Literature DB >> 8925580

Temporal relation between ischemic episodes and activation of the coagulation system in unstable angina.

L M Biasucci1, G Liuzzo, G Caligiuri, G Quaranta, F Andreotti, G Sperti, W van de Greef, A G Rebuzzi, C Kluft, A Maseri.   

Abstract

BACKGROUND: Although a major role of coronary thrombosis in the pathogenesis of unstable angina has been demonstrated, the results of a series of studies have suggested that activation of the hemostatic system may not be confined to ischemic episodes. The purpose of this study was to investigate the temporal relation between ischemic episodes and activation of the coagulation system in unstable angina. METHODS AND
RESULTS: Thrombin-antithrombin III (TAT) and prothrombin fragment 1 + 2 (F1 + 2) levels were measured in 13 patients during spontaneous ischemic episodes (time 0, 5, and 15 minutes and 1 hour) to evaluate the time course of the activation of the coagulation system associated with the development of ischemia (protocol A). TAT and F1 + 2 levels were also measured in 28 patients with unstable angina on admission to hospital (every 6 hours for 24 hours and daily for 3 days) to assess their temporal relation with ischemic episodes (protocol B). In protocol A, TAT and F1 + 2 levels were elevated in 10 of 13 patients (77%) in at least 1 sample. The median value of TAT showed a peak at 5 minutes and returned to baseline within 15 minutes (P < .05), consistent with its plasma half-life of 5 minutes, whereas the median value of F1 + 2 showed no significant changes, possibly because of its longer half-life, which tends to dampen sudden bursts of thrombin production. In protocol B, activation of the clotting system was found in 10 of 33 samples (30%) temporally related to ischemia and also in 23 of 150 (15%, P = .07) of those not temporally related to ischemia.
CONCLUSIONS: Our study demonstrates that patients with active unstable angina develop frequent bursts of thrombin production not necessarily associated with ischemic episodes and that, conversely, some ischemic episodes are not associated with evidence of thrombin activation.

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Year:  1996        PMID: 8925580     DOI: 10.1161/01.cir.93.12.2121

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  4 in total

1.  Thrombotic reactant markers in non-ST segment elevation acute coronary syndromes treated with either enoxaparin (low molecular weight heparin) or unfractionated heparin.

Authors:  E Gurfinkel; E Duronto; C Colorio; G Bozovich; M Cohen; B Mautner
Journal:  J Thromb Thrombolysis       Date:  1999-10       Impact factor: 2.300

2.  Platelet and Thrombin Activity Following Cardiac Catheterization Despite Treatment with Aspirin.

Authors: 
Journal:  J Thromb Thrombolysis       Date:  1998-09       Impact factor: 2.300

3.  Relationship between minor myocardial damage and inflammatory acute-phase reaction in acute coronary syndromes.

Authors:  Hans Martin Hoffmeister; Raila Ehlers; Evi Büttcher; Armin Steinmetz; Silke Kazmaier; Uwe Helber; Sebastian Szabo; Martin E Beyer; Ludger Seipel
Journal:  J Thromb Thrombolysis       Date:  2003-02       Impact factor: 2.300

4.  Interleukin-10 deficiency increases atherosclerosis, thrombosis, and low-density lipoproteins in apolipoprotein E knockout mice.

Authors:  Giuseppina Caligiuri; Mats Rudling; Véronique Ollivier; Marie-Paule Jacob; Jean-Baptiste Michel; Göran K Hansson; Antonino Nicoletti
Journal:  Mol Med       Date:  2003 Jan-Feb       Impact factor: 6.354

  4 in total

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