Silent Myocardial Infarction Due to Kounis Syndrome

Bee stings can cause mortal anaphylactic reactions, which are also precursors to some other mortal events. Kounis syndrome (KS), or allergic myocardial infarctions, are well known concomitant events with every type of allergic reaction. KS should be considered in all patients with allergic events and concomitant chest pain admitted to emergency rooms. The clinical symptoms may not always be clear in these cases. The symptom of chest pain may not be seen in some mono- and poli-neuropathic conditions, particularly in diabetes, transplantation and drug user patients. We present a patient with KS secondary to bee sting. Case Study


INTRODUCTION
The rate of mortal anaphylaxis is as high as 0.8% in bee stings. However, the anaphylactic reactions are not the sole mortal events after bee stings. Kounis syndrome (KS), or allergic myocardial infarctions (MI), are well known concomitant events with every type of allergic reaction. Irrespective of the underlying reasons, KS should be considered in all patients with allergic events and concomitant chest pain symptoms [1,2].

CASE PRESENTATION
A 46 year old farm worker was brought to the emergency room for allergic symptoms (pruritis) after bee sting. While he had no cutaneous rash, the patient said severe pruritus over his entire body. The patient did not report dyspnea, laryngeal irritation or chest pain. In his history, there was no atopic or chronic disease, and he did not use any drugs. He had been smoking one package of cigarettes a day for about twenty years. He was conscious and communicative. His blood pressure was 160/110 mmHg, his pulse was 110 beat/min and his oxygen saturation was 98%. The appearance of tonsilla, pharynx and uvula was normal, with no pathologic pulmonary sound. While the anti-allergic treatment was being initiated, he developed cardiac arrest. He was successfully revived after cardiopulmonary resuscitation. Electrocardiography (ECG) was performed, which revealed minimal ST elevation of D2, D3 and aVF in addition to ST depression for V1,2 ( Fig. 1). The patient was given oxygen support and 300 mg of clopidogrel. The percutaneous coronary intervention (PCI) operation also showed a 90% constriction of the circumflex artery (LAD: 50% stenosis, LMCA and RCA: Normal) (Fig. 2). Troponin I levels of the patient, increased (10,36 ng/ml) during follow-up in intensive care unit. He was discharged seven days later.

DISCUSSION
The term KS involves ACSs that occur soon after anaphylactic reactions. They were firstly defined by Kounis et al. in 1991. KS may be linked to drugs, contrast materials, foods, insect bites, bee stings and latex contacts [2,3]. There are two subgroups of KS, or allergic MI. Type 1 is related to a coronary spasm, which is mediated by histamine, thromboxane and leukotrienes in patients who are lacking any atherosclerotic or coronary artery disease (CAD) history. Type 2 events are seen in CAD patients with the same mediators and are mainly related to vasospasm, perforation and erosion of intravascular plaques. Recently, a type 3 KS was defined and linked to drug secreting stent implants; thrombus samples were showing eosinophiles and mast cells in these cases [3]. Our patient was a chronic smoker, and he had hypertension (160/110 mmHg) at admission (although no prior history of hypertension was mentioned). Accordingly, he had two risk factors for CAD. The PCI showed evidence of stenosis, so this case fits into the KS type 2 category (i.e., patients with underlying CAD developing MI during allergic events).
Cardiac troponins T, I and C are cardiac regulatory proteins that constitute a complex able to control the calcium-mediated interaction between actin and myosin. Troponin I inhibits the interaction of myosin with actin. In a study by Lippi et al. 31 patients admitted to the emergency department and suffering from anaphylaxis, angioedema and urticaria were found to have significantly increased troponin I serum levels. The authors emphasised the importance of cardiac enzymes to demonstrate potential cardiac injury in patients admitted to the emergency department with acute allergic reactions (especially anaphylaxis) without any accompanying symptoms of myocardial ischemia [4,5].
When we look at the literature, many allergens (e.g., insect bites, bee stings and drugs) may cause KS among different ages and patient groups. In the literature, there are some case reports, including the following: a 36-year-old woman with clarithromycin use by Bilgin et al. [6], a 14-year-old boy with metronidazole use by Terlemez et al. [7], a 60-year-old diabetic male after a bee sting by Ralpawana et al. [8], a 14year-old female with oral contraceptives use by Erol et al. [9], and a 43-year-old male with allergic MI after pseudoephedrine use by Celikler et al. [10]. Our patient's KS was observed after a bee sting.

CONCLUSION
In our case, the symptoms of chest pain, dyspnea, syncope and hypotension were lacking. Moreover, conditions such as regular drug use, diabetic disease or neuropathy were also not reported. As a conclusion, we suggest an ECG examination and a cardiac biomarker analysis in all severe allergic cases for detection of KS.

CONSENT
All authors declare that 'written informed consent was obtained from the patient (or other approved parties) for publication of this case report and accompanying images.

ETHICAL APPROVAL
It is not applicable.