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    Allergic myocardial infarction in childhood: Kounis syndrome
    (Springer Nature, 2009) Biteker, Murat; Ekşi Duran, Nilüfer; Sungur Biteker, Funda; Ayyıldız Civan, Hasret; Kaya, Hasan; Gökdeniz, Tayyar; Yıldız, Mustafa; Özkan, Mehmet
    Kounis Syndrome was first described by Kounis as "allergic angina syndrome" progressing to "allergic myocardial infarction". This report describes the first children in the literature presented with Kounis syndrome.
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    Broken heart syndrome in an 83-year-old woman
    (National Library of Medicine, 2008) Biteker, Murat; Ekşi Duran, Nilüfer; Gündüz, Sabahattin; Candan, Özkan; Sungur Biteker, Funda; Gökdeniz, Tayyar; Güler, Ahmet; Özkan, Mehmet
    An 83?year?old woman was admitted to the emergency department because of severe chest pain that had begun 2 hours before and radiated to the neck and left arm. Except for advanced age, she had no coronary risk factors. Her husband had died that day after 58 years of marriage. On admission, physical examination revealed no pathological findings other than slightly high blood pressure and tachycardia. Her blood pressure was 175/90?mmHg, and heart rate was 110?beats/min. Electrocardiogram showed sinus tachycardia and 2?mm ST elevation in leads I, aVL, and V2 to V6 (Figure 1A). After being given 300?mg of aspirin and 5,000?U of intravenous heparin the patient was taken to the coronary intensive care unit. Transthoracic echocardiography (TTE), performed in the coronary intensive care unit immediately, revealed apical akinesia, midventricular hypokinesia and basal hyperkinesia of the left ventricle, moderate mitral regurgitation with ejection frequency of 30%. To exclude coronary artery disease, coronary angiography was performed, which revealed noncritical coronary plaques in the left anterior descending and circumflex artery. Ventriculography showed apical and midventricular ballooning with basal hyperkinesia (Figure 1B). Chest pain disappeared spontaneously. Cardiac enzyme and troponin levels were high and reached maximal degrees (creatine kinase, 623?U/L; creatine kinase?MB, 98?U/L; troponin I, 4.2??g/L) on the second day. Her hospital course was uneventful. TTE, performed on the seventh day, revealed normal left ventricular systolic function without any segmental wall motion abnormality. Her ejection fraction was 58%, with trace mitral regurgitation. On the seventh day, myocardial perfusion scintigraphy was performed, and there was no sign of ischemia. With these findings, TC was diagnosed, and a consultation with a psychiatrist was recommended. The patient was discharged from the hospital in excellent condition and at a 1?month follow?up visit was doing well.
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    Kounis syndrome secondary to amoxicillin/clavulanic acid use in a child
    (Elsevier, 2009) Biteker, Murat; Ekşi Duran, Nilüfer; Sungur Biteker, Funda; Ertürk, Emre; Çağrı Aykan, Ahmet; Ayyıldız Civan, Hasret; Özkan, Mehmet
    The concurrence of acute coronary syndromes with allergic or hypersensitivity as well as with anaphylactic or anaphylactoid reactions is increasingly encountered in clinical practice and there are several reports associating mast cell activation with acute cardiovascular events in adults. It was first described by Kounis as “allergic angina syndrome” progressing to “allergic myocardial infarction”. The main mechanism proposed is the vasospasm of coronary arteries. This condition has not been described in childhood. We present a 13-year-old boy, admitted to our hospital with thoracic pain, 30 min after the ingestion of an oral dose of 500 mg of amoxicillin/clavulanic acid.
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    Kounis syndrome secondary to cefuroxime-axetil use in an octogenarian
    (National Library of Medicine, 2008) Biteker, Murat; Ekşi Duran, Nilüfer; Sungur Biteker, Funda; Gündüz, Sabahattin; Gökdeniz, Tayyar; Kaya, Hasan; Astarcıoğlu, Mehmet Ali; Özkan, Mehmet
    A 90-year-old man who had been hospitalized for urinary tract infection developed chest pain and pruritic skin rashes. His complaints had started approximately 10 minutes after intramuscular injection of 750 mg of cefuroxime-axetil. His physical examination was normal upon admission, and his electrocardiogram showed ST segment elevations in leads II, III, aVF, V4, V5, and V6 (Figure 1). He had no history of coronary artery disease, diabetes mellitus, hypertension, or hyperlipidemia. Transthoracic echocardiography, performed in the coronary intensive care unit, revealed inferior wall hypokinesia. Complete blood count and liver and kidney function tests were normal except for mild leukocytosis. Coronary angiography performed to exclude coronary artery disease revealed noncritical coronary plaques in the left anterior descending and circumflex artery. Troponin-I estimated 4 hours after admission was 4 ng/mL (reference: 0–0.1 ng/mL) and rose to 22 ng/mL. Creatine kinase-MB fraction estimated 4 hours after admission was 42 U/L (reference: 0–25 U/L) and rose to 85 U/L on the second day. Total immunoglobulin E estimated on arrival was 54 IU/mL (reference: 0–100), and serum tryptase was 43.5 mg/L (reference: 5.6–13.5 mg/L). Subsequent daily estimations of serum tryptase were within normal limits. The patient was diagnosed to have Kounis syndrome type I variant, secondary to cefuroxime-axetil. He was treated with oral antihistamines and 8 mg of prednisolone every 6 hours for 5 days. Cefuroxime-axetil was stopped, and he was treated with levofloxacin for urinary tract infection. Five days later, the repeated cardiac markers were within normal limits, with resolution of electrocardiographic abnormalities and inferior wall motion echocardiographic changes. The man was discharged from hospital in excellent condition and was doing well at a 3-week follow-up visit.