Key result
Allergic inflammation effector cells contribute to CAD pathogenesis and adverse events after stent implantation.
Highlights the unrecognized role of allergic inflammation in coronary artery disease and post-stent adverse events, pointing to novel therapeutic targets.
Allergic inflammation may contribute to CAD and stent complications; leaves open whether targeting these pathways improves outcomes.
Inflammation is an important player both for the initiation and progression of coronary artery disease and for coronary plaque instability. Moreover, inflammation contributes to stent thrombosis and in-stent restenosis after percutaneous coronary intervention. In the past several decades, most studies evaluated the involvement of cellular effectors of classic inflammatory responses, such as monocytes/macrophages, neutrophils, and T cells. Yet, besides classic inflammation, mounting evidence derived from both experimental and clinical studies suggests an important, often unrecognized, role for effector cells of allergic inflammation in both the pathogenesis of coronary artery disease and adverse events following stent implantation. In this review, we discuss the role of effector cells of allergic inflammation in the setting of coronary artery disease progression and instability, and in the occurrence of adverse events following stent implantation, as well. Moreover, we discuss possible therapeutic approaches targeting different specific pathways of allergic inflammatory activation.
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Niccoli et al. (2018) conducted a review in Coronary Artery Disease. Effector cells of allergic inflammation play an important role in the pathogenesis of coronary artery disease and adverse events following stent implantation.
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