Medline ® Abstracts for References 62,63
of 'Anaphylaxis: Emergency treatment'
Coronary hypersensitivity disorder: the Kounis syndrome.
Clin Ther. 2013 May;35(5):563-71. Epub 2013 Mar 13.
BACKGROUND: When allergy or hypersensitivity and anaphylactic or anaphylactoid insults lead to cardiovascular symptoms and signs, including acute coronary events, the result might be the recently defined nosologic entity Kounis syndrome. Vasospastic allergic angina, allergic myocardial infarction, and stent thrombosis with occluding thrombus infiltrated by eosinophils and/or mast cells are the 3 reported variants of this syndrome.
OBJECTIVE: The purpose of this review was to highlight and consolidate the recent literature on allergic angina and allergic myocardial infarction and to propose new therapeutic modalities for stabilizing mast cells.
METHODS: A search for current literature on the pathophysiology, causality, clinical appearance, variance, prevention, and treatment of Kounis syndrome was conducted.
RESULTS: Kounis syndrome is caused by inflammatory mediators such as histamine; neutral proteases, including tryptase, chymase, and cathepsin-D; arachidonic acid products; platelet-activating factor; and a variety of cytokines and chemokines released during the mast-cell activation. Platelets with Fcγreceptor (FcγR)Ι, FcγRII, FcεRI, and FcεRII also have a role in the activation cascade. The same mediators released from the similar inflammatory cells are involved in acute coronary events of nonallergic etiology. These cells are not only present in the involved region before plaque erosion or rupture but also release their contents just before an acute coronary event. Pro-inflammatory mediators similar to those found in Kounis syndrome are found in some cases with nonallergic etiology, suggesting that this is a more general problem. The acute coronary and cerebrovascular events in Kounis syndrome may be prevented by the inhibition of mast-cell degranulation. Substances and natural molecules that protect the mast-cell surface and stabilize the mast-cell membrane are emerging as novel agents in the prevention of acute coronary and other arterial events.
CONCLUSIONS: The 3 reported variants of Kounis syndrome-vasospastic allergic angina, allergic myocardial infarction, and stent thrombosis with occluding thrombus-are caused by inflammatory mediators. Agents that inhibit mast-cell degranulation may be efficacious in preventing the acute coronary and cerebrovascular events of Kounis syndrome.
Department of Medical Sciences, Patras Highest Institute of Education and Technology, Patras, Greece. firstname.lastname@example.org
Allergy and the cardiovascular system.
Triggiani M, Patella V, Staiano RI, Granata F, Marone G
Clin Exp Immunol. 2008;153 Suppl 1:7.
The most dangerous and life-threatening manifestation of allergic diseases is anaphylaxis, a condition in which the cardiovascular system is responsible for the majority of clinical symptoms and for potentially fatal outcome. The heart is both a source and a target of chemical mediators released during allergic reactions. Mast cells are abundant in the human heart, where they are located predominantly around the adventitia of large coronary arteries and in close contact with the small intramural vessels. Cardiac mast cells can be activated by a variety of stimuli including allergens, complement factors, general anesthetics and muscle relaxants. Mediators released from immunologically activated human heart mast cells strongly influence ventricular function, cardiac rhythm and coronary artery tone. Histamine, cysteinyl leukotrienes and platelet-activating factor (PAF) exert negative inotropic effects and induce myocardial depression that contribute significantly to the pathogenesis of anaphylactic shock. Moreover, cardiac mast cells release chymase and renin that activates the angiotensin system locally, which further induces arteriolar vasoconstriction. The number and density of cardiac mast cells is increased in patients with ischaemic heart disease and dilated cardiomyopathies. This observation may help explain why these conditions are major risk factors for fatal anaphylaxis. A better understanding of the mechanisms involved in cardiac mast cell activation may lead to an improvement in prevention and treatment of systemic anaphylaxis.
Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy. email@example.com