脂蛋白(a)与老年人冠状动脉钙化和骨密度的关系。

IF 0.6
Ece Yurtseven, Gizem Timoçin Yığman, Gizem Yaşa, Nigar Bakhshaliyeva, Kayhan Çetin Atasoy, Erol Gürsoy, Kemal Baysal, Saide Aytekin, Vedat Aytekin
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引用次数: 0

摘要

目的:冠状动脉钙化(CAC)和骨质疏松症是常见的与年龄相关的疾病,可能有共同的潜在机制,如炎症和脂质失调。脂蛋白(a) [Lp(a)]被认为是这两个过程的潜在贡献者。本研究旨在探讨未使用他汀类药物的老年人群中CAC、骨密度(BMD)和Lp(a)水平之间的关系。方法:这项回顾性研究包括310例年龄≥55岁的患者,他们接受了冠状动脉ct血管造影和Lp(a)测量。目测CAC,用椎体霍斯菲尔德单位测量骨密度。根据Lp(a)水平将患者分为≤30mg /dL、30-49 mg/dL和≥50mg /dL三组。对年龄和性别进行倾向评分匹配。结果:CAC患者Lp(a)水平升高[36.4 +- 33.2 vs. 21.7 +- 27.8 mg/dL, P < 0.001],高密度脂蛋白胆固醇(HDL-C)降低[52.6 +- 14.6 vs. 57.5 +- 17.9 mg/dL, P = 0.010],骨密度降低[152.9 +- 50.2 vs. 169.1 +- 51.0 HU, P = 0.009]。在多变量分析中,Lp(a)和HDL-C都是CAC的独立预测因子。低骨密度和CAC患病率在不同的Lp(a)层逐渐增加:在Lp(a)≤30 mg/dL的患者中,28.9%的人存在低骨密度,52.6%的人存在CAC;Lp(a) 30 ~ 49 mg/dL组分别为37.2%和66.7%;Lp(a)≥50 mg/dL组分别为58.6%和80.3% (P = 0.002和P = 0.001)。结论:Lp(a)升高与CAC和低BMD相关。Lp(a)≥50 mg/dL可作为识别血管和骨骼同时恶化风险个体的共享生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Association of Lipoprotein(a) with Coronary Artery Calcification and Bone Mineral Density in Elderly Individuals.

Objective: Coronary artery calcification (CAC) and osteoporosis are common age-related conditions that may share underlying mechanisms such as inflammation and lipid dysregulation. Lipoprotein(a) [Lp(a)] has been suggested as a potential contributor to both processes. This study aims to investigate the relationship between CAC, bone mineral density (BMD), and Lp(a) levels in a statin-naive elderly population.

Method: This retrospective study included 310 patients aged ≥ 55 years who underwent coronary computed tomography angiography and Lp(a) measurement. CAC was assessed visually, and BMD was measured using vertebral Hounsfield units. Patients were stratified into three groups according to Lp(a) levels: ≤ 30, 30-49, and ≥ 50 mg/dL. Propensity score matching was performed for age and sex.

Results: Patients with CAC had higher Lp(a) levels [36.4 +- 33.2 vs. 21.7 +- 27.8 mg/dL, P < 0.001], lower high-density lipoprotein cholesterol (HDL-C) [52.6 +- 14.6 vs. 57.5 +- 17.9 mg/dL, P = 0.010], and lower BMD [152.9 +- 50.2 vs. 169.1 +- 51.0 HU, P = 0.009]. In multivariate analysis, both Lp(a) and HDL-C were independent predictors of CAC. Low BMD and CAC prevalence increased stepwise across Lp(a) strata: in patients with Lp(a) ≤ 30 mg/dL, low BMD was present in 28.9% and CAC in 52.6%; in those with Lp(a) 30-49 mg/dL, 37.2% and 66.7%; and in those with Lp(a) ≥ 50 mg/dL, 58.6% and 80.3%, respectively (P = 0.002 and P = 0.001).

Conclusion: Elevated Lp(a) is associated with both CAC and low BMD. Lp(a) ≥ 50 mg/dL may serve as a shared biomarker to identify individuals at risk for concurrent vascular and skeletal deterioration.

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