THROMBOSIS-RELATED MARKERS IN UNSTABLE ANGINA-PECTORIS

While thrombus formation has been implicated in the pathogenesis of unstable angina, the value of thrombus-related markers for distinguishing unstable from stable angina is not well defined. Fibrin D-dimer and plasminogen activator inhibitor were prospectively analyzed in the peripheral blood of 46 patients (26 with unstable angina and 20 with stable angina or normal coronary arteries). Baseline blood samples were drawn within 24 h after rest pain in patients with unstable angina and in 19 of these 26 patients in < 6 h. In patients with unstable angina, mean +/- SD (median) values for fibrin D-dimer and plasminogen activator inhibitor values measured 0.09 +/- 0.06 (0.07) mu-g/ml and 9.1 +/- 9.6 (5.9) IU, respectively, compared to 0.11 +/- 0.10 (0.05) mu-g/ml and 5.5 +/- 1.9 (5.0) IU/ml, in patients in the control group (p = NS for all comparisons between the two groups). Recurrent in-hospital pain, coronary anatomy and need for intervention showed no relation to the levels of these markers. In 19 additional patients (9 with unstable angina and 10 control patients) samples from the coronary sinus and the peripheral blood were also analyzed. Again, in patients with unstable angina all samples were drawn < 24 h after rest pain; in six of nine patients samples were drawn in < 6 h. A coronary sinus to peripheral blood gradient for either of these markers could not be demonstrated. The differences between peripheral and coronary sinus D-dimer and plasminogen activator inhibitor concentrations were also similar in patients with unstable angina and control patients. In conclusion, peripheral blood and even coronary sinus samples of D-dimer and plasminogen activator inhibitor could not distinguish patients with unstable angina from control patients. Although plaque disruption with thrombus formation appears to be the most important pathogenetic mechanism in unstable angina pectoris, the amount of thrombus may be too small to be detected by these assays. In addition, ongoing acute thrombus formation with a resultant decrease in coronary perfusion may be unimportant as a mechanism of rest pain.