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A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Percutaneous coronary intervention triggers a systemic inflammatory response in patients treated for in-stent
M Kozinski1, A Krzewina-Kowalska, J Kubica
1Department of Cardiology and Internal Diseases, The Ludwik Rydygier Medical University in Bydgoszcz, Sklodowskiej-Curie 9, 85-094 Bydgoszcz, Poland. jkubica@amb.bydgoszcz.pl
Insights
Percutaneous coronary intervention (PCI) triggers a systemic inflammatory response in patients with in-stent restenosis (ISR), differing from stable (SA) and unstable angina (UA) patients. Higher preprocedural tumor necrosis factor alpha (TNF-alpha) in ISR patients suggests a role in restenosis.
Area of Science:
- Cardiology
- Immunology
- Interventional Cardiology
Background:
- The systemic inflammatory response post-percutaneous coronary intervention (PCI) may influence long-term outcomes in stable (SA) and unstable angina (UA) patients.
- Understanding the inflammatory response in in-stent restenosis (ISR) is crucial for managing restenosis after angioplasty.
Purpose of the Study:
- To investigate the presence, pattern, and magnitude of systemic inflammation following balloon angioplasty in ISR patients.
- To compare the inflammatory response in ISR patients with that observed in SA and UA patients undergoing PCI.
Main Methods:
- Prospective study involving 80 patients: 59 SA, 10 UA, and 11 ISR.
- Measurement of C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor alpha (TNF-alpha), and interleukin 10 (IL-10) before and after the procedure at multiple time points.
- Comparison of inflammatory markers between SA/UA patients undergoing stenting and ISR patients undergoing balloon angioplasty alone.
Main Results:
- Comparable CRP and SAA response patterns were observed in ISR and SA groups, with a higher magnitude in UA patients.
- CRP and SAA levels peaked at 24 hours post-procedure, correlating with baseline levels.
- Preprocedural TNF-alpha was elevated in ISR patients, with a further increase post-PCI, unlike SA and UA patients who showed delayed increases.
Conclusions:
- PCI induces a systemic inflammatory response in ISR patients, with distinct patterns compared to SA and UA patients.
- Elevated preprocedural TNF-alpha and its post-PCI increase in ISR patients warrant further investigation for a potential role in the restenosis process.
Objective And Design:
It is believed that the magnitude of the systemic inflammatory response induced by percutaneous coronary intervention (PCI) impacts on the long-term outcomes in patients with stable angina (SA) and unstable angina (UA). We aimed to determine whether an inflammatory response appears in in-stent restenosis (ISR) patients undergoing balloon angioplasty and to assess its pattern and magnitude in relation to SA and UA subjects.
Subjects:
80 patients (59 with SA, 10 with UA, 11 with ISR) were enrolled into the prospective study.
Treatment:
SA and UA patients undergoing single vessel coronary balloon angioplasty followed by stenting versus ISR subjects in whom only balloon angioplasty was performed.
Methods:
C-reactive protein (CRP), serum amyloid A (SAA), tumor necrosis factor alpha (TNF-alpha) and interleukin 10 (IL-10) were measured in blood samples collected before and 6, 24 h and 1 month after the procedure.
Results:
A comparable pattern of inflammatory response in terms of CRP and SAA concentrations in subjects undergoing PCI due to ISR and SA was discovered while in unstable patients its magnitude was substantially higher. CRP and SAA levels increased significantly in each group with the peak value at 24 h and the baseline levels remarkably correlated with the highest markers' concentrations. In contrast, preprocedural TNF-alpha concentrations were higher in ISR group when compared with SA and UA patients. Additionally, in ISR group a twofold increase in their values of borderline significance at 6 h was noted. SA and UA subjects were found to have significantly lower TNF-alpha levels at 6 and 24 h after the intervention though the marker concentrations markedly increased with peak values at 1 month. The levels of IL-10 did not differ at any time point between the groups.
Conclusions:
We suggest that PCI triggers a systemic inflammatory response in patients with ISR and considerable differences in its pattern when compared with SA and UA patients were demonstrated. Moreover, a high preprocedural TNF-alpha level and its increase provoked by PCI in the ISR group warrant the need for further investigation of its possible involvement in the restenosis process.
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