Willeit J, Kiechl S, Santer P, Oberhollenzer F, Egger G, Jarosch E, Mair A
Department of Neurology, University Clinic Innsbruck, Austria.
Stroke. 1995 Sep;26(9):1582-7. doi: 10.1161/01.str.26.9.1582.
Elevated levels of lipoprotein(a) [Lp(a)] have been reported in association with symptomatic coronary and carotid artery disease. Relevancy of Lp(a) as a risk predictor of presymptomatic atherosclerosis in general populations is not well established.
Serum Lp(a) distribution and its relation to sonographically assessed carotid atherosclerosis were examined in a random sample of 885 men and women aged 40 to 79 years (Bruneck Study).
Logistic regression analysis revealed a binary-type association between Lp(a) and carotid artery disease, with the threshold level of Lp(a) for an enhanced atherosclerosis risk defined at 32 mg/dL. The strength of relation increased with advancing severity of carotid atherosclerosis (odds ratios for Lp(a), 1.8 for nonstenotic and 4.7 for stenotic carotid artery disease; P < .001). Lp(a) was unaffected by environmental factors except for a significant decrease in women taking hormone replacement therapy (P < .05). In a multivariate approach, Lp(a) turned out to be an independently significant predictor of carotid atherosclerosis (P < .001). No differential effect of Lp(a) on atherosclerosis (effect modification) was observed for sex, age, low-density lipoprotein cholesterol, apolipoprotein A-I and B, fasting glucose, diabetes, or hypertension. However, the Lp(a)-atherosclerosis relation was significantly modified by fibrinogen (P < .01) and antithrombin III (P < .05).
The present study demonstrates a strong and independent association between elevated Lp(a) levels and carotid atherosclerosis in a large randomized population and provides evidence of a potential role of Lp(a) in the evolution of carotid stenosis. Apart from atherogenicity of Lp(a) cholesterol, interference with fibrinolysis of atheroma-associated clots and fibrin deposits in the arterial wall may achieve pathophysiological significance.
已有报道称，脂蛋白(a)[Lp(a)]水平升高与有症状的冠状动脉和颈动脉疾病相关。Lp(a)作为一般人群无症状性动脉粥样硬化风险预测指标的相关性尚未完全确立。
在一个包含885名年龄在40至79岁的男性和女性的随机样本中（布伦内克研究），检测血清Lp(a)分布及其与超声评估的颈动脉粥样硬化的关系。
逻辑回归分析显示Lp(a)与颈动脉疾病之间存在二元关联，将Lp(a)导致动脉粥样硬化风险增加的阈值水平定义为32mg/dL。随着颈动脉粥样硬化严重程度的增加，两者关系的强度也增加（Lp(a)的优势比，非狭窄性颈动脉疾病为1.8，狭窄性颈动脉疾病为4.7；P<.001）。除接受激素替代治疗的女性Lp(a)显著降低外（P<.05），Lp(a)不受环境因素影响。在多变量分析中，Lp(a)被证明是颈动脉粥样硬化的独立显著预测指标（P<.001）。未观察到Lp(a)对动脉粥样硬化有性别、年龄、低密度脂蛋白胆固醇、载脂蛋白A-I和B、空腹血糖、糖尿病或高血压的差异影响（效应修正）。然而，纤维蛋白原（P<.01）和抗凝血酶III（P<.05）显著改变了Lp(a)与动脉粥样硬化的关系。
本研究表明，在一个大型随机人群中，Lp(a)水平升高与颈动脉粥样硬化之间存在强烈且独立的关联，并为Lp(a)在颈动脉狭窄发展中的潜在作用提供了证据。除Lp(a)胆固醇的致动脉粥样硬化作用外，干扰动脉壁中与动脉粥样硬化相关的血栓和纤维蛋白沉积物的纤维蛋白溶解可能具有病理生理学意义。
