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.
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Oltrona, L., Merlini, P.A., Savonitto, S. et al. Lack of Correlation Between Activation of Hemostatic Mechanism and Inflammation in Unstable Angina Pectoris. J Thromb Thrombolysis 5, 169–173 (1998). https://doi.org/10.1023/A:1008890314994
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DOI: https://doi.org/10.1023/A:1008890314994