George N. Kounis

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

Stent components acting as potential antigens and promoting intracoronary mast cell activation can lead to catastrophic intrastent thrombosis. Patients with drug-eluting stent (DES) implantation are prone to hypersensitivity reactions from five potential antigens namely, nickel strut, polymer coating, eluted drug, as well as, concomitant drugs clopidogrel and aspirin. These events may be more common than suspected because it is hard to document them, unless they become systemic, in which case they manifest themselves as the Kounis syndrome characterized by the concurrence of acute coronary events with hypersensitivity reactions. This report concerns of a patient with implanted DES who developed an acute myocardial infarction in the stent area following an allergic reaction to contrast material.

Nickel allergy, Kounis syndrome and intracardiac metal devices

Metal-induced allergic reactions are not rare in every day practice but nickel, cobalt and chromium are the most common offenders. Other metal anions and metal alloys represent also emerging causes for hypersensitivity reaction in humans. The metal struts of endovascular and intracardiac devices are usually alloys containing nickel and constitute causes for allergic reactions with possible intracardiac and intracoronary mast cell activation resulting in the Kounis hypersensitivity coronary syndrome. Newer intracoronary stents avoid nickel thus making them less allergenic. It is advisable that, before any device implantation, careful history of any metal allergy should be taken and efforts should be made for the development of new devices with better biocompatibility.

Kounis syndrome: Two extraordinary cases

Acute myocardial infarction occurring during the course of an allergic reaction constitutes the Kounis syndrome. This syndrome is caused by inflammatory mediators released mainly from activated mast cells and the interrelated via bidirectional stimuli macrophages and T-lymphocytes. Since activated mast cells abound at the areas of plaque erosion or rupture in patients suffering from acute myocardial infarction a common pathway between allergic and non allergic coronary events seems to exist. Two cases of this syndrome are described, the first following nicorette transdermal application and subsequent finger pricking by fish bone and the second after ciprofloxacin administration.

Hypersensitivity to proton pump inhibitors: Lansoprazole-induced Kounis syndrome

Proton pump inhibitors are commonly used in clinical practice for the treatment of peptic ulcer and gastroesophageal reflux and are well tolerated by the patients. Their use is rarely associated with hypersensitivity and anaphylactic reactions. According to the reports in the Uppsala Monitoring Center database the frequency of hypersensitivity reactions out of all reported adverse reactions for proton pump inhibitors and H2-histamine receptor antagonists was between 0.2% and 0.7%. A few cases of hypersensitivity to lansoprazole have been reported. We report a patient who developed Kounis syndrome after taking 30 mg of lansoprazole. This is the first report of Kounis syndrome associated with lansoprazole administration in the world literature.

Coronary artery spasm associated with eosinophilia: another manifestation of Kounis syndrome?

W read with interest the article published in this Journal [1], associating eosinophilia and coronary artery spasm (CAS). So far, the mechanism and precipitating factors of CAS are not well understood. Endothelial dysfunction, smooth muscle calcium hypersensitivity, increased autonomic tone increased oxidative stress and genetic susceptibility have been incriminated [2]. In a recent editorial [3], concerning the mechanism of CAS, the possibility of involvement of bone marrow-derived cells such as mast cells and their products was mentioned. Eosinophils are bone marrow-derived granulocytic leukocytes, which normally reside in tissues and express H4 h c d i a a c a H

The conundrum of hypersensitivity cardiac disease: Hypersensitivity myocarditis, acute hypersensitivity coronary syndrome (Kounis Syndrome) or both?

Abstract Hypersensitivity or allergic inflammatory processes can affect the cardiac structures during allergic insults. The myocardium, the conduction system and the coronary arteries can be the targets of these insults resulting in Kounis syndrome (hypersensitivity coronary syndrome) or hypersensitivity myocarditis. Kounis syndrome and hypersensitivity myocarditis can be clinically indistinguishable and masquerade each other. Simultaneous occurrence of both entities has not been reported. We report on a patient who presented with signs and symptoms of type I variant of Kounis syndrome but cardiac magnetic resonance imaging showed that he had hypersensitivity myocarditis.

Tryptase levels in coronary syndromes and in hypersensitivity episodes: A common pathway towards Kounis syndrome

Evidence exists today, that the same mediators released from imilar cells such mast cells are present in both acute coroary events and acute hypersensitivity episodes [1]. It seems ikely that a common pathway exists between the hypersensiivity coronary syndrome the so called Kounis syndrome [2] and on-hypersensitivity coronary syndromes [3]. One of these comon mediators is the mast cell derived specific neutral protease ryptase. In the very important paper, concerning 270 Chinese patients, ublished in this Journal [4] it was found that serum tryptase evels were significantly higher in patients with substantial coroary heart disease including unstable angina and acute myocardial nfarction than in patients with unsubstantial disease namely atients with less than 50% or without luminal narrowing of the ain coronary arteries. The authors of this report suggested that ryptase and the brother protease chymase are important indepenent biomarkers for atherosclerotic plaque vulnerability. Although n this cohort, patients with any kind of autoimmunity, allergic iseases, cancer, and renal failure were correctly excluded other atients with conditions known to have also elevated baseline erum tryptase levels [5] such as mastocytosis, refractory aneias, myelodysplastic syndromes, hypereosinophilic syndrome, nd patients receiving recombinant human stem cell factor should ad been excluded also. However, several other studies have also shown that elevated ryptase levels are present during acute coronary syndromes and

Foods, Drugs and Environmental Factors: Novel Kounis Syndrome Offenders

Kounis syndrome is hypersensitivity coronary disorder induced by various types of environmental exposures, drugs, conditions and stents. Allergic, hypersensitivity, anaphylactic and anaphylactoid reactions are associated with this syndrome. The disorder manifests as coronary spasms, acute myocardial infarction and stent thrombosis and affects the cerebral and mesenteric as well as coronary arteries. Importantly, its manifestations are broad and its etiology is continuously increasing. Recently, a variety of unusual etiologies have been reported including Anisakis simplex, scombroid syndrome, the use of Gelofusin or ultrasound contrast agents, kiwifruit, fly bites, and bee stings. Furthermore, losartan and the paradox of corticosteroid allergy have been implicated as possible causes. Although not rare, Kounis syndrome is infrequently diagnosed. Therefore, awareness of its etiology, manifestations and pathophysiology is important for providing the proper diagnosis and treatment and determining prognosis.

Acute stent thrombosis and atopy: Implications for Kounis syndrome

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Kounis syndrome--the killer for Williams syndrome?

The report by Gupta et al. published in this journal[1] raises some important issues concerning sudden cardiac death in Williams syndrome (WS) patients during anesthesia. WS is a complex syndrome comprising of developmental abnormalities, cranofacial dysmorphic features and cardiac anomalies. Although supravalvular aortic stenosis is the classic abnormality associated with 37–73% of the cases and pulmonary artery stenosis is also relatively common, coronary anomalies and obstruction in WS can be present in 6–60% of the cases. Significant coronary artery stenosis with evidence of myocardial infarction has been reported.