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To assess whether activation of the thrombotic system may induce neutrophil degranulation in unstable angina (UA), we studied the time course of the intracellular index of myeloperoxidase (MPXI), a marker of neutrophil activation, in relation to levels of Thrombin-antithrombin III complexes (TAT) and of Fragment 1+2 (FI +2) as markers of activation of the coagulation system in 20 patients (pts) with UA and in 20 healthy volunteeres (N). Samples were taken on admission, and at 6, 24, 48 and 72 hours. Results (median and range): On admission no differences were found between UA and N in TAT e F1+2 values: TAT: 2.05 ng/ml (range 0.5/14.4) vs 2.1 ng/ml (range 1.05/4.2); F1+2: 0.83 nmol/1 (range 0.14/-1.65) vs 0.59 nmol/1 (range 0.41/0.98), conversely MPXI levels were significantly different in UA vs N: respectively -4 (range +5/-15) vs -1.3 (range +5.S/-7, p<0.01). During the study 11 episodes of elevation of TAT and/or F1 +2 (6 symptomatic and 5 asymptomatic) followed by at least one sample for MPXI were observed. No changes in MPXI values after the episodes of activation of the coagulation as compared to baseline values were observed (-3.5, range -11.4/1.2 vs -4.7, range -13.1/4.5 respectively). There was no correlation between MPXI and TAT, and MPXI and F[+2. Conclusions: Our data suggest that activation of the coagulation system doesn't elicit systemic neutrophil activation in unstable angina; this may suggests that a primary, yet unknown inflammatory cause, may be responsible for the neutrophil activation observed in unstable angina.

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