LACK OF CORRELATION BETWEEN ACTIVATION OF HEMOSTATIC MECHANISM AND INFLAMMATION IN UNSTABLE ANGINA-PECTORIS

In the acute phase of unstable angina, activation of the hemostatic me chanism is demonstrated by an increase in the plasma levels of markers of thrombin generation (prothrombin fragment 1+2) and thrombin activi ty (fibrinopeptide A). Increased concentrations of plasma C-reactive p rotein, an acute-phase reactant, have also been reported in patients w ith unstable angina. However, whether there is a correlation between t he activation of the hemostatic mechanism and the acute-phase reaction of inflammation remains unclear. We measured the plasma levels of pro thrombin fragment 1+2, fibrinopeptide A, and C-reactive protein in 91 patients consecutively hospitalized with recent-onset rest angina (Cla ss IIIB Braunwald's classification), finding that they were above the normal limits in 48 (53%), 45 (49%), and 30 (33%) patients, respective ly. There was no correlation between prothrombin fragment 1+2 and fibr inopeptide A (P = 0.34), prothrombin fragment 1+2 and C-reactive prote in (P = 0.10), or fibrinopeptide A and C-reactive protein (P = 0.75). Plasma levels of prothrombin fragment 1+2 and fibrinopeptide A were bo th above normal levels in 32% of patients; 19% had both prothrombin fr agment 1+2 and C-reactive protein, and 18% both fibrinopeptide A and C -reactive protein levels above the upper normal limits. Ail three mark ers were abnormally high in 11% of patients. According to the kappa co efficient test, the agreement between the elevation of the plasma conc entrations of the markers was ''random.'' In approximately half of the patients with acute unstable angina, there was an increase in the mar kers of the activation of the hemostatic mechanism and, in a smaller p roportion, an increase in plasma C-reactive protein levels. The activa tion of the coagulation cascade and the acute-phase reaction of inflam mation were infrequently associated in individual patients.