Calori G, D'Angelo A, Della Valle P, Ruotolo G, Ferini-Strambi L, Giusti C, Errera A, Gallus G
Epidemiology Unit, Istituto Scientifico H S. Raffaele, Milano, Italy.
Thromb Haemost. 1996 Jan;75(1):14-8.
The association of cigarette smoking with the development of occlusive vascular disease is firmly established. Unfavourable changes in a series of variables held independent risk factors for the development of vascular lesions (HDL-cholesterol, haematocrit, white blood cell count, fibrinogen and plasminogen activator inhibitor-1 (PAI-1)) are thought to be directly influenced by cigarette smoking. However, the role played by the genotype in the effect of smoking on the above parameters has not been investigated. To control the genotype, we studied the relationship between cigarette smoking and a series of cardiovascular risk factors in 27 monozygotic twin pairs (7 male and 20 female pairs, mean age +/- SD: 47.4 +/- 12.9 yrs) with a life-long discordance for smoking. Smoking twins had a life-long dose of smoking (Brickman index) of 287.3 +/- 241.5. Body mass index, blood pressure, haematocrit, haemoglobin and red blood cell counts, total cholesterol levels and the acute phase reactants alpha 1-acid glycoprotein and C-reactive protein were similar in smokers and non-smokers. Triglyceride was higher by 12.6% (9.5-35%, 95% confidence interval, p = 0.02) and HDL-cholesterol lower by 7.5% (0.2-15%, p = 0.04) in the smoking co-twins, who also had 8.4% (-0.2-17%, p = 0.06) higher white blood cell counts and 4.1% (1.2-7%, p < 0.01) larger mean platelet volume. There was no significant difference in clottable fibrinogen (by two methods) or in the activity of plasminogen activator inhibitor-1 between the two groups, nor was the within-pair difference in these parameters related to the smoking dose. Echo-doppler examination of the carotid arteries of 24 twin pairs showed mostly minor atherosclerotic lesions in 46% and 42% of the smoking and non-smoking co-twins. After adjustment for age, systolic blood pressure and platelet count and volume were the only variables significantly associated to the presence of vascular lesions. Cigarette smoking is associated with an atherogenic lipid profile and with changes in platelets and white cells potentially reflecting endothelial cell damage. When controlling the genotype, fibrinogen and PAI-1 activity levels did not seem directly influenced by cigarette smoking.
吸烟与闭塞性血管疾病的发生之间的关联已得到确证。一系列被认为是血管病变发生独立危险因素的变量（高密度脂蛋白胆固醇、血细胞比容、白细胞计数、纤维蛋白原和纤溶酶原激活物抑制剂-1（PAI-1））的不利变化被认为直接受吸烟影响。然而，基因型在吸烟对上述参数影响中所起的作用尚未得到研究。为了控制基因型，我们研究了27对单卵双胞胎（7对男性和20对女性，平均年龄±标准差：47.4±12.9岁）中吸烟情况终生不一致者吸烟与一系列心血管危险因素之间的关系。吸烟的双胞胎终生吸烟量（布里克曼指数）为287.3±241.5。吸烟者和不吸烟者的体重指数、血压、血细胞比容、血红蛋白和红细胞计数、总胆固醇水平以及急性期反应物α1-酸性糖蛋白和C反应蛋白相似。吸烟的同卵双胞胎甘油三酯高12.6%（9.5-35%，95%置信区间，p = 0.02），高密度脂蛋白胆固醇低7.5%（0.2-15%，p = 0.04），白细胞计数高8.4%（-0.2-17%，p = 0.06），平均血小板体积大4.1%（1.2-7%，p < 0.01）。两组之间可凝固纤维蛋白原（两种方法检测）或纤溶酶原激活物抑制剂-1的活性无显著差异，这些参数的同卵双胞胎之间差异也与吸烟量无关。对24对双胞胎的颈动脉进行超声多普勒检查发现，46%的吸烟同卵双胞胎和42%的不吸烟同卵双胞胎大多有轻微动脉粥样硬化病变。在对年龄进行调整后，收缩压以及血小板计数和体积是与血管病变存在显著相关的仅有的变量。吸烟与致动脉粥样硬化的血脂谱以及血小板和白细胞的变化有关，这些变化可能反映了内皮细胞损伤。在控制基因型时，纤维蛋白原和PAI-1活性水平似乎不受吸烟直接影响。
