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      Anatolian Journal of Cardiology
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          Abstract

          To the Editor, We thank you for the interest in and positive reviews for our case report published in the Anatolian Journal of Cardiology entitled “Bonsai-induced Kounis Syndrome in a young male patient” (1). The most important step of the diagnosis of Kounis syndrome is determining the presence of allergic symptoms accompanying chest pain. Systemic allergic reaction is manifest with skin, mucosa, respiratory system, cardiovascular system, or gastrointestinal system signs in minutes/hours after exposure to the allergen. The clinical picture is variable in a wide spectrum from mild skin lesions that might be unnoticed to anaphylactic shock. The course of the allergic reaction occurring in this case was chest pain without skin involvement. No skin lesion was encountered in this patient. However, skin lesions may be absent in majority of the cases (2). The patient was questioned and examined for skin lesions; nevertheless, the mild nature of the skin lesions should be considered so that they may be unnoticeable (3). Leukocytosis, eosinophilia, and increased IgE levels were detected in this case, and other tests could not be performed because of technical unavailability. The skin prick test may be helpful in diagnosis; however, its rate of usage is found to be low in the literature (4). Primary treatment of Kounis syndrome is AKS management and suppression of the allergic reaction. Because the primary mechanism is coronary vasospasm in young and otherwise healthy patients who have no risk factors for coronary artery disease and are considered to have Type I variant Kounis syndrome, the first-line treatment is nitrates and calcium channel blockers. Suppression of allergy by steroids and antihistamines alone may even alleviate coronary vasospasm. AKS management in those patients, on the other hand, is unclear. Debatable applications have been reported, particularly on the antiaggregants. Because aspirin is a basic building block treatment in the management of AKS, we started aspirin (5). However, as you have mentioned, aspirin has the potential to increase the continuing allergic reaction in patients with Kounis syndrome. It may be more suitable to prefer clopidogrel in patients with hypersensitivity to aspirin.

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          Clinical features and severity grading of anaphylaxis.

          Existing grading systems for acute systemic hypersensitivity reactions vary considerably, have a number of deficiencies, and lack a consistent definition of anaphylaxis. The aims of this study were to develop a simple grading system and definition of anaphylaxis and to identify predictors of reaction severity. Case records from 1149 systemic hypersensitivity reactions presenting to an emergency department were analyzed retrospectively. Logistic regression analyses of the associations between individual reaction features and hypotension and hypoxia were used to construct a grading system. Epinephrine use, etiology, age, sex, comorbidities, and concurrent medications were then assessed for their association with reaction grade. Confusion, collapse, unconsciousness, and incontinence were strongly associated with hypotension and hypoxia and were used to define severe reactions. Diaphoresis, vomiting, presyncope, dyspnea, stridor, wheeze, chest/throat tightness, nausea, vomiting, and abdominal pain had weaker, albeit significant, associations and were used to define moderate reactions. Reactions limited to the skin (urticaria, erythema, and angioedema) were defined as mild. These grades correlated well with epinephrine usage. Older age, insect venom, and iatrogenic causes were independent predictors of severity. Preexisting lung disease was associated with an increased risk of hypoxia. This simple grading system has potential value for defining reaction severity in clinical practice and research settings. The moderate and severe grades provide a workable definition of anaphylaxis. Age, reaction precipitant, and preexisting lung disease appear to be the major determinants of reaction severity.
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            A case of Kounis syndrome after a hornet sting and literature review

            Background Acute coronary syndrome after hymenoptera stings or exposure to environment toxins is referred to as the Kounis syndrome or allergic myocardial ischaemia with or without infarction. We report a case of hornet (Vespa affinis) sting causing Kounis syndrome in Sri Lanka and present a review of literature. Case presentation A 60-year -old female with diabetes mellitus and known allergy to bee venom was stung by a hornet on the right hand. Within 30 minutes she developed hypotension and wide spread T wave inversion in the 12 leads ECG that remained unchanged about 5 hours and reversed back to normal. Conclusion Hymenoptera stings can induce acute coronary syndrome either by direct effect of venom constituents on the coronary endothelium or through inflammatory mediators induced allergic reaction on coronary vasculature. Early recognition of Kounis syndrome is needed in hornet stings to implement necessary treatments.
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              Bonsai-induced Kounis Syndrome in a young male patient

