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Published on: May 28, 2019
Cardiac release and kinetics of cytokines after elective bare metal coronary stenting
NourEddine ElMokhtari1, Sascha Zschernitz, Susanne Sebens
1Department of Cardiology, University Hospital Schleswig-Holstein, Campus Kiel, Schittenhelmstr. 12, Kiel 24105, Germany.
Insights
Percutaneous coronary intervention (PCI) causes cardiac release of interleukin-6 (IL-6) due to endothelial injury, not myocardial ischemia. This finding is crucial for understanding post-PCI inflammation and recovery.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Interventional Cardiology
Background:
- Cytokine release following cardiovascular procedures is not fully understood.
- Interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and tumor-necrosis-factor-α (TNF-α) are key inflammatory mediators.
- Assessing cytokine kinetics after coronary interventions is important for patient outcomes.
Purpose of the Study:
- To evaluate the cardiac release kinetics of IL-1ß, IL-6, and TNF-α after bare metal stent implantation.
- To differentiate between cytokine release due to myocardial ischemia versus endothelial injury post-PCI.
- To compare cytokine levels in patients undergoing PCI with a control group.
Main Methods:
- Prospective study comparing 10 patients with coronary intervention to 11 controls.
- Measurement of IL-1ß, IL-6, and TNF-α in coronary sinus and peripheral blood samples.
- Monitoring of myocardial ischemia using lactate metabolism and ECG.
Main Results:
- A significant increase in IL-6 was observed post-PCI, peaking at 6 hours.
- Higher IL-6 levels in the coronary sinus compared to peripheral veins indicated cardiac IL-6 release.
- No significant changes in IL-1ß or TNF-α were found in either group; myocardial ischemia was excluded.
Conclusions:
- Uncomplicated percutaneous coronary intervention (PCI) leads to significant cardiac release of IL-6.
- The observed IL-6 release is attributed to endothelial injury, not myocardial ischemia.
- These findings highlight the inflammatory response post-PCI and guide further research into managing post-procedural inflammation.
Abstract:
The study was designed to assess the cardiac release kinetics of the cytokines interleukin-1ß (IL-1ß), interleukin-6 (IL-6) and tumor-necrosis-factor-α (TNF-α) in patients with significant stenosis of the ramus interventricularis anterior. Ten patients were treated by bare metal stent implantation, 11 patients who underwent a diagnostic coronary angiography without intervention served as a control group. Cytokines paired blood samples were withdrawn from the coronary sinus and a peripheral vein immediately before and 1, 2, 6 h after the intervention. Myocardial ischemia was monitored by means of cardiac lactate metabolism and 12-lead electrocardiogram. After coronary intervention IL-6 gradually increased from a common baseline level of 1.34 ± 1.56 pg/ml to a maximum of 10.58 ± 5.7 pg/ml in the peripheral vein and 15.81 ± 6.98 pg/ml in the coronary sinus within 6 h with persistent higher levels in the coronary sinus indicating coronary IL-6 release. After 12 h the peripheral venous concentration of IL-6 returned to baseline levels. Neither in the study group for IL-1ß and TNF-α nor in the control group for any cytokine level significant changes were found. Myocardial ischemia was excluded in all patients. Uncomplicated percutaneous coronary intervention (PCI) was followed by a significant cardiac IL-6 release due to endothelial injury and not to myocardial ischemia.
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