Transient increase of plasma lipoprotein(a) in patients with unstable angina pectoris. Does lipoprotein(a) alter fibrinolysis?

It has been shown that lipoprotein(a) (Lp[a]) may interfere with the fibrinolytic system and that the Lp(a) level in an individual remains constant. To evaluate the effects of Lp(a) on the fibrinolytic system in patients with unstable angina, we measured plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, and the thrombin-antithrombin III complex. The latter is a marker of thrombin generation, and the alpha 2-plasmin inhibitor-plasmin complex is an indicator of plasminogen activation. Venous plasma samples were taken from 18 patients with unstable angina and 18 patients with stable exertional angina who had been matched for clinical variables. On admission, plasma levels of Lp(a) were significantly higher in patients with unstable angina than in those with stable exertional angina (319 +/- 193 mg/l versus 191 +/- 141 mg/l, respectively; p less than 0.05). On admission, plasma levels of the alpha 2-plasmin inhibitor-plasmin complex and of the thrombin-antithrombin III complex were also significantly higher in patients with unstable angina than in those with stable exertional angina (0.78 +/- 0.42 micrograms/ml and 3.6 +/- 1.3 ng/ml versus 0.41 +/- 0.13 micrograms/ml and 1.9 +/- 0.5 ng/ml, respectively; p less than 0.01). In nine of the 18 patients with unstable angina, serial changes of plasma levels of Lp(a), the alpha 2-plasmin inhibitor-plasmin complex, the thrombin-antithrombin III complex, and the acute-phase proteins C-reactive protein and alpha 1-antitrypsin were examined for 3 weeks after admission.(ABSTRACT TRUNCATED AT 250 WORDS)