Lack of correlation between activation of hemostatic mechanism and inflammation in unstable angina pectoris

Luigi Oltrona, Fiera A. Merlini, Stefano Savonitto, Marco Broccolino, Gioachino Giarratana, Antonio Pezzano, Pier M. Mannucci, Diego Ardissino

Research output: Contribution to journalArticle

Abstract

In the acute phase of unstable angina, activation of the hemostatic mechanism is demonstrated by an increase in the plasma levels of markers of thrombin generation (prothrombin fragment 1 + 2) and thrombin activity (fibrinopeptide A). Increased concentrations of plasma C-reactive protein, an acute-phase reactant, have also been reported in patients with unstable angina. However, whether there is a correlation between the activation of the hemostatic mechanism and the acute-phase reaction of inflammation remains unclear. We measured the plasma levels of prothrombin fragment 1 + 2, fibrinopeptide A, and C-reactive protein in 91 patients consecutively hospitalized with recent-onset rest angina (Class IIIB Braunwald's classification), finding that they were above the normal limits in 48 (53%), 45 (49%), and 30 (33%) patients, respectively. There was no correlation between prothrombin fragment 1 + 2 and fibrinopeptide A (P = 0.34), prothrombin fragment 1 + 2 and C-reactive protein (P = 0.10), or fibrinopeptide A and C-reactive protein (P = 0.75). Plasma levels of prothrombin fragment 1 + 2 and fibrinopeptide A were both above normal levels in 32% of patients; 19% had both prothrombin fragment 1 + 2 and C-reactive protein, and 18% both fibrinopeptide A and C-reactive protein levels above the upper normal limits. All three markers were abnormally high in 11% of patients. According to the kappa cofficient test, the agreement between the elevation of the plasma concentrations of the markers was 'random.' In approximately half of the patients with acute unstable angina, there was an increase in the markers of the activation of the hemostatic mechanism and, in a smaller proportion, an increase in plasma C-reactive protein levels. The activation of the coagulation cascade and the acute-phase reaction of inflammation were infrequently associated in individual patients.

Original languageEnglish
Pages (from-to)169-173
Number of pages5
JournalJournal of Thrombosis and Thrombolysis
Volume5
Issue number2
DOIs
Publication statusPublished - 1998

Keywords

  • Hemostatic mechanism
  • Inflammation
  • Unstable angina pectoris

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine

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