Transmyocardial fibrinolytic activity in patients with unstable angina pectoris.

OBJECTIVES: This study was performed to investigate local (transmyocardial) fibrinolytic activity in patients with unstable angina.

BACKGROUND: Previous studies have reported decreased intrinsic fribrinolytic activity-increased systemic plasminogen activator inhibitor-1 (PAI-1) activity and/or decreased systemic tissue plasminogen activator (t-PA) activity-in patients with acute myocardial infarction. In contrast, the role of intrinsic fibrinolytic activity in patients with unstable angina is not well understood.

METHODS: We studied 67 consecutive patients (52 men and 15 women, aged 38-82 years) undergoing cardiac catheterization for chest pain within 24 h of acute presentation: 17 with unstable angina, 33 with stable angina, and 17 with atypical chest pain with angiographically normal coronary arteries. In each, blood samples were obtained simultaneously from the aorta and coronary sinus for measurement of t-PA and PAI-1 activities.

RESULTS: There was no difference in coronary sinus or systemic (aortic) t-PA activity among the three groups. The coronary sinus t-PA activity was 0.092 +/- 0.054, 0.088 +/- 0.038, and 0.080 +/- 0.050 IU/ml in the control, unstable angina, and stable angina groups, respectively [not significant (NS)], and the aortic t-PA activity was 0.114 +/- 0.053, 0.099 +/- 0.057, and 0.090 +/- 0.056 IU/ml in the control unstable angina, and stable angina groups, respectively (NS). Similarly, there was no difference in coronary sinus or systemic (aortic) PAI-1 activity among the three groups: the coronary sinus PAI-1 activity was 8.2 +/- 2.0, 7.4 +/- 2.0, and 8.0 +/- 2.5 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). The aortic PAI-1 activity was 7.8 +/- 2.1, 7.2 +/- 1.4, and 8.0 +/- 1.8 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS).

CONCLUSIONS: Although it has been suggested that alterations in local (transmyocardial) t-PA and PAI-1 activities may be of pathophysiologic importance in the genesis of unstable angina, our data show no difference in transmyocardial fibrinolytic activity in patients with unstable angina, stable angina, and noncardiac chest pain.