Acute Lipoprotein (a) Reduction after PCI and the Incidence of Restenosis: a Clinical Study

Abstract

Background: Lipoprotein (a) [Lp(a)] is a well-documented independent risk factor for Coronary Artery Disease (CAD) that also affects the lipid and coagulation systems. Nevertheless, the influence of Lp (a) on the manifestation of restenosis after Percutaneous Coronary Intervention (PCI) is not fully explored. We investigate Lp (a), fibrinogen, and plasminogen levels pre- and post-Percutaneous Coronary Intervention (PCI) to assess interaction of Lp (a) with the coagulation system. Methods: Patients with CAD and PCI with bare metal stents were recruited between August 1998 and June 1999. Blood samples to measure Lp (a), plasminogen, and fibrinogen were taken pre-PCI, immediately after PCI, and on days one and three after PCI. Patients were followed up after six months by scheduled Coronary Angiogram (CAG). Results: A total of 89 patients were recruited, 81 of which were examined by CAG, and 28 had restenosis after PCI (34.5%). Following PCI, patients with restenosis had a larger decrease in Lp (a) levels and fibrinogen neither of both had reached baseline by day three (Lp (a) p=0.008, fibrinogen p=0.0121). Conclusions: From the fact that neither Lp (a), nor fibrinogen, or plasminogen had returned to baseline levels by day three after PCI, we hypothesise that there may exist a bridge between Lp (a) and the thrombosis and fibrinolysis pathways at the site of vascular injury after PCI which promotes restenosis after PCI.