HIGH PAI ACTIVITY WITH CORRELATION TO TRIGLYCERIDE AND HDL CHOLESTEROL VALUES IN PATIENTS WITH CORONARY-ARTERY DISEASE WITH NO DIFFERENCE IN SURVIVORS OF MYOCARDIAL-INFARCTION

被引:7
作者
IHNKEN, K
SPEISER, W
RUF, W
THIEL, W
SCHLEPPER, M
MULLERBERGHAUS, G
机构
[1] MAX PLANCK INST PHYSIOL & KLIN FORSCHUNG,KERCKHOFF KLIN,DIV HEMOSTASEOL & TRANSFUS MED,D-61231 BAD NAUHEIM,GERMANY
[2] MAX PLANCK INST PHYSIOL & KLIN FORSCHUNG,KERCKHOFF KLIN,DIV CARDIOL,D-61231 BAD NAUHEIM,GERMANY
关键词
CORONARY ARTERY DISEASE; PAI ACTIVITY; HYPERLIPIDEMIA; MYOCARDIAL INFARCTION; TISSUE-TYPE PLASMINOGEN ACTIVATOR;
D O I
10.1007/BF01715054
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The fibrinolytic capacity of blood depends mainly on the amount of tissue-type plasminogen activator (t-PA) activity and plasminogen activator inhibitor type-1 (PAI-1) activity. Previous studies linked high PAI activity or low t-PA activity with the development of atherosclerosis and thromboembolic diseases. Yet, there are conflicting reports in the literature as to whether there is higher PAI activity in patients with myocardial infarction (MI) than in patients with coronary artery disease (CAD) without previous MI. In this retrospective study, t-PA activity, t-PA antigen, and PAI activity before and after a venous occlusion test (VOT) of 10 min were assessed in 109 patients with angiographically documented CAD, in two subgroups of CAD patients with (n = 66) or without (n = 43) previous MI, and in subgroups of CAD patients according to their triglyceride levels and other risk factors. The mean values of t-PA activity in the whole patient group showed a 100-fold increase and a 3.1-fold increase in t-PA antigen after VOT (0.03+/-0.03 to 3.0+/-6.8 U/ml and 16.5+/-6.9 to 51.0+/-25.4 ng/ml, p<0.05). PAI activity was 24.4+/-11.0 before and 19.6+/-13.2 U/ml after VOT. Within the CAD group, no difference was found between patients without MI and survivors of previous MI in PAI activity before VOT (24.6+/-10.7 vs. 24.3+/-11.3 U/ml) and after VOT (19.0+/-12.1 vs 20.0+/-14.0 U/ml), or t-PA activity before (0.03+/-0.01 vs. 0.04+/-0.04 U/ml) and after VOT (2.8+/-7.0 vs. 3.2+/-6.7 U/ml). In 39.4% of CAD patients elevated plasma PAI activity before VOT (>25 U/ml) was found. This subgroup of patients represented the highest PAI activity after VOT (p<0.05), the lowest t-PA activity after VOT (p<0.001), and the highest triglyceride levels (p<0.05). In 11% of the patients, a small increase in t-PA activity (less than 0.5 U/ml) after VOT was seen. This group showed the lowest t-PA antigen after VOT (p<0.001) and the highest fibrinogen level (p<0.05). Both subgroups showed the same distribution among patients with and without MI. CAD patients with triglyceride levels over 200 mg/dl had the highest PAI activity values before VOT (28.3+/-11.8 U/ml; p<0.01) and after VOT (24.9+/-13.2 U/ml; p<0.01), resulting in low t-PA activity after VOT (p<0.01). Additionally, a negative correlation was found between PAI activity and HDL cholesterol (p<0.001). No differences were found between subgroups of CAD patients separated according to smoking habits, blood pressure, cholesterol, and severity of CAD. This study confirms former findings of elevated PAI activity in patients with coronary artery disease. In contrast to some reports, it did not demonstrate a difference between patients with and without previous MI. Further studies may clarify whether changes in lipid metabolism influence the function of endothelial cells in synthesis or secretion of PAI. Prospective studies are necessary to determine whether high PAI activity is a risk factor for the development of coronary artery disease or MI.
引用
收藏
页码:237 / 244
页数:8
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