Kotzé Retha C M, Ariëns Robert A S, de Lange Zelda, Pieters Marlien
Centre of Excellence for Nutrition, North-West University, Potchefstroom, South Africa.
Theme Thrombosis, Division of Cardiovascular and Diabetes Research, Multidisciplinary Cardiovascular Research Centre and Leeds Institute for Genetics, Health and Therapeutics, School of Medicine, University of Leeds, UK.
Thromb Res. 2014 Nov;134(5):963-9. doi: 10.1016/j.thromres.2014.08.018. Epub 2014 Aug 29.
Cardiovascular disease (CVD) risk factors are associated with total fibrinogen concentration and/or altered clot structure. It is however, unclear whether such associations with clot structure are ascribed to fibrinogen concentration or other independent mechanisms. We aimed to determine whether CVD risk factors associated with increased total and/or γ' fibrinogen concentration, were also associated with altered fibrin clot properties and secondly whether such associations were due to the fibrinogen concentration or through independent associations.
In a plasma setting CVD risk factors (including total and γ' fibrinogen concentration) were cross-sectionally analysed in 2010 apparently healthy black South African participants. Kinetics of clot formation (lag time, slope and maximum absorbance) as well as clot lysis times were calculated from turbidity curves.
Of the measured CVD risk factors age, metabolic syndrome, C-reactive protein (CRP), high density lipoprotein (HDL)-cholesterol and homocysteine were significantly associated with altered fibrin clot properties after adjustment for total and or γ' fibrinogen concentration. Aging was associated with thicker fibres (p=0.004) while both metabolic syndrome and low HDL-cholesterol levels were associated with lower rates of lateral aggregation (slope), (p=0.0004 and p=0.0009), and the formation of thinner fibres (p=0.007 and p=0.0004). Elevated CRP was associated with increased rates of lateral aggregation (p=0.002) and consequently thicker fibres (p<0.0001). Hyperhomocysteinemia was associated with increased rates of lateral aggregation (p=0.0007) without affecting fibre thickness.
Final clot structure may contribute to increased CVD risk in vivo through associations with other CVD risk factors independent from total or γ' fibrinogen concentration.
心血管疾病(CVD)风险因素与纤维蛋白原总浓度和/或血凝块结构改变有关。然而,尚不清楚这种与血凝块结构的关联是归因于纤维蛋白原浓度还是其他独立机制。我们旨在确定与总纤维蛋白原和/或γ'纤维蛋白原浓度增加相关的CVD风险因素是否也与纤维蛋白凝块特性改变有关,其次,这种关联是由于纤维蛋白原浓度还是通过独立关联导致的。
在血浆环境中,对2010名表面健康的南非黑人参与者进行了CVD风险因素(包括总纤维蛋白原和γ'纤维蛋白原浓度)的横断面分析。从浊度曲线计算凝块形成动力学(滞后时间、斜率和最大吸光度)以及凝块溶解时间。
在调整总纤维蛋白原和/或γ'纤维蛋白原浓度后,所测量的CVD风险因素中,年龄、代谢综合征、C反应蛋白(CRP)、高密度脂蛋白(HDL)胆固醇和同型半胱氨酸与纤维蛋白凝块特性改变显著相关。衰老与更粗的纤维相关(p = 0.004),而代谢综合征和低HDL胆固醇水平均与较低的横向聚集率(斜率)相关(p = 0.0004和p = 0.0009),以及形成更细的纤维(p = 0.007和p = 0.0004)。CRP升高与更高的横向聚集率相关(p = 0.002),因此纤维更粗(p < 0.0001)。高同型半胱氨酸血症与更高的横向聚集率相关(p = 0.0007),但不影响纤维厚度。
最终的凝块结构可能通过与其他独立于总纤维蛋白原或γ'纤维蛋白原浓度的CVD风险因素的关联,在体内导致CVD风险增加。