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Thrombosis and intrinsic fibrinolysis in percutaneous transluminal angioplasty
B Jørgensen1, J D Nielsen, P Helligsø
1Vascular Surgery Unit, Skejby Hospital, Aarhus University Hospital, Denmark.
Insights
Percutaneous transluminal angioplasty (PTA) activates coagulation and fibrinolysis, increasing thrombus formation. Standard heparin doses do not prevent thrombosis and can cause bleeding complications after femoropopliteal PTA.
Area of Science:
- Vascular Biology
- Hemostasis and Thrombosis
- Interventional Cardiology
Background:
- Femoropopliteal artery lesions often require percutaneous transluminal angioplasty (PTA).
- The impact of PTA on coagulation and fibrinolysis in claudicants is not fully understood.
- Understanding these hemostatic changes is crucial for optimizing patient outcomes.
Purpose of the Study:
- To investigate the dynamic changes in coagulation and fibrinolysis markers following PTA in patients with femoropopliteal artery lesions.
- To assess the relationship between these markers and the occurrence of thrombus formation or bleeding complications.
- To evaluate the efficacy of conventional heparin administration in managing hemostatic balance post-PTA.
Main Methods:
- 14 claudicants undergoing femoropopliteal PTA were studied.
- Peripheral blood samples were analyzed for cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (t-PA) antigen, fibrinopeptide A (FPA), and plasminogen activator inhibitor-1 (PAI-1) activity.
- Measurements were taken at baseline and at various time points after PTA.
- Heparin dosage and bleeding complications were recorded.
Main Results:
- PTA significantly increased XL-FDP and t-PA levels, indicating thrombus formation and fibrinolytic activation.
- FPA and PAI-1 levels decreased post-PTA, with heparin showing a sparing effect on PAI-1 consumption.
- Higher heparin doses (>5600 IU) were associated with increased groin hematoma incidence.
- Patients with rethrombosis showed significantly higher XL-FDP and residual FPA levels compared to those with an uncomplicated course.
Conclusions:
- PTA of femoropopliteal lesions triggers both pro-coagulant and fibrinolytic responses, driven by thrombin activation.
- The balance between coagulation and fibrinolysis appears unstable post-PTA, potentially leading to thrombosis.
- Conventional heparinization strategies may be insufficient to prevent thrombosis and can increase bleeding risk, suggesting a need for alternative antithrombotic approaches.
Abstract:
Coagulation and fibrinolysis were investigated in 14 claudicants undergoing percutaneous transluminal angioplasty (PTA) for femoropopliteal artery lesions. Cross-linked fibrin degradation products (XL-FDP), tissue plasminogen activator (t-PA) antigen, fibrinopeptide A (FPA), and plasminogen activator inhibitor-1 (PAI-1) activity were measured in peripheral blood. XL-FDP and t-PA increased, and FPA and PAI-1 decreased significantly after angioplasty. XL-FDP increased from baseline 266 +/- 72 ng/ml to 481 +/- 239 ng/ml (p < 0.0005) 30 min after PTA, indicating mural thrombus formation in spite of the significant fall in FPA influenced by heparin. A groin haematoma developed after PTA in 4/6 patients, who received more than 5600 IU heparin and in 1/8 patients receiving smaller dosages. The alterations in PAI-1 showed no correlation with those of t-PA, whereas heparin had a sparing effect on PAI-1 consumption. These findings may indicate that PAI-1 acts as a thrombin inhibitor following deep vessel wall injury by angioplasty. In two patients, who had signs of rethrombosis on the next day, residual FPA was relatively high, XL-FDP peaked at 3530 +/- 1170 ng/ml, and t-PA increased by 2.6 +/- 1.0 ng/ml. The corresponding values in patients with an uncomplicated course were 406 +/- 89 ng/ml (p < 0.0001) and 0.1 +/- 0.5 ng/ml (p < 0.02). We conclude that thrombin promotes activation of coagulation and fibrinolysis in femoropopliteal PTA. Instability between these counteracting systems resulting in thrombosis is not prevented by conventional heparin administration at dosages causing bleeding complications.