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Hypothesis-generating for eosinophil role in late stent events; prospective trials needed before any clinical implications.
In-stent restenosis (ISR) and stent thrombosis are the main adverse reactions to coronary stent implantation, where an important role is played by individual susceptibility, along with procedural and stent-related factors [1]. In particular, the individual inflammatory reaction profoundly affects vessel response to the implanted stent. In the bare-metal stent (BMS) era, many studies suggested that C-reactive protein levels were able to predict the risk of ISR, while its role in predicting stent thrombosis was less established [1]. Drug-eluting stents (DES) have abated ISR rates occurring in the classical 1-year window, but new concern is emerging regarding late restenosis and thrombosis [2]. Interestingly, in this setting, baseline inflammation as assessed by C-reactive protein levels has been associated with stent thrombosis but not to ISR [3]. Along with common inflammatory pathways involving neutrophils, monocytes and lymphocytes, a new role is emerging for allergic inflammation involving eosinophils in determining the clinical outcome after DES implantation. Indeed, the pathogenesis of late events seems to be related to delayed healing and to allergic reactions to polymers, a process in which eosinophils play an important role [4]. Of note, a possible role for eosinophils in ISR and stent thrombosis has also been reported for BMS [5,6]. In addition to histological studies, the potential role of an allergic reaction to implanted stents also derives from studies utilizing patch test or, more recently, serum levels of eosinophil cationic protein (ECP), a marker of eosinophil activation.
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Crea et al. (2011) studied this question.
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