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Published on: September 22, 2020
Complement component C5a predicts restenosis after superficial femoral artery balloon angioplasty
Walter S Speidl1, Markus Exner, Jasmin Amighi
1Departments of Internal Medicine II, Medical University of Vienna, Austria. walter.speidl@meduniwien.ac.at
Insights
Superficial femoral artery angioplasty increases C5a levels, a marker of inflammation. Higher baseline C5a levels predict a greater risk of restenosis after the procedure.
Area of Science:
- Vascular Biology
- Immunology
- Interventional Cardiology
Background:
- Restenosis remains a significant complication following superficial femoral artery (SFA) balloon angioplasty (PTA).
- Inflammatory processes, including complement activation, are implicated in the development of post-angioplasty restenosis.
- C5a, a potent anaphylatoxin, is a key mediator in complement-driven inflammation.
Purpose of the Study:
- To determine if SFA balloon angioplasty elevates serum C5a levels.
- To assess whether baseline C5a levels can predict the risk of restenosis after SFA angioplasty.
Main Methods:
- Serum C5a antigen levels were measured in 131 patients before and 8 hours after successful SFA balloon angioplasty.
- Patients were monitored for a median of 10 months for restenosis, defined as >50% narrowing by duplex ultrasound.
Main Results:
- Median C5a levels significantly increased from baseline to 8 hours post-intervention (p<0.001).
- A significant association was found between higher baseline C5a levels (quartiles) and an increased risk of restenosis (p=0.0092).
- This association remained significant after adjusting for C-reactive protein, indicating independence from general inflammation.
Conclusions:
- Balloon angioplasty of the SFA leads to increased C5a levels.
- Elevated baseline C5a is a significant predictor of restenosis after SFA angioplasty.
- Targeting complement activation pathways, specifically C5a, may offer a therapeutic strategy to improve long-term patency rates.
Purpose:
To investigate whether balloon angioplasty of the superficial femoral artery (SFA) increases serum levels of C5a and whether C5a predicts risk of restenosis.
Methods:
C5a antigen was measured at baseline and 8 hours after intervention in 131 consecutive patients (76 women; median age 72 years) with intermittent claudication who underwent successful primary SFA balloon angioplasty. Patients were followed for a median 10 months [interquartile range (IQR) 6 to 14] for the occurrence of >50% restenosis by duplex ultrasound.
Results:
Median C5a levels increased significantly from 39.7 ng/mL (IQR 27.8 to 55.0) at baseline to 53.8 ng/mL (IQR 35.6 to 85.1, p<0.001) 8 hours post intervention. During the follow-up period, 70 (53%) patients developed restenosis. Increasing levels of C5a (quartiles) at baseline were significantly associated with an increased risk for restenosis (p=0.0092). Adjusted hazard ratios (95% confidence intervals) for restenosis with increasing quartiles of baseline serum C5a levels were 1.24 (0.60 to 2.58), 1.93 (0.95 to 3.93), and 2.08 (1.02 to 4.21), respectively, compared to the lowest quartile. This effect was independent of nonspecific inflammation as reflected by plasma levels of C-reactive protein.
Conclusion:
Inflammatory mechanisms play a major role in the development of restenosis after angioplasty. The complement component C5a exerts strong chemotactic and proinflammatory effects. Enhanced complement activation prior to PTA, as measured by higher levels of C5a, was significantly associated with restenosis after SFA balloon angioplasty. Pathways of complement inhibition thus may be worth investigating with respect to improving patency rates.
