Markus H S, Kapadia R, Sherwood R A
Department of Neurology, King's College School of Medicine and Dentistry, London, UK.
Ann Clin Biochem. 1997 Jul;34 ( Pt 4):360-5. doi: 10.1177/000456329703400404.
In vitro studies provide mechanisms by which elevated lipoprotein (a) [Lp(a)] concentrations may promote both thrombosis and atherogenesis. Case-control studies have reported raised Lp(a) concentrations in patients with stroke, but prospective studies have failed to confirm the association. A potential confounding factor is that Lp(a) may rise acutely after stroke. We determined Lp(a) concentrations in 164 patients studied at least 21 days after stroke or transient ischaemic attack, and in 91 controls. In the patient group we correlated Lp(a) concentrations with both the degree of carotid stenosis estimated on duplex ultrasonography, and with stroke subtype (large vessel disease, lacunar infarction, and cardioembolic and unknown pathogenesis). There was no difference between Lp(a) concentration in cases and controls [median (quartiles) 0.10 (0.04, 0.39) versus 0.12 (0.04, 0.30) g/L, P = 0.34]. There was no difference in the proportion of cases compared with controls with a markedly elevated Lp(a) of > 0.4 g/L (21.3 versus 16.5%, P = 0.34). There was non-significant trend towards higher median Lp(a) concentrations in women [median (quartiles) 0.16 (0.04, 0.32) g/L versus 0.12 (0.04, 0.28) g/L, P = 0.3]. In view of this trend we analysed the differences between cases and controls for each sex separately. Lp(a) concentrations in men were median (quartiles) 0.08 (0.04, 0.26) g/L in the 101 cases and 0.12 (0.04, 0.28) g/L in the 43 controls (P = 0.6). Lp(a) concentrations in women were median (quartiles) 0.25 (0.04, 0.44) g/L in the 63 cases, and 0.16 (0.04, 0.32) g/L in the 48 controls (P = 0.16). Within the patient group there was no difference between Lp(a) concentrations in the different stroke subgroups. There was no relationship between Lp(a) concentrations and mean percentage carotid stenosis (rs = 0.14, P = 0.07). Our results suggest that in an unselected population of men studied more than 3 weeks post event there is no relationship between lipoprotein(a) concentrations and either stroke/transient ischaemic attack, or carotid atheroma. The relationship in women requires further study.
体外研究揭示了脂蛋白(a)[Lp(a)]浓度升高可能促进血栓形成和动脉粥样硬化的机制。病例对照研究报告称中风患者的Lp(a)浓度升高，但前瞻性研究未能证实这种关联。一个潜在的混杂因素是Lp(a)可能在中风后急性升高。我们测定了164例在中风或短暂性脑缺血发作后至少21天接受研究的患者以及91名对照者的Lp(a)浓度。在患者组中，我们将Lp(a)浓度与经双功超声检查估计的颈动脉狭窄程度以及中风亚型（大血管疾病、腔隙性梗死、心源性栓塞和病因不明）进行了关联分析。病例组和对照组的Lp(a)浓度没有差异[中位数（四分位数间距）0.10（0.04，0.39）对0.12（0.04，0.30）g/L，P = 0.34]。Lp(a)显著升高> 0.4 g/L的病例与对照的比例没有差异（21.3%对16.5%，P = 0.34）。女性的Lp(a)中位数浓度有非显著性升高趋势[中位数（四分位数间距）0.16（0.04，0.32）g/L对0.12（0.04，0.28）g/L，P = 0.3]。鉴于这一趋势，我们分别分析了男女病例组和对照组之间的差异。101例男性病例的Lp(a)浓度中位数（四分位数间距）为0.08（0.04，0.26）g/L，43名男性对照为0.12（0.04，0.28）g/L（P = 0.6）。63例女性病例的Lp(a)浓度中位数（四分位数间距）为0.25（0.04，0.44）g/L，48名女性对照为0.16（0.04，0.32）g/L（P = 0.16）。在患者组中，不同中风亚组的Lp(a)浓度没有差异。Lp(a)浓度与颈动脉狭窄平均百分比之间没有关系（rs = 0.14，P = 0.07）。我们的结果表明，在事件发生3周后研究的未经过筛选的男性人群中，脂蛋白(a)浓度与中风/短暂性脑缺血发作或颈动脉粥样硬化之间没有关系。女性中的这种关系需要进一步研究。
