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The Fibrinolytic System Is Not Impaired in Older Men With Hypertension

 

作者: Christopher A. DeSouza,   Donald R. Dengel,   Marc A. Rogers,   Kim Cox,   Richard F. Macko,  

 

期刊: Hypertension  (OVID Available online 1996)
卷期: Volume 27, issue 5  

页码: 1053-1058

 

ISSN:0194-911X

 

年代: 1996

 

出版商: OVID

 

数据来源: OVID

 

摘要:

The fibrinolytic system is thought to be impaired in older hypertensive adults, thus contributing to the elevated risk of atherothrombosis, stroke, and acute myocardial infarction in this population. However, studies that have examined the fibrinolytic system in hypertensive individuals have failed to control for the confounding effects of other metabolic risk factors, making it difficult for one to determine the independent effect of hypertension on the fibrinolytic system. The purpose of the present study was to test the hypothesis that the fibrinolytic system is not impaired in older sedentary hypertensive men when the confounding effects of cardiovascular disease, diabetes, and dyslipidemia are controlled. Plasma concentrations of tissue-type plasminogen activator antigen and activity as well as plasminogen activator inhibitor-1 antigen and activity were measured under resting conditions in 12 hypertensive (69.4 plus/minus 1.4 years) and 11 normotensive (65.2 plus/minus 1.3 years) older men. The hypertensive and normotensive subjects had similar anthropometric and metabolic characteristics. There were no significant differences between the hypertensive and normotensive men in tissue-type plasminogen antigen (7.3 plus/minus 0.5 versus 6.1 plus/minus 0.6 ng/mL) and activity (1.8 plus/minus 0.3 versus 1.7 plus/minus 0.2 IU/mL) or plasminogen activator inhibitor-1 antigen (14.1 plus/minus 2.3 versus 10.8 plus/minus 2.2 ng/mL) and activity (17.4 plus/minus 1.2 versus 17.5 plus/minus 1.8 arbitrary units [AU]/mL) levels. In addition, the molar concentration ratio of active tissue-type plasminogen activator to active plasminogen activator inhibitor-1 did not differ between the hypertensive (1:9.7 plus/minus 2.3 mmol/L) and normotensive (1:10.5 plus/minus 2.2 mmol/L) subjects, indicative of no impairment in fibrinolytic potential in either group. These results support the hypothesis that hypertension does not directly result in impaired fibrinolytic function in older adults. Furthermore, our findings suggest that abnormalities in fibrinolytic function in older hypertensive men are likely due to the primary effects of other metabolic disorders that usually accompany hypertension, such as hyperinsulinemia and dyslipidemia. (Hypertension. 1996;27:1053-1058.)

 



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