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The fibrinolytic system is not impaired in older men with hypertension
C A DeSouza1, D R Dengel, M A Rogers
1Department of Kinesiology, University of Maryland, College Park, USA. desouzac@stripe
Insights
Hypertension does not directly impair the fibrinolytic system in older men. This study found no differences in fibrinolytic function between hypertensive and normotensive individuals when controlling for other metabolic factors.
Area of Science:
- Cardiovascular Science
- Gerontology
- Thrombosis Research
Background:
- The fibrinolytic system's impairment is linked to increased atherothrombosis risk in older hypertensive adults.
- Previous studies lacked control for confounding metabolic factors, obscuring hypertension's independent effect.
Purpose of the Study:
- To investigate if hypertension directly impairs the fibrinolytic system in older men, independent of other metabolic risk factors.
- To test the hypothesis that the fibrinolytic system is not impaired in older sedentary hypertensive men when cardiovascular disease, diabetes, and dyslipidemia are controlled.
Main Methods:
- Measured plasma concentrations of tissue-type plasminogen activator (t-PA) antigen and activity.
- Measured plasminogen activator inhibitor-1 (PAI-1) antigen and activity in resting older hypertensive and normotensive men.
- Controlled for confounding effects of cardiovascular disease, diabetes, and dyslipidemia.
Main Results:
- No significant differences were observed in t-PA or PAI-1 antigen and activity levels between hypertensive and normotensive groups.
- The ratio of active t-PA to active PAI-1, indicating fibrinolytic potential, was similar in both groups.
- Anthropometric and metabolic characteristics were comparable between the hypertensive and normotensive subjects.
Conclusions:
- Hypertension does not appear to directly cause impaired fibrinolytic function in older adults.
- Abnormalities in fibrinolytic function in older hypertensive men are likely attributable to co-existing metabolic disorders like hyperinsulinemia and dyslipidemia.
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.