Serum tryptase levels in acute coronary syndromes with ST elevation

Baldomà, Nuria; Cosmen, Cristina Rodríguez; Galinski, Susana Fernández; García, Luis Moltó; Gracia, Luis Recasens; Villén, Fernando Escolano

doi:10.1016/j.ijcard.2007.07.101

Cited by 14 publications

(11 citation statements)

References 8 publications

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“…[1][2][3][4][5][6][7][8][9][10][11][12][13][14] We present a case of recurrent acute myocardial infarction associated with an allergic reaction in an 83-year-old Italian woman. On July 1, 2008, an 83-year-old Italian woman was admitted to the emergency department with chest pain.…”

Section: Case Reportmentioning

confidence: 98%

Recurrent acute myocardial infarction and Kounis syndrome

Patanè¹,

Marte²,

Currò³

et al. 2010

International Journal of Cardiology

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Section: Case Reportmentioning

confidence: 98%

Recurrent acute myocardial infarction and Kounis syndrome

Patanè¹,

Marte²,

Currò³

et al. 2010

International Journal of Cardiology

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“…The cause of the above symptomatology has been attributed to Inflammatory mediators released via activation of mast cell and other interrelated and interacting inflammatory cells such as eosinophils, macrophages and T-lymphocytes. The culprit inflammatory mediators include histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines and chemokines released during the activation process (29)(30)(31). In Kounis hypersensitivity-associated thrombotic syndrome, platelets are activated via the high-affinity and low-affinity IgE hypersensitivity receptors FCγRΙ, FCγRII, FCεRI and FCεRII.…”

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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“…Some examinations are helpful to prove simultaneous occurrence of cardiac damage and allergic reaction and support the diagnosis. Laboratory tests such as measurement of serum cardiac enzymes, tryptase [4], and histamine, eosinophil number and total IgE level may be helpful [2]. It was reported that histological analysis of the aspirated thrombi by hematoxylin-eosin and Giemsa staining showed the presence of eosinophils and mast cells [5].…”

Section: Discussionmentioning

confidence: 99%

A case of Kounis syndrome associated with transcatheter arterial chemoembolization for hepatocellular carcinoma

Iyonaga

Ichiki

Watanabe

et al. 2015

Journal of Cardiology Cases

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Simultaneous occurrence of acute coronary syndrome and allergic reactions is known as Kounis Syndrome, which was described by Kounis and Zavras in 1991 [1]. Although the pathophysiology of Kounis syndrome is not completely understood, allergic reaction-induced coronary inflammation and vasospasm are suggested to play a role. Kounis syndrome is caused by various factors, such as foods, drugs, environmental exposures, and medical conditions, all of which induce allergic reactions. Allergens cause mast cell degranulation and several inflammatory mediators such as histamine, tryptase, chymase, neutral proteases, arachidonic acid products, platelet activating factor, and various cytokines and chemokines are released. These mediators cause coronary arterial spasm, plaque rupture, and thrombosis, resulting in acute coronary syndrome. We report a case of Kounis syndrome that was induced by transcatheter arterial chemoembolization (TACE) for the treatment of hepatocellular carcinoma (HCC). Two similar cases that we experienced are also reviewed. Case report A 79-year-old man with a history of HCC treatment by TACE was admitted to our hospital for another TACE. He had been treated with TACE for five times before without allergic reactions. His medical history was unremarkable except for essential hypertension with medication. There was no history of allergic diseases. And he had never complained of anterior chest pain suggestive of angina pectoris. Approximately 30 min after successful TACE with iopamidol, an iodinated contrast media, and ethylester of iodinated poppy-seed oil fatty acid injection, he complained of anterior chest pain and then lost consciousness. His systolic blood pressure was decreased to 40 mmHg, and his heart rate was 50 beats per minute. His spontaneous breathing stopped. We assisted his breathing with bag valve mask ventilation. Intravenous infusion of normal saline and dopamine (3.0 mg/min/kg) was

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Serum tryptase levels in acute coronary syndromes with ST elevation

Cited by 14 publications

References 8 publications

Recurrent acute myocardial infarction and Kounis syndrome

Recurrent acute myocardial infarction and Kounis syndrome

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

A case of Kounis syndrome associated with transcatheter arterial chemoembolization for hepatocellular carcinoma

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