Rallidis L S, Megalou A A, Papageorgakis N H, Trikas A G, Chatzidimitriou G I, Tsitouris G K
Department of Cardiology, Evangelismos Hospital, Athens, Greece.
Thromb Haemost. 1996 Sep;76(3):417-21.
To assess whether plasminogen activator inhibitor 1 (PAI-1) activity is elevated in the progeny of young coronary men, 193 young subjects were recruited and divided into two groups. Group A consisted of 104 children whose fathers had suffered a myocardial infarction before the age of 55 ("cases"). Eighty-nine young subjects matched for age, sex, body mass index (BMI) and smoking habits without familial history of coronary artery disease (CAD) served as controls (group B). Children with a family history of diabetes mellitus or hypertension were excluded from both groups. We measured PAI-1 activity, tissue-type plasminogen activator (t-PA) antigen, a2-antiplasmin, fibrinogen, lipids and apolipoproteins in both groups. PAI-1 activity levels were also determined in the men who suffered a premature myocardial infarction 4 months after their discharge. PAI-1 activity levels were higher in cases compared to controls (3.13 +/- 1.9 vs 2.17 +/- 1.9 U/ml, p = 0.0014). t-PA antigen and a2-antiplasmin did not differ significantly between the two groups, while fibrinogen, total cholesterol, low-density lipoprotein cholesterol, apolipoprotein B and lipoprotein(a) were significantly higher in group A. PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. There was also a positive correlation between PAI-1 activity levels of the affected fathers and their children (r = 0.30, p = 0.01). The present data support the hypothesis that elevated PAI-1 levels in the offspring of men with premature myocardial infarction impair their fibrinolytic capacity contributing to their familial predisposition to CAD.
为评估年轻冠心病男性后代的纤溶酶原激活物抑制剂1(PAI-1)活性是否升高,招募了193名年轻受试者并将其分为两组。A组由104名儿童组成,他们的父亲在55岁之前曾发生过心肌梗死(“病例组”)。89名年龄、性别、体重指数(BMI)和吸烟习惯相匹配且无冠心病(CAD)家族史的年轻受试者作为对照组(B组)。两组均排除有糖尿病或高血压家族史的儿童。我们测量了两组的PAI-1活性、组织型纤溶酶原激活物(t-PA)抗原、α2-抗纤溶酶、纤维蛋白原、血脂和载脂蛋白。还测定了发生过早发心肌梗死的男性出院4个月后的PAI-1活性水平。病例组的PAI-1活性水平高于对照组(3.13±1.9 vs 2.17±1.9 U/ml,p = 0.0014)。两组间t-PA抗原和α2-抗纤溶酶无显著差异,而A组的纤维蛋白原、总胆固醇、低密度脂蛋白胆固醇、载脂蛋白B和脂蛋白(a)显著更高。病例组中PAI-1与甘油三酯(r = 0.22,p = 0.024)、载脂蛋白B(r = 0.21,p = 0.039)和纤维蛋白原(r = 0.22,p = 0.029)呈正相关,在病例组和对照组中均与BMI呈正相关(病例组r = 0.37,p = 0.0003;对照组r = 0.23,p = 0.044)。在逐步多元回归分析中,病例组中只有载脂蛋白B(p = 0.008)和BMI(p = 0.0014)是PAI-1活性的显著决定因素。受影响父亲及其子女的PAI-1活性水平之间也存在正相关(r = 0.30,p = 0.01)。目前的数据支持以下假设:过早发心肌梗死男性后代中PAI-1水平升高会损害其纤溶能力,导致他们患CAD的家族易感性。