Histamine induced coronary artery spasm, fish consumption and Kounis syndrome

Kounis, Nicholas G.; Patsouras, Nicholas; Grapsas, Nicholas; Hahalis, George

doi:10.1016/j.ijcard.2015.05.038

Cited by 192 publications

(290 citation statements)

References 22 publications

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“…However, the detailed description of the "allergic angina syndrome" as coronary spasm, which represents a manifestation of endothelial dysfunction or microvascular angina and progresses to allergic acute myocardial infarction, was not described until 1991 [7].…”

Section: Historical Backgroundmentioning

confidence: 99%

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

Kounis¹

2016

Clinical Chemistry and Laboratory Medicine (CCLM)

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Kounis syndrome has been established as a hypersensitivity coronary disorder induced by various conditions, drugs, environmental exposures, foods and coronary stents. Allergic, hypersensitivity, anaphylactic and anaphylactoid reactions are associated with this syndrome. Vasospastic allergic angina, allergic myocardial infarction and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells constitute are the three reported, so far, variants of this syndrome. Apart from coronary arteries, it affects the cerebral and mesenteric arteries. Its manifestations are broadening and its etiology is continuously increasing. Kounis syndrome is a ubiquitous disease which represents a magnificent natural paradigm and nature's own experiment in a final trigger pathway implicated in cases of coronary artery spasm and plaque rupture. Kounis syndrome seems to be not a rare disease but an infrequently diagnosed clinical entity which has revealed that the same mediators released from the same inflammatory cells are also present and in acute coronary events of non allergic etiology. These cells are not only present in the culprit region before plaque erosion or rupture but they release their contents just before an actual coronary event. Therefore, awareness of etiology, epidemiology, pathogenesis and clinical manifestations seems to be important for its prognosis, diagnosis, treatment, prevention.

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Section: Historical Backgroundmentioning

confidence: 99%

Kounis syndrome: an update on epidemiology, pathogenesis, diagnosis and therapeutic management

Kounis¹

2016

Clinical Chemistry and Laboratory Medicine (CCLM)

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322

421

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“…Kounis hypersensitivity-associated thrombotic syndrome and stent thrombosis Kounis syndrome was described more than 25 years ago (28) and has been defined as the coincidental occurrence of chest pain, chest discomfort, dyspnea, faintness, nausea, vomiting, syncope, pruritus, urticaria, hypotension, diaphoresis, pallor, palpitations and bradycardia with conditions associated with mast cell activation including allergic, hypersensitivity, anaphylactic or anaphylactoid episodes. 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.…”

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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“…Though uncommon, the systemic manifestations include anaphylaxis, dyspnea, bronchospasm, generalized edema, vasculitis, acute renal failure, neuritis, encephalitis, and serum sickness. 3 Acute coronary syndrome after hymenoptera stings is rare and seldom reported. 3 In 1991, Kounis et al described the syndrome of allergic angina 3 as the occurrence of acute coronary syndrome with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults due to allergic hypersensitivity reactions.…”

Section: Discussionmentioning

confidence: 99%

“…3 Acute coronary syndrome after hymenoptera stings is rare and seldom reported. 3 In 1991, Kounis et al described the syndrome of allergic angina 3 as the occurrence of acute coronary syndrome with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults due to allergic hypersensitivity reactions. Numerous causes such as hymenoptera sting, viper venom, food allergy, idiopathic anaphylaxis, mastocytosis, and serum sickness, and drugs such as NSAIDS, contrast media, antibiotics, and antineoplastic drugs capable of causing Kounis syndrome have been documented.…”

Section: Discussionmentioning

confidence: 99%

“…Numerous causes such as hymenoptera sting, viper venom, food allergy, idiopathic anaphylaxis, mastocytosis, and serum sickness, and drugs such as NSAIDS, contrast media, antibiotics, and antineoplastic drugs capable of causing Kounis syndrome have been documented. 3 This immune mediated injury is postulated to be triggered by mast cell activation and degranulation induced by IgE or non-IgE mechanism. The release of vasoactive inflammatory mediators such as histamine, serotonin, neutral proteases, arachidonic acid metabolites (thromboxane and leukotrines), and various cytokines and chemokines cause vasospasm, platelet and …”

Section: Discussionmentioning

confidence: 99%

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