Impaired Fibrinolytic Capacity and Tissue Plasminogen Activator Release in Patients with Restenosis after Percutaneous Transluminal Coronary Angioplasty (PTCA)

Abstract

SummaryTo assess the role of the fibrinolytic system in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA), we determined the components of this system in a retrospective study, including 16 patients with restenosis (gr. A) and 19 patients with long-term success (gr. B). In both groups at baseline fibrinolytic activity (FA) is unchanged, whereas tissue plasminogen activator antigen (tPA-Ag) is significantly increased (gr. A: 147.0%; gr. B: 139.8%; p <0.01). Fibrinolytic capacity (FC) and tPA-Ag release are significantly reduced in the restenosis group (FC: 46.5%, p <0.05; tPA-Ag release: 48.3%, p <0.01) compared to normal controls as well as to gr. B (FC: 84.3%, p <0.05; tPA-Ag release: 79.0%, p <0.05).Relating to the contact activation system, F XII (79.5%, p <0.05) is significantly, and F XI (82.3%) is clearly reduced in gr. A. Protein C (PC) is significantly elevated in gr. B (117.5%, p <0.05). There is a negative correlation between plasminogen activator inhibitor (PAI 1) and HDL-cholesterol (r = 0.37, p <0.05).It appears, that there is a typical pattern of defective fibrinolysis in patients with restenosis after PTCA and that this might be a pathogenetic factor in the development of restenosis.

Augmented Plasma Protein C Activity after Coronary Thrombolysis with Urokinase in Patients with Acute Myocardial Infarction

“…* rnent (UK). p < 0.05 vs. before urokinase treatpotentiating the activity of plasminogen acti vators [6,7], which is independent of protein S [10], Recent reports suggested the efficacy of protein C as an extrinsic antithrombotic agent [ l l-l 3] or as an agent to prevent reste nosis after percutaneous transluminal coro nary angioplasty [ 14],…”

Preclinical Restenosis Models: Challenges and Successes

“…This response to vessel wall injury is substantially different across species (Kirschstein et al, 1989;Mason and Read, 1971;Schwartz et al, 1992bSchwartz et al, , 1993, and different amounts of mural thrombus can be seen depending the animal model used. In the rat carotid and canine models, significant fibrin-rich thrombus is rarely if ever found.…”

“…However, dogs have high fibrinolytic activity (Mason and Read, 1971), markedly different from the human coagulation system (Kirschstein et al, 1989). In addition, the canine vessel wall produces only a thin neointima when compared with other animal models (Figure 2).…”

Plasma Plasminogen Activator Inhibitor-1, Tissue Plasminogen Activator and Serum Lipoprotein(a) after Reperf usion Therapy in Acute Myocardial Infarction: Comparison between Sequential and Direct Percutaneous Transluminal Coronary Angioplasty

“…Previous studies have demonstrated that plasma PAI-1 and t-PA derived from the vascular endothelial cells play important roles in thrombogenesis or thrombolysis, re spectively [7][8][9], It has also been noted that, once arterial injuries occur, the plasma levels of PAI-1 and t-PA change markedly [10], In our study, 4-24 h after PTCA plasma PAI-1 concen trations were significantly higher than control levels in group D. Similarly, 8-18 h after PTCA plasma t-PA levels were also significantly higher than control values. These changes seem to result from the injury of the endothelial …”