Otto C, Ritter M M, Richter W O, Minkenberg R, Schwandt P
Medical Department 2, Klinikum Grosshadern, University of Munich, Germany.
Metabolism. 2001 Feb;50(2):166-70. doi: 10.1053/meta.2001.20192.
Dyslipoproteinemias are associated with hemorrheologic abnormalities (elevated fibrinogen concentration, higher viscosity of plasma and blood). Epidemiologic data suggest that not only elevated lipoprotein concentrations (eg, low-density lipoprotein [LDL] cholesterol), but also hemorrheologic abnormalities could causally be involved in the atherosclerotic process. To elucidate potential effects of hemorrheological disturbances, we investigated patients suffering from primary hyperlipoproteinemias with both low (familial hypertriglyceridemia, n = 25) and high (type III hyperlipoproteinemia, n = 21; familial hypercholesterolemia, n = 19; mixed hyperlipoproteinemia, n = 19) atherosclerotic risk, as well as healthy controls (n = 49) in a cross-sectional design. Dyslipoproteinemias were classified by lipoprotein measurements (using ultracentrifugation), family history, and apolipoprotein E phenotype. Hemorrheology was characterized by the measurement of fibrinogen concentration, viscosity of plasma and blood at different shear rates, and red cell aggregation (RCA) at stasis and low shear. Fibrinogen concentration was lower in controls (2.38 +/- 0.09 g/L) compared with familial hypercholesterolemia (3.19 +/- 0.19 g/L), to type III hyperlipoproteinemia (3.02 +/- 0.12 g/L), to familial hypertriglyceridemia (2.95 +/- 0.21 g/L) and to mixed hyperlipoproteinemia (3.01 +/- 0.12 g/L) (P < .05, respectively) without differences between dyslipoproteinemia groups. Plasma viscosity was higher in patients with type III hyperlipoproteinemia (1.42 +/- 0.03 mPas), with familial hypertriglyceridemia (1.47 +/- 0.04 mPas), and with mixed hyperlipoproteinemia (1.43 +/- 0.02 mPas) compared with controls (1.29 +/- 0.01 mPas) (P < .05, respectively). After including 6 lipoprotein parameters in a general linear model, plasma viscosity, blood viscosity, and RCA were higher in familial hypertriglyceridemia compared with healthy controls and familial hypercholesterolemia (P < .05, respectively). As most of the hemorrheologic abnormalities were still significant after adjusting for lipoprotein concentrations, they seem to be at least partly independent from direct lipoprotein effects. Hemorrheologic abnormalities in familial hypertriglyceridemia (low atherosclerotic risk) were at least as marked as in dyslipoproteinemias with high atherosclerotic risk, suggesting that it might be most important to determine lipoprotein concentrations and to define exactly the type of dyslipoproteinemia for estimating the individual cardiovascular risk in these patients.
异常脂蛋白血症与血液流变学异常（纤维蛋白原浓度升高、血浆和血液粘度增加）有关。流行病学数据表明，不仅脂蛋白浓度升高（如低密度脂蛋白[LDL]胆固醇），而且血液流变学异常也可能在动脉粥样硬化过程中起因果作用。为了阐明血液流变学紊乱的潜在影响，我们采用横断面设计，对原发性高脂血症患者进行了研究，这些患者既有低动脉粥样硬化风险（家族性高甘油三酯血症，n = 25），也有高动脉粥样硬化风险（III型高脂血症，n = 21；家族性高胆固醇血症，n = 19；混合型高脂血症，n = 19），并设置了健康对照组（n = 49）。异常脂蛋白血症通过脂蛋白测量（使用超速离心法）、家族史和载脂蛋白E表型进行分类。血液流变学特征通过测量纤维蛋白原浓度、不同剪切速率下的血浆和血液粘度以及静态和低剪切力下的红细胞聚集（RCA）来表征。与家族性高胆固醇血症（3.19±0.19 g/L）、III型高脂血症（3.02±0.12 g/L）、家族性高甘油三酯血症（2.95±0.21 g/L）和混合型高脂血症（3.01±0.12 g/L）相比，对照组的纤维蛋白原浓度较低（2.38±0.09 g/L）（P均<.05），而各异常脂蛋白血症组之间无差异。III型高脂血症患者（1.42±0.03 mPas）、家族性高甘油三酯血症患者（1.47±0.04 mPas）和混合型高脂血症患者（1.43±0.02 mPas）的血浆粘度高于对照组（1.29±0.01 mPas）（P均<.05）。在将6个脂蛋白参数纳入一般线性模型后，家族性高甘油三酯血症患者的血浆粘度、血液粘度和RCA高于健康对照组和家族性高胆固醇血症患者（P均<.05）。由于在调整脂蛋白浓度后，大多数血液流变学异常仍然显著，因此它们似乎至少部分独立于脂蛋白的直接作用。家族性高甘油三酯血症（低动脉粥样硬化风险）中的血液流变学异常至少与高动脉粥样硬化风险的异常脂蛋白血症一样明显，这表明在评估这些患者的个体心血管风险时，确定脂蛋白浓度并准确界定异常脂蛋白血症的类型可能最为重要。
