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Hypertension. 1996;27:1053-1058

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(Hypertension. 1996;27:1053-1058.)
© 1996 American Heart Association, Inc.


Articles

The Fibrinolytic System Is Not Impaired in Older Men With Hypertension

Christopher A. DeSouza; Donald R. Dengel; Marc A. Rogers; Kim Cox; Richard F. Macko

From the Department of Kinesiology, University of Maryland, College Park (C.A.D., M.A.R.), and Division of Gerontology, Department of Medicine (D.R.D., R.F.M.) and Department of Neurology (K.C., R.F.M.), University of Maryland Medical School and Baltimore Veterans Affairs Medical Center Geriatric, Research, Education, and Clinical Center, Baltimore.

Correspondence to Christopher DeSouza, PhD, University of Colorado, Department of Kinesiology, Campus Box 354, Boulder, CO 80309. E-mail desouzac@stripe.Colorado.EDU.

Abstract 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±1.4 years) and 11 normotensive (65.2±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±0.5 versus 6.1±0.6 ng/mL) and activity (1.8±0.3 versus 1.7±0.2 IU/mL) or plasminogen activator inhibitor–1 antigen (14.1±2.3 versus 10.8±2.2 ng/mL) and activity (17.4±1.2 versus 17.5±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±2.3 mmol/L) and normotensive (1:10.5±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.


Key Words: fibrinolytic system • aging • alteplase




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