Kounis syndrome: A manifestation of drug-eluting stent thrombosis associated with allergic reaction to contrast material

Kogias, J.; Papadakis, Emmanouil; Tsatiris, Constantinos G.; Hahalis, George; Kounis, George N.; Mazarakis, Andreas; Batsolaki, Maria; Gouvelou-Deligianni, Georgia V.; Kounis, Nicholas G.

doi:10.1016/j.ijcard.2008.08.026

Cited by 46 publications

(25 citation statements)

References 15 publications

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“…Main pathophysiological mechanism is vasospasm of epicardial coronary arteries due to increased inflammatory mediators that are released during a hypersensitivity reaction [1]. The trigger may be drugs [2][3][4][5][6][7], chemicals [9], foreign bodies [10][11][12][13][14], environmental exposures [8,[24][25][26][27][28] or some other conditions that give rise to inflammatory mediator release [15]. Anaphylactic or anaphylactoid reactions can make clinical situation even more serious.…”

Section: Introductionmentioning

confidence: 99%

Kounis Syndrome secondary to cefuroxime axetil use in an asthmatic patient

Erkan

Güvenç

Poyraz

et al. 2009

International Journal of Cardiology

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Section: Introductionmentioning

confidence: 99%

Kounis Syndrome secondary to cefuroxime axetil use in an asthmatic patient

Erkan

Güvenç

Poyraz

et al. 2009

International Journal of Cardiology

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“…For example, allergic reactions from propyphenazone (37), contrast material (38), insect stings (39) and snake bites (40) were accompanied by in-stent thrombosis denoting that stents constitute the area of possible mast cell and platelet activation in order to cause Kounis syndrome. An astonishing event is that even an allergic reaction to clopidogrel (41), the drug that is given to prevent stent thrombosis, itself has induced stent thrombosis (42)!…”

Section: Causes Of Stent Thrombosismentioning

confidence: 99%

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

et al. 2017

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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.

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“…Indeed, susceptible individuals expressing a magnified mast cell degranulation effect may be per se more vulnerable to coronary artery spasm and plaque erosion or rupture [4]. This topic is an important one since patients affected by ischemic heart disease receiving stent implantation can be prone to hypersensitivity reactions from five potential antigens, namely nickel strut, polymer coating, eluted drug, clopidogrel and aspirin [10]. Some hypersensitivity cases have indeed been associated with implantation of drug eluting coronary stents [11][12][13] and between them a case of intra-stent thrombosis in a subject with allergy to larvae of fly carvaria [14].…”

Section: Discussionmentioning

confidence: 99%