Centre for Heart Lung Innovation, University of British Columbia, Vancouver, British Columbia, Canada; Program in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of Harvard, Cambridge, Massachusetts, USA. Electronic address: https://twitter.com/marketrinder.
Program in Medical and Population Genetics and the Cardiovascular Disease Initiative, Broad Institute of Harvard, Cambridge, Massachusetts, USA; Cardiology Division, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, USA; Cardiovascular Research Center, Massachusetts General Hospital, Boston, Massachusetts, USA.
J Am Coll Cardiol. 2022 Feb 22;79(7):617-628. doi: 10.1016/j.jacc.2021.11.055.
BACKGROUND: When indicated, guidelines recommend measurement of lipoprotein(a) for cardiovascular risk assessment. However, temporal variability in lipoprotein(a) is not well understood, and it is unclear if repeat testing may help refine risk prediction of coronary artery disease (CAD). OBJECTIVES: The authors examined the stability of repeat lipoprotein(a) measurements and the association between instability in lipoprotein(a) molar concentration with incident CAD. METHODS: The authors assessed the correlation between baseline and first follow-up measurements of lipoprotein(a) in the UK Biobank (n = 16,017 unrelated individuals). The association between change in lipoprotein(a) molar concentration and incident CAD was assessed among 15,432 participants using Cox proportional hazards models. RESULTS: Baseline and follow-up lipoprotein(a) molar concentration were significantly correlated over a median of 4.42 years (IQR: 3.69-4.93 years; Spearman rho = 0.96; P < 0.0001). The correlation between baseline and follow-up lipoprotein(a) molar concentration were stable across time between measurements of <3 (rho = 0.96), 3-4 (rho = 0.97), 4-5 (rho = 0.96), and >5 years (rho = 0.96). Although there were negligible-to-modest associations between statin use and changes in lipoprotein(a) molar concentration, statin usage was associated with a significant increase in lipoprotein(a) among individuals with baseline levels ≥70 nmol/L. Follow-up lipoprotein(a) molar concentration was significantly associated with risk of incident CAD (HR per 120 nmol/L: 1.32 [95% CI: 1.16-1.50]; P = 0.0002). However, the delta between follow-up and baseline lipoprotein(a) molar concentration was not significantly associated with incident CAD independent of follow-up lipoprotein(a) (P = 0.98). CONCLUSIONS: These findings suggest that, in the absence of therapies substantially altering lipoprotein(a), a single accurate measurement of lipoprotein(a) molar concentration is an efficient method to inform CAD risk.
背景：当需要时，指南建议测量脂蛋白(a)以进行心血管风险评估。然而，脂蛋白(a)的时间变异性尚不清楚，也不清楚重复检测是否有助于改善冠心病（CAD）的风险预测。
目的：作者研究了重复脂蛋白(a)测量的稳定性，以及脂蛋白(a)摩尔浓度不稳定与 CAD 事件之间的关系。
方法：作者评估了 UK Biobank 中脂蛋白(a)基线和第一次随访测量之间的相关性（n=16017 个无血缘关系的个体）。在 15432 名参与者中，使用 Cox 比例风险模型评估了脂蛋白(a)摩尔浓度变化与 CAD 事件之间的关系。
结果：中位随访时间为 4.42 年（IQR：3.69-4.93 年）时，脂蛋白(a)摩尔浓度的基线和随访值具有显著相关性（Spearman rho=0.96，P<0.0001）。在测量间隔<3（rho=0.96）、3-4（rho=0.97）、4-5（rho=0.96）和>5 年（rho=0.96）时，脂蛋白(a)摩尔浓度的基线与随访之间的相关性均稳定。尽管他汀类药物的使用与脂蛋白(a)摩尔浓度的变化之间存在微小到适度的关联，但他汀类药物的使用与基线水平≥70 nmol/L 的个体中脂蛋白(a)水平的显著升高有关。随访脂蛋白(a)摩尔浓度与 CAD 事件风险显著相关（每增加 120 nmol/L 的 HR：1.32[95%CI：1.16-1.50]；P=0.0002）。然而，在不考虑随访脂蛋白(a)的情况下，随访和基线脂蛋白(a)摩尔浓度之间的差值与 CAD 事件之间没有显著相关性（P=0.98）。
结论：这些发现表明，在没有明显改变脂蛋白(a)的治疗方法的情况下，单次准确测量脂蛋白(a)摩尔浓度是一种有效的方法，可以为 CAD 风险提供信息。
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