Author + information
- Nicholas G. Kounis, MD, PhD⁎ ()
- ↵⁎Department of Medical Sciences, Patras Highest Institute of Education and Technology, Queen Olgas Square, 7 Aratou Street, Patras 26221, Greece
In their white paper, Holmes, Jr. et al. (1) do not refer to hypersensitivity coronary syndrome.
However, I strongly believe that stent thrombosis (ST) is principally a manifestation of Kounis hypersensitivity coronary syndrome (2), caused by an “antigenic complex” of nickel alloys, polymers, eluted drugs, and possibly concomitant oral antiplatelet drugs and environmental exposures. Thus far, all clinical reports and reported pathologic findings in all patients who have died of ST, and all animal studies and experiments, point toward hypersensitivity inflammation with infiltration of various interrelated and interacting inflammatory cells, including eosinophils, macrophages, T cells, and mast cells. Following are some examples (3–5):
• In patients who developed ST associated with generalized allergic reactions, induced by environmental causes, stents act like magnets attracting inflammatory cells and constitute the area of possible intracoronary mast cell and platelet activation in order to develop ST.
• In the Research on Adverse Drug Events and Reports project, definite ST cases showed peripheral eosinophilia and raised immunoglobulin E titers over 5 times normal, together with eosinophilic thrombus infiltration.
• In serum sickness–like reactions after sirolimus-eluting stent implantation, symptoms did not resolve after the discontinuation of clopidogrel and substitution with ticlopidine, but they resolved with prednisone. However, prednisone abolished symptoms despite aspirin and clopidogrel continuation.
• In occluded biliary stents, pathology revealed infiltration of eosinophils and lymphocytes compatible with nickel allergic reaction.
• In thrombus sections stained with hematoxylin and eosin, neutrophils and eosinophils were associated with stent apposition, suggesting an allergic hypersensitivity reaction.
• In sirolimus-eluting stents, localized coronary hypersensitivity vasculitis and acute myocardial infarction were induced from late ST.
• In patients who received stents and died of multivessel spasm, histologic findings revealed inflammatory cells in the intima and adventitia. Giemsa staining showed few scattered mast cells.
I wonder how many of us have noticed that manufacturers' information sheets accompanying the new generation of stents state clearly that they are contraindicated for use in patients with hypersensitivity to any stent component.
In conclusion, antigen-free stents should be implanted to avoid catastrophic ST.
- American College of Cardiology Foundation
- Holmes D.R. Jr..,
- Kereiakes D.J.,
- Garg S.,
- et al.
- Kounis N.G.,
- Kounis G.N.,
- Kouni S.N.,
- Soufras G.D.,
- Niarchos C.,
- Mazarakis A.
- Chen J.P.,
- Hou D.,
- Pendyala L.,
- Goudevenos J.A.,
- Kounis N.G.