The Evolving Role of Inflammatory Biomarkers in Risk Assessment After Stent Implantation

Abstract

The main adverse reactions to coronary stents are in-stent restenosis (ISR) and stent thrombosis. Along with procedural factors, individual susceptibility to these events plays an important role. In particular, inflammatory status, as assessed by C-reactive protein levels, predicts the risk of ISR after bare-metal stent implantation, although it does not predict the risk of stent thrombosis. Conversely, C-reactive protein levels fail to predict the risk of ISR after drug-eluting stent (DES) implantation, although they appear to predict the risk of stent thrombosis. Of note, DES have abated ISR rates occurring in the classical 1-year window, but new concern is emerging regarding late restenosis and thrombosis. The pathogenesis of these late events seems to be related to delayed healing and allergic reactions to polymers, a process in which eosinophils seem to play an important role by enhancing restenosis and thrombosis. The identification of high-risk individuals based on biomarker assessment may be important for the management of patients receiving stent implantation. In this report, we review the evolving role of inflammatory biomarkers in predicting the risk of ISR and stent thrombosis.

Comparative Analysis of Plaque Growth after Arterial Stent Implant with Anti-Inflammatory Chemokine and Serine Protease Inhibitors Treatment

“…Excess bleeding was not seen after treatment with either agent. The fact that there was no significant difference in adverse events and specifically thrombotic and hemorrhagic events would support prior studies form other researchers that have linked excess inflammation in stent implant areas with later stent thrombosis [7][8][9][10][35][36][37][38][39][40][41][42][43]. Specific or selective inflammatory cell responses werenot examined here and remain to be determined.…”

“…Acute thrombosis is reduced with dual antiplatelet therapy and acute post stent infarction may be reduced with high dose statin therapy [34]. However the most effective treatment, proven to reduce restenosis after angioplasty or stent implant is the use of bare metal stents when compared to balloon angioplasty alone or the use of drug eluting stents when compared to balloon angioplastyor BMS [7][8][9][10][35][36][37]. Multiple studies report correlations between acute and chronic inflammatory cell invasion and activation with restenosis as well as later stent thrombosis [7][8][9][10]38,39].…”

“…However the most effective treatment, proven to reduce restenosis after angioplasty or stent implant is the use of bare metal stents when compared to balloon angioplasty alone or the use of drug eluting stents when compared to balloon angioplastyor BMS [7][8][9][10][35][36][37]. Multiple studies report correlations between acute and chronic inflammatory cell invasion and activation with restenosis as well as later stent thrombosis [7][8][9][10]38,39]. Agents targeting inflammatory reactions have been reported in preclinical animal studies and small clinical trials to alter restenosis after stent implant but this work remains investigational [38][39][40][41][42][43].…”

“…Acute stent thrombosis has high associated morbidity and mortality. While the advent of BMS reduced the incidence of restenosis when compared to balloon angioplasty and coated DES stents further reduced restenosis, both types of stents are associated with persistent risk of restenosis and thrombosis, particularly in the absence of adequate antiplatelet therapy [10].…”

“…Circulating chemokines, e.g. monocyte chemoattractant protein-1 (MCP-1, MIP1α, CCR2, CX3CR1) and also the serine (uPA, tPA) and the matrix metalloproteases (MMP2, MMP9) and the serpin plasminogen activator inhibitor-1 (PAI-1) [9,10] are increased in unstable angina, non ST elevation MI (NSTEMI) and immediately after stent implant [18,19]. PAI-1 is seen in both increased and decreased restenosis [19,20].…”