SHORT-TERM ACE-INHIBITION MAY INFLUENCE EXERCISE-INDUCED CHANGES IN HEMOSTASIS IN HEALTHY-SUBJECTS

Citation
D. Prisco et al., SHORT-TERM ACE-INHIBITION MAY INFLUENCE EXERCISE-INDUCED CHANGES IN HEMOSTASIS IN HEALTHY-SUBJECTS, Fibrinolysis & proteolysis, 11(4), 1997, pp. 187-192
Citations number
28
Categorie Soggetti
Hematology,"Medicine, Research & Experimental
Journal title
ISSN journal
13690191
Volume
11
Issue
4
Year of publication
1997
Pages
187 - 192
Database
ISI
SICI code
0268-9499(1997)11:4<187:SAMIEC>2.0.ZU;2-D
Abstract
Experimental studies have indicated that the renin-angiotensin system may regulate plasminogen activation and fibrinolysis and that angioten sin-converting enzyme (ACE) inhibitors are able to reduce the rate of myocardial infarction, possibly by interfering with haemostatic system . However, no data are available on the effect of ACE inhibition on ha emostasis in healthy subjects. The aim of this study was to evaluate t he effects of short-term ACE inhibition on haemostasis, both in baseli ne conditions and after a standardized exercise stress test in healthy subjects. Ten male control subjects (age 25-40 years) were enrolled i n a randomized, double blind, placebo-controlled crossover study. They assumed enalapril 20 mg or placebo once daily for 7 days, then, after a 15-day washout period, treatments were crossed. Treadmill stress te st was performed before and after each 7-day treatment period. Blood s ampling for fibrinolysis and coagulation studies were performed before exercise and after maximal exercise. The exercise-induced decrease in ELT and plasminogen activator inhibitor-1 and the increase in tissue plasminogen activator were more marked after enalapril than after plac ebo. No differences were seen in signs of exercise-induced clotting ac tivation. These data indicate that a short-term treatment with enalapr il in healthy subjects is able to affect fibrinolysis response to a ph ysiological stimulation such as physical effort. These results may be of help in the study of complex relationships among ACE inhibition, ha emostasis and reduction in myocardial infarction.