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      Bonsai-induced coronary artery spasm

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      Anatolian Journal of Cardiology
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          Abstract

          To the Editor, I have read the article by İnci et al. (1) entitled “Bonsai-induced Kounis Syndrome in a young male patient” with great interest, which was published in Anatol J Cardiol 2015, 15: 952-3. The authors presented an unusual form of acute coronary syndrome, which developed following the synthetic cannabinoid “Bonsai” use. I would like highlight some points regarding this article. Although there are no definite diagnostic criteria to differentiate prinzmetal angina from Kounis syndrome, systemic allergic reactions associated with acute myocardial ischemia in a patient should suggest that the patient has Kounis syndrome (2). Are there any signs and symptoms of systemic allergic reactions such as generalized erythema or urticarial rashes in the patient? Also, after clinical stabilization, additional allergy tests, including skin prick test, may be helpful for diagnosis. I also would like to highlight a specific point in the treatment of the abovementioned patient. In the cases where type 1 Kounis syndrome progresses to acute myocardial infarction with increased cardiac enzymes and troponins, anti-allergic treatment, including administration of H1 and H2 blockers together with corticosteroids combined with classical treatment of acute coronary syndromes, is recommended (3). Also, in patients with non-ST-elevation acute coronary syndromes, dual antiplatelet therapy with aspirin and clopidogrel has been recommended for 1 year over aspirin alone, irrespective of the revascularization strategy and stent type according to the current guidelines (4). However, the utilization of aspirin is controversial because of the underlying anaphylactic reaction in Kounis syndrome. Acetylsalicylic acid can cause allergic reactions and induce anaphylaxis; therefore, the safety of aspirin use in patients with Kounis syndrome is unknown (5). I would like to kindly ask the authors whether there is any specific reason for the treatment of aspirin in this case? In conclusion, because the use of synthetic cannabinoid is gradually increasing in our country, rapid diagnosis and appropriate treatment in these patients has great importance because of the complex and complicated course of acute coronary syndromes associated with allergic reactions.

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          Kounis syndrome (allergic angina and allergic myocardial infarction): a natural paradigm?

          Inflammatory mediators including histamine, neutral proteases, arachidonic acid products, platelet activating factor and a variety of cytokines and chemokines are increased in blood or urine in both allergic episodes and acute coronary syndromes. The release of mediators during allergic insults has been incriminated to induce coronary artery spasm and/or atheromatous plaque erosion or rupture. A common pathway between allergic and non-allergic coronary syndromes seems to exist. Today, there is evidence that mast cells not only enter the culprit region before plaque erosion or rupture but they release their contents before an actual coronary episode. Kounis syndrome is the concurrence of acute coronary syndromes with conditions associated with mast cell activation including allergic or hypersensitivity and anaphylactic or anaphylactoid insults. It is caused by inflammatory mediators released through mast cell activation. Kounis syndrome, as consequence, of the above pathophysiologic association is regarded as nature's own experiment and magnificent natural paradigm showing novel way in an effort to prevent acute coronary syndromes. Drugs and natural molecules which stabilize mast cell membrane and monoclonal antibodies that protect mast cell surface could emerge as novel therapeutic modalities capable to prevent acute coronary and cerebrovascular events.
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            Treatment of Kounis syndrome.

            Kounis syndrome is potentially a life-threatening medical emergency with both a severe allergic reaction and acute coronary syndrome. Most of the information about this syndrome has come from the case reports. The management of these patients may be challenging for clinicians, and unfortunately guidelines have not been established yet. In this article, we review the current guidelines of acute coronary syndromes and anaphylaxis along with the published cases with Kounis syndrome secondary to beta-lactam antibiotics. We have summarized our recommendations for the work-up and treatment of Kounis syndrome from available data. Obviously, larger prospective studies are needed to establish definitive treatment guidelines for these patients. Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.
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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
                : 226-227
                Affiliations
                [1]Department of Cardiology, Atatürk State Hospital, Antalya- Turkey
                Author notes
                Address for Correspondence: Dr. Can Ramazan Öncel Atatürk Devlet Hastanesi, Kardiyoloji Kliniği Anafartalar Cad., 07040, Antalya- Türkiye E-mail: r_oncel@ 123456hotmail.com
                Article
                AJC-16-226c
                10.14744/AnatolJCardiol.2016.6918
                5336827
                27067575
                4432a132-b4d7-425a-8f09-325989187344
                Copyright © 2016 Turkish Society of Cardiology

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

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