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Evidence for priming and activation of neutrophils early after coronary angioplasty
P G Steg1, C Pasquier, T P Huu
1Service de Cardiology, INSERM U294, Hôpital Bichat, Paris, France.
Insights
Percutaneous transluminal coronary angioplasty (PTCA) primes and activates neutrophils, indicated by increased oxidative response and plasma lactoferrin. This neutrophil activation, along with complement system changes, may contribute to post-angioplasty complications.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Interventional Cardiology
Background:
- Percutaneous transluminal coronary angioplasty (PTCA) causes arterial injury and ischemia.
- The impact of PTCA on neutrophil and complement system activation requires further elucidation.
Purpose of the Study:
- To investigate the potential for PTCA to induce neutrophil priming and activation.
- To assess the role of the complement system following PTCA.
Main Methods:
- Blood samples collected pre- and post-PTCA (n=7) and pre- and post-coronary angiography (n=7).
- Neutrophil priming assessed via ex vivo whole blood chemiluminescence.
- Neutrophil activation measured by plasma lactoferrin levels.
Main Results:
- PTCA significantly increased neutrophil chemiluminescence and plasma lactoferrin.
- Coronary angiography alone did not induce these changes.
- A mild decrease in complement factors (CH50, C3, C4, B factor) was observed after both procedures.
Conclusions:
- PTCA leads to neutrophil priming and activation, evidenced by enhanced oxidative response and increased lactoferrin.
- Mild complement system activation, possibly contrast-agent related, may contribute to neutrophil priming.
- Neutrophil activation post-PTCA might play a role in vasoconstriction, myocardial dysfunction, and inflammation.
Objectives:
Percutaneous transluminal coronary angioplasty (PTCA) induces deep arterial wall injury and transient ischaemia. The aim of this study was to demonstrate that PTCA could result in priming or activation of the neutrophils and the complement system.
Methods:
Blood was drawn from the coronary sinus before and immediately after PTCA in 7 patients and before and immediately after coronary angiography in 7 patients (to ensure that the changes observed after PTCA were not solely related to the angiographic procedure). Neutrophil priming was assessed ex vivo by whole blood chemiluminescence stimulated in vitro by formyl-methionyl-leucyl-phenylalanine, phorbol myristate and opsonized zymosan. Neutrophil activation was assessed by measurement of plasma lactoferrin.
Results:
Whole blood chemiluminescence increased after PTCA, regardless of the stimulus used, while it did not after arteriography. After PTCA, lactoferrin increased 2-fold (p < 0.02) whereas after arteriography a non-significant increase was observed. Neutrophil count and adherence properties were not modified by either PTCA or arteriography. Total haemolytic complement (CH50), C3, C4 and B factor decreased slightly (7 to 16%) after both PTCA and arteriography.
Conclusions:
Early after PTCA, the neutrophil oxidative response, assessed by stimulated whole blood chemiluminescence, increased, suggesting a "priming" effect of PTCA on neutrophils. In addition, plasma lactoferrin levels increased, indicating neutrophil activation. Finally, there was a mild global activation of the complement system, most likely related to the contrast agent, and which may play a role in the "priming" process. Neutrophil priming and activation may participate in several phenomena occurring after angioplasty such as enhanced vasoconstriction and post-ischaemic myocardial dysfunction. In addition, it may participate in triggering local inflammatory processes.