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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Merlini, P. Articles by Mannucci, P. Search for Related Content PubMed PubMed Citation Articles by Merlini, P. Articles by Mannucci, P. Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Activation of the hemostatic mechanism during thrombolysis in patients with unstable angina pectoris PA Merlini, D Ardissino, KA Bauer, L Oltrona, A Spinola, P Diotallevi, RD Rosenberg and PM Mannucci 2nd Division of Cardiology, Ca'Granda Niguarda Hospital, Milan, Italy. In patients with myocardial infarction, thrombolytic therapy induces a paradoxical activation of the hemostatic mechanism. In patients with unstable angina, the effect of thrombolysis on the coagulation cascade is unknown. We prospectively measured the plasma concentrations of prothrombin fragment 1 + 2 and fibrinopeptide A in consecutive patients with unstable angina randomized to receive placebo alone (n = 23), streptokinase 1,500,000 IU over 1 hour followed by a 48-hour placebo infusion (n = 21), or streptokinase 250,000 over 1 hour followed by a continuous infusion of 100,000 IU per hour over 48 hours (n = 20). All the patients received intravenous heparin for 72 hours. The plasma levels of the different markers were measured at baseline, 90 minutes, 24 hours, and 48 hours after the start of therapy. The median baseline plasma concentrations of prothrombin fragment 1 + 2 and fibrinopeptide A were similar in the three treatment groups. In comparison with placebo, an increase in plasma prothrombin fragment 1 + 2 and fibrinopeptide A, was observed after 90 minutes in the two groups receiving thrombolysis. After 24 and 48 hours, the prothrombin fragment 1 + 2 levels remained significantly higher only in the patients receiving the 48-hour streptokinase infusion. In patients with unstable angina, thrombolytic therapy induces an activation of the hemostatic mechanism, despite concomitant heparin administration; in those receiving a prolonged streptokinase infusion, the activation of coagulation persists for as long as the drug is administered. Volume 86, Issue 9, pp. 3327-3332, 11/01/1995 Copyright © 1995 by The American Society of Hematology CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. J. Szarka, E. G. Sihota, H. R. Habibi, and S.-L. Wong Staphylokinase as a Plasminogen Activator Component in Recombinant Fusion Proteins Appl. Envir. Microbiol., February 1, 1999; 65(2): 506 - 513. [Abstract] [Full Text]

	Copyright © 1995 by American Society of Hematology         Online ISSN: 1528-0020