International Journal of Cardiology 179 (2015) 16

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Letter to the editor

Takotsubo cardiomyopathy or Kounis syndrome or both? Gurbet Özge Mert a, Funda Sungur Biteker b, Kadir Uğur Mert a,⁎, Özcan Başaran a, Volkan Doğan a, Murat Biteker a a b

Muğla Sıtkı Koçman University, Faculty of Medicine, Department of Cardiology, Turkey Muğla Sıtkı Koçman University, Faculty of Medicine, Department of Infectious Diseases and Clinical Microbiology, Turkey

a r t i c l e

i n f o

Article history: Received 15 October 2014 Accepted 20 October 2014 Available online xxxx Keywords: Takotsubo Cardiomyopathy Takotsubo cardiomyopathy Kounis syndrome

We read with interest the article recently published by Bernards et al. entitled “Transient left ventricular apical ballooning syndrome in a patient with allopurinol induced skin rash” [1]. However, we have some concerns about the article. Kounis syndrome is described as the concurrence of acute coronary events with allergic or hypersensitivity reactions as well as anaphylactic or anaphylactoid reaction [2]. There are several causes that have been reported as capable of inducing Kounis syndrome [2, 3]. These include a number of conditions, several drugs, foods, insect stings, etc. In recent years, an association between Kounis syndrome and takotsubo cardiomyopathy (also called stressinduced cardiomyopathy, transient left ventricular apical ballooning or broken heart syndrome) is argued [4]. However, differential diagnosis of takotsubo cardiomyopathy or Kounis syndrome may be very challenging. Cardiac signs and symptoms, and electrocardiographic and laboratory signs may be similar. Coronary angiography usually reveals a normal coronary angiogram in takotsubo cardiomyopathy and type I variant of Kounis syndrome [5]. Complete resolution of left ventricle contractile abnormalities within weeks is also characteristics of these two syndromes. We would like to remind another laboratory tool for the differential diagnosis of takotsubo cardiomyopathy or Kounis syndrome. Mast cells are necessary for the development of allergic reactions, through crosslinking of their surface receptors for IgE leading to degranulation. Following mast cell degranulation, several vasoconstricting and collagen-degrading compounds are released locally and in the peripheral ⁎ Corresponding author at: Muğla Sıtkı Koçman Üniversitesi Tıp Fakültesi, Orhaniye Mah. Haluk Özsoy Cad., 48000 Muğla, Turkey. E-mail address: [email protected] (K.U. Mert).

http://dx.doi.org/10.1016/j.ijcard.2014.10.059 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

circulation. These compounds include preformed mediators such as histamine, neutral proteases (tryptase, chymase), platelet activating factor, and newly synthesized mediators such as an array of cytokines and chemokines and others by the metabolism of arachidonic acid through activation of a phospholipase [6]. Histamine is short lived and circulates only for 8 min following the allergic insult, but tryptase has a half-life of 90 min. The increased levels of tryptase suggest an acute allergic reaction, where tryptase has been incriminated to induce coronary artery spasm and/or plaque erosion or rupture [7]. The utility of serum mast cell tryptase to diagnose anaphylaxis had a sensitivity of 73% and specificity of 98%, and serial measurements of total serum tryptase in serum or plasma may increase the sensitivity and the specificity of the test [7]. In summary, chest pain, during an allergic insult, with electrocardiographic ischemic changes but with normal cardiac enzymes, negative troponins, normal coronary angiogram and positive tryptase or histamine test are in favor of type I variant of the syndrome. In addition to the routine work-up of patients with acute coronary syndromes (ECG, cardiac enzymes and troponin, complete blood count, D-dimer, brain natriuretic peptide, serum cholesterol levels), serum histamine, tryptase, specific IgE antibody, complement proteins (C4 and C1 inhibitor levels), and eosinophil levels can help differentiate takotsubo cardiomyopathy and Kounis syndrome. References [1] J. Bernards, K. Van Kolen, E. Govaerts, F.J. Somville, M. von Stritzky, Transient left ventricular apical ballooning syndrome in a patient with allopurinol induced skin rash: a case report, Int. J. Cardiol. (Oct 8 2014), http://dx.doi.org/10.1016/j.ijcard. 2014.09.130 (pii: S0167-5273(14)01850-6 [Epub ahead of print]). [2] M. Biteker, Current understanding of Kounis syndrome, Expert Rev. Clin. Immunol. 6 (5) (2010) 777–788. [3] M. Biteker, N.E. Duran, F.S. Biteker, E. Ertürk, A.C. Aykan, H.A. Civan, M. Ozkan, Kounis syndrome secondary to amoxicillin/clavulanic acid use in a child, Int. J. Cardiol. 136 (1) (2009) e3–e5. [4] Y. Yanagawa, K. Nishi, N. Tomiharu, T. Kawaguchi, A case of takotsubo cardiomyopathy associated with Kounis syndrome, Int. J. Cardiol. 132 (2) (Feb 20 2009) e65–e67. [5] M. Biteker, A new classification of Kounis syndrome, Int. J. Cardiol. 145 (3) (2010) 553. [6] M. Biteker, N.E. Duran, F. Biteker, et al., Kounis syndrome: first series in Turkish patients, Anadolu Kardiyol. Derg. 9 (1) (2009) 59–60. [7] S.J. Galli, S. Nakae, M. Tsai, Mast cells in the development of adaptive immune responses, Nat. Immunol. 6 (2) (2005) 135–142.

Takotsubo cardiomyopathy or Kounis syndrome or both?

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