,吸烟、Lp(a) ≥ 28 mg/dL 和累积 LDL-C 暴露 ≥ 10600 mg-年/dL 的人群患 CAD 的风险显著增加至 85.7%(几率比:46.5,95%CI:5.3-411.4,p<0.001):本研究表明,脂蛋白(a)和累积低密度脂蛋白胆固醇暴露对 HeFH 患者的 CAD 有叠加效应。该研究表明,脂蛋白(a)和累积低密度脂蛋白胆固醇暴露对 HeFH 患者的 CAD 有叠加效应,与传统危险因素(尤其是吸烟和累积低密度脂蛋白胆固醇暴露)相互作用,极大地增加了该人群的心血管风险。
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Clinical Impact of Lipoprotein (a) and Cumulative Low-Density Lipoprotein Cholesterol Exposure on Coronary Artery Disease in Patients with Heterozygous Familial Hypercholesterolemia.

Aims: Elevated lipoprotein (a) (Lp[a]), predominantly determined by genetic variability, causes atherosclerotic cardiovascular disease (ASCVD), particularly in patients with familial hypercholesterolemia (FH). We aimed to elucidate the clinical impact of Lp(a) and cumulative exposure to low-density lipoprotein cholesterol (LDL-C) on CAD in patients with FH.

Methods: One hundred forty-seven patients clinically diagnosed with heterozygous familial hypercholesterolemia (HeFH) were retrospectively investigated. Patients were divided into 2 groups according to the presence of CAD. Their clinical characteristics and lipid profiles were evaluated.

Results: There were no significant differences in untreated LDL-C levels between the 2 groups (p=0.4), whereas the cumulative exposure to LDL-C and Lp(a) concentration were significantly higher in patients with CAD (11956 vs. 8824 mg-year/dL, p<0.01; 40 vs. 14 mg/dL, p<0.001, respectively). A receiver operating characteristic (ROC) curve analysis demonstrated that the cutoff values of Lp(a) and cumulative LDL-C exposure to predict CAD in patients with FH were 28 mg/dL (AUC 0.71) and 10600 mg-year/dL (AUC 0.77), respectively. A multivariate analysis revealed that cumulative LDL-C exposure ≥ 10600 mg-year/dL (p<0.0001) and Lp(a) level ≥ 28 mg/dL (p<0.001) were independent predictors of CAD. Notably, the risk of CAD remarkably increased to 85.7% with smoking, Lp(a) ≥ 28 mg/dL, and cumulative LDL-C exposure ≥ 10600 mg-year/dL (odds ratio: 46.5, 95%CI: 5.3-411.4, p<0.001).

Conclusions: This study demonstrated an additive effect of Lp(a) and cumulative LDL-C exposure on CAD in patients with HeFH. Interaction with traditional risk factors, particularly smoking and cumulative LDL-C exposure, enormously enhances the cardiovascular risk in this population.

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来源期刊
CiteScore
6.60
自引率
15.90%
发文量
271
审稿时长
1 months
期刊介绍: JAT publishes articles focused on all aspects of research on atherosclerosis, vascular biology, thrombosis, lipid and metabolism.
期刊最新文献
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