Thrombotic responses to coronary stents, bioresorbable scaffolds and the Kounis hypersensitivity-associated acute thrombotic syndrome

Abstract

Percutaneous transluminal coronary angioplasty with coronary stent implantation is a lifesaving medical procedure that has become, nowadays, the most frequent performed therapeutic procedure in medicine. Plain balloon angioplasty, bare metal stents, first and second generation drug-eluting stents, bioresorbable and bioabsorbable scaffolds have offered diachronically a great advance against coronary artery disease and have enriched our medical armamentarium. Stented areas constitute vulnerable sites for endothelial damage, endothelial dysfunction, flow turbulence, hemorheologic changes, platelet dysfunction, coagulation changes and fibrinolytic disturbances. Implant surface attracts several proteins such as albumin, fibronectin, fibrinogen, and complement that lead to complement system activation. Macrophages recognize the implant as foreign substance due to protein adsorption and its continuous presence results in macrophage differentiation and fusion into foreign body giant cells. Polymer coating, stent metallic platforms and the released drugs can act as strong antigenic complex that apply continuous, repetitive, persistent and chronic hypersensitivity irritation to the coronary intima. The concomitant administration of oral antiplatelet drugs and environmental exposures can induce hypersensitivity inflammation. A class of platelets, activated via high-affinity and low-affinity IgE hypersensitivity receptors FCγRI, FCγRII, FCεRI and FCεRII, can induce Kounis hypersensitivity-associated thrombotic syndrome inside the stented coronaries. Type III variant of this syndrome is diagnosed when coronary artery stent thrombosis is associated with thrombus infiltrated by eosinophils or mast cells and/or when coronary intima, media and adventitia adjacent to stent, is infiltrated by eosinophils or mast cells. Careful history of hypersensitivity reactions to all implanted materials and concomitant drugs with monitoring of inflammatory mediators as well as lymphocyte transformation studies to detect hypersensitivity must be undertaken in order to avoid disastrous consequences. Food and Drug Administration recommendations for coronary stent implantation should be applied also to bioresorbable scaffolds. Further studies with inert and non-allergenic implants are necessary.

Cinnamic aldehyde inhibits vascular smooth muscle cell proliferation and neointimal hyperplasia in Zucker Diabetic Fatty rats

“…Drug-eluting stents are currently the most effective therapy for restenosis as they inhibit all cellular proliferation and migration within the vessel, but their use increases the risk of thrombosis by preventing vessel reendothelialization [9]. Thus, emerging therapies aim to prevent the proliferation and migration of VSMC and fibroblasts after injury without inhibiting endothelialization.…”

Plaque Rupture-Induced Myocardial Infarction and Mechanical Circulatory Support in Alpha-Gal Allergy

“…Culprit components include the polymer coating, metallic platform, and the released drugs, which are thought to result in chronic and repetitive hypersensitivity irritation to the coronary intima [11]. This eventually results in attracting several proteins, mainly fibrinogen and complement, leading to complement system activation [11]. As such, this constitutes a variant of allergic acute coronary syndrome, manifesting as stent thrombosis, which is unlikely in our patient given the sequence of events.…”

“…Furthermore, stents themselves may act as antigenic stimuli and induce hypersensitivity reactions [11]. Culprit components include the polymer coating, metallic platform, and the released drugs, which are thought to result in chronic and repetitive hypersensitivity irritation to the coronary intima [11]. This eventually results in attracting several proteins, mainly fibrinogen and complement, leading to complement system activation [11].…”

Where Are the Secrets of Increased Thrombosis and Aneurysm Formation With the Current Bioresorbable Vascular Scaffolds Hidden?

“…1 It has the potential advantage of progressive early re-absorption and maintaining the cyclic pulsatility and vasomotion that could not be offered by the metallic drug-eluting stents (DES). However, scaffold remnants have been traced even 44 months after bioresorbable scaffold implantation, 2 and there is increasing evidence that aneurysm formation, restenosis and thrombosis are frequent with this technology.…”