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Published on: January 28, 2020
Drug-eluting coronary stents mediate inflammation-associated protein signature in an experimental in vitro study
Vera Paar1, Xuanchao Feng2, Kristen Kopp1
1Department of Internal Medicine II, Paracelsus Medical University, Salzburg, Austria.
Insights
Drug-eluting stents (DES) can trigger inflammation by activating immune cells and releasing inflammatory proteins. Stent design, material, and drug coating influence this inflammatory response, with zotarolimus-eluting stents showing lower reactivity.
Area of Science:
- Biomedical Engineering
- Immunology
- Cardiovascular Research
Background:
- Drug-eluting stents (DES) are crucial for treating ischemic heart diseases but can cause late stent thrombosis.
- Thrombosis and inflammation are closely linked, involving inflammatory cell activation and cytokine release.
Purpose of the Study:
- To investigate the in vitro inflammatory response of human peripheral blood mononuclear cells (PBMCs) to various DES.
- To assess how DES structure, drug coating, and material influence inflammatory markers.
Main Methods:
- Isolated human PBMCs were incubated with different DES types for 48 hours.
- Cytokine, chemokine, cell adhesion molecule, and growth factor secretion were measured using ELISA.
- Inflammation-associated protein expression was analyzed.
Main Results:
- DES significantly increased the secretion of IL-1β, IL-6, IL-8, ICAM-1, ANG, and FGF-basic.
- Zotarolimus-eluting stents demonstrated the lowest inflammation-associated protein expression.
- Inflammatory reactions were dependent on DES size, material, and polymer coating type; thinner alloys showed a trend towards lower inflammation.
Conclusions:
- DES can potentially induce an increased inflammatory reaction.
- Understanding these inflammatory responses can guide the optimization of DES composition and drug selection for improved safety and efficacy.
Abstract:
Drug eluting stents (DES) are a first-line treatment for ischemic heart diseases. Due to their direct contact with the blood stream, late stent thromboses are a common complication. Thrombosis and inflammation are tightly linked to each other, and are characterized by the activation of inflammatory cells and the secretion of cytokines and chemokines. To date, the influence of DES on the activation of the inflammatory cascade and its corresponding players has not yet been investigated. We performed an in vitro study to observe any potential response of isolated human peripheral blood mononuclear cells (PBMCs) to the structure and drug-coating of different DES. PBMCs from healthy volunteers were incubated with different DES types for 48 h. We measured the secretion of cytokines and chemokines, as well as cell adhesion molecules, and selected growth factors by ELISA. DES were found to significantly increase the cytokine and chemokine secretion of IL-1β, IL-6, IL-8, and ICAM-1, as well as the growth factors ANG and FGF-basic. We further showed that zotarolimus presents with the lowest inflammation-associated protein expression. Our data further revealed that the inflammatory reaction is highly dependent on the DES size, material, and the polymer type of the DES coating. Finally, we tendentially showed that thinner alloys are associated with a lower inflammatory reaction. Our results indicate that DES may potentially lead to an increased inflammatory reaction, considering the different DES designs and properties. This would potentially help to further improve composition and drug selection.
