Schreiner P J, Heiss G, Tyroler H A, Morrisett J D, Davis C E, Smith R
Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, 55454-1015, USA.
Arterioscler Thromb Vasc Biol. 1996 Mar;16(3):471-8. doi: 10.1161/01.atv.16.3.471.
The association of lipoprotein(a) [Lp(a)] with preclinical atherosclerotic disease is not well established in any race group, particularly African Americans. This report examined the association of Lp(a) with preclinical extracranial carotid atherosclerosis in middle-aged black and white participants in the Atherosclerosis Risk in Communities (ARIC) Study. Study participants (15 124: 2417 black women, 1522 black men, 5907 white women, and 5278 white men) who were 45 to 64 years old at baseline were examined during the period 1987 to 1989. Carotid intimal-medial far-wall thickness was determined by B-mode ultrasonography and expressed as the overall wall thickness mean at six sites to approximate atherosclerosis in the carotid system. Lp(a) was measured as its total protein component, Lp(a) protein, by a double-antibody ELISA for apolipoprotein(a) detection. Mean Lp(a) protein levels were higher in blacks than whites (169.1 and 147.0 microgram/mL in black women and black men, respectively, compared with 86.6 and 75.1 micrograms/mL in white women and white men). Mean carotid wall thickness (in millimeters) varied by race and gender: 0.798 in white men, 0.779 in black men, 0.718 in black women and 0.695 in white women. Multivariable-adjusted Lp(a) protein was independently associated with wall thickness (in millimeters) in white men and black men; among women, however, this association appeared to be stronger when smoking and diabetes were present. A 100-microgram/mL difference in Lp(a) protein was associated with 0.049- and 0.043-mm higher wall thickness values in black men and white men, respectively. Among white women who smoked, the difference in wall thickness was 0.051 mm compared with 0.032 mm for former/never smokers and 0.21 mm in black female diabetics compared with 0.031 mm in black female nondiabetics. These results suggest that Lp(a) is associated with preclinical carotid atherosclerosis in both blacks and whites, but that this association may be affected by the presence of other cardiovascular risk factors, particularly in women.
脂蛋白(a)[Lp(a)]与临床前动脉粥样硬化疾病之间的关联在任何种族群体中都尚未完全明确,尤其是非裔美国人。本报告在社区动脉粥样硬化风险(ARIC)研究中,调查了中年黑人和白人参与者中Lp(a)与临床前颅外颈动脉粥样硬化的关联。研究参与者(共15124人:2417名黑人女性、1522名黑人男性、5907名白人女性和5278名白人男性)在1987年至1989年期间接受检查,他们在基线时年龄为45至64岁。通过B型超声测定颈动脉内膜中层远壁厚度,并表示为六个部位的总体壁厚度平均值,以近似颈动脉系统中的动脉粥样硬化情况。通过用于载脂蛋白(a)检测的双抗体ELISA法,将Lp(a)作为其总蛋白成分即Lp(a)蛋白进行测量。黑人的平均Lp(a)蛋白水平高于白人(黑人女性和黑人男性分别为169.1和147.0微克/毫升,而白人女性和白人男性分别为86.6和75.1微克/毫升)。平均颈动脉壁厚度(以毫米为单位)因种族和性别而异:白人男性为0.798,黑人男性为0.779,黑人女性为0.718,白人女性为0.695。多变量调整后的Lp(a)蛋白与白人男性和黑人男性的壁厚度(以毫米为单位)独立相关;然而,在女性中当存在吸烟和糖尿病时,这种关联似乎更强。Lp(a)蛋白每相差100微克/毫升,黑人男性和白人男性的壁厚度值分别增加0.049毫米和0.043毫米。在吸烟的白人女性中,壁厚度差异为0.051毫米,而既往吸烟者/从不吸烟者为0.032毫米;在黑人女性糖尿病患者中为0.21毫米,而黑人女性非糖尿病患者为0.031毫米。这些结果表明,Lp(a)与黑人和白人的临床前颈动脉粥样硬化均相关,但这种关联可能会受到其他心血管危险因素的影响,尤其是在女性中。