Department of Neurology and Stroke Center, University Hospital Basel, Basel, Switzerland.
Department of Clinical Research, University of Basel, Basel, Switzerland.
Swiss Med Wkly. 2024 Apr 2;154:3633. doi: 10.57187/s.3633.
Lipoprotein (a) [Lp(a)] serum levels are highly genetically determined and promote atherogenesis. High Lp(a) levels are associated with increased cardiovascular morbidity. Serum Lp(a) levels have recently been associated with large artery atherosclerosis (LAA) stroke. We aimed to externally validate this association in an independent cohort.
This study stems from the prospective multicentre CoRisk study (CoPeptin for Risk Stratification in Acute Stroke patients [NCT00878813]), conducted at the University Hospital Bern, Switzerland, between 2009 and 2011, in which Lp(a) plasma levels were measured within the first 24 hours after stroke onset. We assessed the association of Lp(a) with LAA stroke using multivariable logistic regression and performed interaction analyses to identify potential effect modifiers.
Of 743 patients with ischaemic stroke, 105 (14%) had LAA stroke aetiology. Lp(a) levels were higher for LAA stroke than non-LAA stroke patients (23.0 nmol/l vs 16.3 nmol/l, p = 0.01). Multivariable regression revealed an independent association of log10and#xA0;Lp(a) with LAA stroke aetiology (aOR 1.47 [95% CI 1.03and#x2013;2.09], p = 0.03). The interaction analyses showed that Lp(a) was not associated with LAA stroke aetiology among patients with diabetes.
In a well-characterised cohort of patients with ischaemic stroke, we validated the association of higher Lp(a) levels with LAA stroke aetiology, independent of traditional cardiovascular risk factors. These findings may inform randomised clinical trials investigating the effect of Lp(a) lowering agents on cardiovascular outcomes. The CoRisk (CoPeptin for Risk Stratification in Acute Patients) study is registered on ClinicalTrials.gov.
NCT00878813.
脂蛋白(a)[Lp(a)]血清水平高度受遗传决定,并促进动脉粥样硬化形成。高 Lp(a)水平与心血管发病率增加相关。最近,血清 Lp(a)水平与大动脉粥样硬化性(LAA)卒中相关。我们旨在一个独立队列中对这种关联进行外部验证。
本研究源于前瞻性多中心 CoRisk 研究(CoPeptin 用于急性卒中患者风险分层[临床试验编号:NCT00878813]),该研究于 2009 年至 2011 年在瑞士伯尔尼大学医院进行,在卒中发病后 24 小时内测量 Lp(a)血浆水平。我们使用多变量逻辑回归评估 Lp(a)与 LAA 卒中的相关性,并进行交互分析以确定潜在的效应修饰因子。
在 743 例缺血性卒中患者中,105 例(14%)具有 LAA 卒中病因。Lp(a)水平在 LAA 卒中患者中高于非 LAA 卒中患者(23.0 nmol/l 比 16.3 nmol/l,p = 0.01)。多变量回归显示 log10Lp(a)与 LAA 卒中病因独立相关(优势比 1.47 [95%可信区间 1.03-2.09],p = 0.03)。交互分析显示,在糖尿病患者中,Lp(a)与 LAA 卒中病因无关。
在一个特征明确的缺血性卒中患者队列中,我们验证了较高的 Lp(a)水平与 LAA 卒中病因相关,这独立于传统心血管危险因素。这些发现可能为正在进行的评估 Lp(a)降低剂对心血管结局影响的随机临床试验提供信息。CoRisk(急性患者 CoPeptin 风险分层)研究在 ClinicalTrials.gov 上注册。
NCT00878813。