George Almpanis

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.

Vascular Complications Following Transradial and Transulnar Coronary Angiography in 1600 Consecutive Patients

Background: Major, noncoronary complications are rarely encountered following transradial coronary procedures. Methods and Results: Among 1600 prospectively studied patients with complete follow-up, 7 patients experienced major complications following coronary forearm procedures corresponding to an incidence of 0.44%. We found inadvertent symptomatic intramyocardial contrast medium injection, 2 cases with compartment syndrome of which 1 was managed surgically, exertional hand ischemia due to radial artery occlusion, a large ulnar artery pseudoaneurysm, an ulnar arteriovenous fistula, and 1 critical hand ischemia due to late occlusion of the distal brachial artery. Conclusions: Although infrequent, surveillance for major complications should be encouraged after forearm coronary procedures.

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

Kounis syndrome following cold urticaria: The swimmer's death

Kounissyndromeisahypersensitivitycoronarydisorderinducedbyconditions,environmentalexposures,drugs,andcoronarystents.Sofar,conditions that have been reported to be associated with Kounissyndrome include angio-edema, bronchial asthma, exercise inducedanaphylaxis, food allergy, idiopathic anaphylaxis, mastocytosis, serumsickness and urticaria [1]. We report a unique case of cold-inducedurticaria complicated by Kounis syndrome during swimming in seawater(swimmersdeath) [2]thatsurvivedbutwithsevereandavoidableimpairment of quality of life (Qol).A 68 year-old female was brought by her friends to the emergencydepartmentcomplainingofitchyfeeling,chestdiscomfortanddifficultyin breathing. Her symptoms had started soon after touching the seawater when she went for swimming about 2 h previously. Her friendsdescribed that she fainted immediately after started swimming andrecovered by external massage. On examination, in the emergencyroom, her body was covered by generalized erythematous rash andwas cold. Her pulse was 90 regular, the blood pressure 140/80 andtemperature 35 °C. Electrocardiogram was normal but the highsensitivity cardiac troponin was 1.33 (normal values 0.00–0.005).Echocardiography revealed global reduction of left ventricularcontractility resembling myocardial stunning with reduced ejectionfraction to 30%. She was treated with diphenydramine corticosteroidsand nitrates intravenously for an allergic reaction associated withmyocardial ischemia. Her symptoms resolved gradually and she wastransferred to a coronary care unit for further investigations. Detailedpast history revealed that six years previously she have had an acutenonST elevation myocardial infarction that had occurred again whileswimming treated conservatively in another hospital. In that hospitalcoronary angiography had revealed normal coronary arteries. Shereported also hospitalization to a dermatology clinic due to a dermalexanthema covering all over her trunk. At that time, she underwentdermal biopsy and allergic skin prick tests that showed reaction toseveral allergens and had been characterized as an atopic person. Shealso mentioned attacks of photodermatitis. During the second day, inour hospital, her condition improved and a coronary angiographyshowed again normal coronary arteries with normalized echocardio-gram and increased ejection fraction to 45%. Laboratory investigationsincluding rheumatoid factor, cryoglobulins, antinuclear antibody titersand checking for thrombophilia were all negative. She was diagnosedas Kounis syndrome type I variant induced by cold urticaria. We didnot perform ice-cube-challenge test on ethical grounds. She wasadvised to avoid cold stimuli with water temperature preferablyb25 °C and to use prophylactic antihistamines and corticosteroids.Kounis syndrome is mast cell degranulation associated with acutecoronary disorder resulting from the action of inflammatory mediatorsreleased during mast cell degranulation in allergic or anaphylacticepisodes. Mast cell degranulation occurs when 2000 nearby antibodiesattached to mast cell surface are bridged by corresponding antigensand make the critical number of 1000 bridges [3]. Such mediators caninduce either coronary artery spasm which can progress to acutemyocardialinfarctionoratheromatousplaqueerosionorruptureculmi-nating to coronary thrombosis [4]. This is a classical pathway to inducean allergic or anaphylactic episode. However, mast cells have also theability to degranulate inresponse tocold and to release their mediatorssuch as histamine [5]. Histamine can induce coronary artery spasm viaH1 receptors situated in the coronary arteries. In general, mast cellscan be activated, in susceptible patients, by physical stimuli such asexposure to cold, exposure to heat or vibration, a condition known asphysically induced urticaria [6]. Despite the direct mast cell activationby physical exposures, a role for IgE mediated activation in thepathogenesis of cold urticaria has been also proposed. This is based onserum transfer studies [7] and successful treatment with the anti-IgEdrug omalizumab [8]. The described patient developed an allergicreaction manifesting as urticaria on two occasions while attempting toswim in cold sea water that was associated with nonST elevationmyocardial infarction. Cold urticaria is an uncommon form of physicalurticaria that can cause life-threatening reactions. Death may occur

Kounis syndrome uncovers critical left main coronary disease: The question of administering epinephrine

This report concerns of a previously asymptomatic patient who developed anaphylactic shock with chest discomfort and generalized erythematous rash after receiving 1 g of amoxicillin orally prior to a dental procedure. He was diagnosed as having Kounis syndrome [1] and during catheterization a 90% of left main coronary artery disease was revealed and needed urgent surgical revascularization. Anaphylaxis was treated with large dose of hydrocortisone and antihistamines but epinephrine was withheld. The 64-year-old asymptomatic male smoker lost consciousness and developed chest discomfort approximately 5 min following 1 g of amoxicillin taken orally for tooth extraction. In the emergency room he was conscious but sweating with generalized erythematous rash covering the whole body and chest discomfort. The blood pressure was undetectable, the pulse was 115 beats per min and an electrocardiogram [Fig. 1] showed sinus tachycardia with generalized ST segment depression but with 2 mm ST elevation in AVL lead. He was diagnosed as having anaphylactic shock from amoxicillin and was treated with 1 g hydrocortisone sodium succinate and 8 mg of dimetindene maleate intravenously. The patient was kept under close surveillance and monitoring, but epinephrine was not given because the electrocardiographic changes in this 64 year old smoker were suggestive of coronary vasospasm.

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.

Kounis syndrome is likely culprit of coronary vasospasm induced by capecitabine

Capecitabine administration has been associated with various allergic reactions including acneiform skin rash, linchenoid photosensitive eruption, exudative non healing scalp, skin reactions, pyogenic granuloma, subacute cutaneous systemic lupus erythematosus, exudative hyponychia dermatitis, and hand–foot syndrome. A patient who developed ventricular fibrillation following capecitabine-induced coronary vasospasm and necessitating cardioverter-defibrillator implantation was published recently in J Oncol Pharm Practice. The authors attributed this reaction to capecitabine cardiotoxicity, but capecitabine hypersensitivity is closely associated with Kounis syndrome. Tests and measures which will help to confirm, prevent and treat cardiac hypersensitivity to antineoplastic agents are recommended.