              Introduction The use of cannabis and its synthetic derivative, bonsai, has recently increased, and it has become an important health problem (1). Kounis syndrome develops by the activation of mast cells, and it is an acute coronary syndrome (ACS) related to allergies, hypersensitivity, anaphylaxis, or anaphylactic reactions (2, 3). Bonsai-induced Kounis syndrome has not been reported in literature. The present study presents the case of a 27-year-old patient who arrived at the emergency clinic with chest pain 6 h after the use of bonsai. Case Report A 27-year-old male patient arrived at the emergency clinic with sudden-onset retrosternal pain in the left arm, vomiting, and sweating. The chest pain was characterized by pressure and burning and lasted for 6 h. The patient did not have any known atherosclerosis risk factor and reported bonsai use for the first time in his life. He expressed that he had used a great amount of bonsai 1 h before the onset of chest pain. All vital signs of the patient were stable. His electrocardiographic (ECG) investigation revealed mild bradycardia and ST segment elevations in the inferior derivations (D2, D3, and AVF) (Fig. 1). The patient was referred to the coronary intensive care unit after the diagnosis of acute inferior MI was made. Bedside echocardiography revealed inferior and septal hypokinesis. Thrombolytic therapy was planned but was then disregarded as the recently recorded ECG showed ST-segment elevations returning to the isoelectric line. Troponin I value showed a typical increase (4 h)- decrease (24-36 h) (peak value 10.722 ng/mL). Mild leukocytosis and eosinophilia (4.9%) were present. The immunoglobulin E level was high (150 mg/L). The patient was referred to a more advanced center for coronary angiography (CAG). CAG indicated that all coronary arteries were patent (Fig. 2). The fibrinogen and homocysteine levels and antithrombin activity were all within normal ranges. The patient was followed-up for three days without any complications and was then dismissed from the hospital with prescriptions for 100-mg aspirin, 90-mg diltiazem, and 40-mg atorvastatin. Figure 1 ST elevation in inferior leads on 12-derivation ECG obtained in the emergency department Figure 2 Demonstrating RCA, LMCA, LAD, and LCx on coronary angiography Discussion To our knowledge, this patient is the first bonsai-induced Kounis syndrome case in literature. Kounis syndrome, in other words allergic MI, has two types depending on the pathophysiology, or the presence of coronary artery disease. In type I, patients exhibit coronary vasospasms induced by allergic mediators such as histamine, thromboxane, and leukotrienes without the presence of atherosclerosis risk factors or coronary artery disease. In type 2, ACS develops due to coronary vasospasms, plaque erosion, or plaque rupture induced by these mediators in patients with atherosclerotic coronary artery disease. Recently, the fact that there are eosinophil and mast cells in the thrombus material excised from some patients in whom stent thrombosis developed after stent implantation with drug release makes us consider hypersensitivity reactions in these patients. This situation is accepted as the type III variant of Kounis Syndrome (4). With these findings, our case is in accordance with the type I variant of Kounis syndrome. Cardiovascular and psychological problems are frequently reported to be associated with the use of bonsai. The main pathophysiology of Kounis syndrome is the release of many allergic mediators as a result of mast cell activation induced by allergic stimulants. It has been demonstrated in experimental studies that some endogenous cannabinoids suppress inflammation by decreasing mast cell activation via receptors; however, some endogenous cannabinoids trigger mast cell activation independent from receptors (5). In our patient, coronary arteries were revealed to be completely patent, and this may cause us to consider that a coronary vasospasm was the reason that was caused via mediators released by the bonsai-induced activation of mast cells. The main cardiovascular effects are coronary vasoconstriction, increase in the synthesis of tissue factor, thrombocyte activation, dysrhythmia development induced by various mechanisms, and plaque erosion (6, 7). In a patient considered to have Kounis syndrome, in addition to appropriate ACS management, the determination of serum histamine, specific Ig E antibodies, and complement proteins and investigation of eosinophilia aid in the diagnosis (2). Leukocyte, eosinophil, and total IgE levels were increased in our patient, but other analyses could not be performed due to technical limitations. Conclusion We hoped to emphasize the consideration of the use of bonsai-type synthetic drugs in a young patient with acute MI signs but without any risk factors.
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                Author and article information

                Journal
                Anatol J Cardiol
                Anatol J Cardiol
                Anatolian Journal of Cardiology
                Kare Publishing (Turkey )
                2149-2263
                2149-2271
                March 2016
                : 16
                : 3
                : 227-228
                Affiliations
                [1]Departmant of Cardiology, Aksaray State Hospital, Aksaray- Turkey
                [1 ]Departmant of Cardiology, Şişli Etfal Education and Tracking Hospital, İstanbul- Turkey
                [2 ]Departmant of Cardiology, Faculty of Medicine, Erciyes University, Kayseri- Turkey
                Author notes
                Address for Correspondence: Dr. Sinan İnci Aksaray Devlet Hastanesi, Zafer Mah., Nevşehir Cad., No:117, Aksaray- Türkiye Phone:+90 382 212 35 02 E-mail: doktorsinaninci@ 123456gmail.com
                Article
                AJC-16-227
                5336828
                27067576
                77fdb21a-f21b-4de8-acba-3f9692d2c75a
                Copyright © 2016 Turkish Society of Cardiology

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License

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