INHIBITORS OF THE HEMOSTASIS AND RELATED SYSTEMS IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION OR UNSTABLE ANGINA-PECTORIS

Citation
Hm. Hoffmeister et al., INHIBITORS OF THE HEMOSTASIS AND RELATED SYSTEMS IN PATIENTS WITH ACUTE MYOCARDIAL-INFARCTION OR UNSTABLE ANGINA-PECTORIS, Fibrinolysis, 9, 1995, pp. 104-108
Citations number
19
Categorie Soggetti
Hematology
Journal title
ISSN journal
02689499
Volume
9
Year of publication
1995
Supplement
1
Pages
104 - 108
Database
ISI
SICI code
0268-9499(1995)9:<104:IOTHAR>2.0.ZU;2-M
Abstract
Background: alterations of the hemostatic and fibrinolytic systems are known in patients with acute coronary syndromes. Objective: to invest igate the meaning of several inhibitors of these systems in patients w ith acute myocardial infarction (n = 20) and unstable angina pectoris (n = 21). Methods: repeated venous blood sampling was performed during the first 10 days after admission, Plasma inhibitors were measured us ing chromogenic substrate tests, Data were compared with controls (n = 25). Results: the C-1-esterase inhibitor did not show a significant d ifference to the controls, but in patients with unstable angina pector is a slight intraindividual increase during the follow-up was observed , az-macroglobulin in contrast was transiently reduced in comparison w ith the controls (p < 0.05) in patients with unstable angina pectoris, whereas no significant alterations were found in patients with acute myocardial infarction, alpha(1)-antitrypsin increased in both groups s ignificantly during the observation period indicating an acute phase r eaction, Antithrombin III was slightly decreased in patients with acut e coronary syndromes during the 10 day follow-up, No significant alter ations were found in alpha(2)-antiplasmin and protein C levels. Conclu sion: our results indicate that besides the known alterations of the p lasminogen activator inhibitor in the fibrinolytic system the other in hibitor systems are only slightly involved, The borderline alterations indicate consumption of some of the inhibitors due to the known activ ation of thrombin generation or the kallikrein-kinin system, but do no t indicate that an inhibitor deficiency is a reason for the activation of the coagulation in acute coronary syndromes.