Osborn waves masquerading as ST-segment elevation myocardial infarction

Osborn waves masquerading as ST-segment elevation myocardial infarction

IJCA-18901; No of Pages 2 International Journal of Cardiology xxx (2014) xxx–xxx Contents lists available at ScienceDirect International Journal of ...

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IJCA-18901; No of Pages 2 International Journal of Cardiology xxx (2014) xxx–xxx

Contents lists available at ScienceDirect

International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard

Letter to the Editor

Osborn waves masquerading as ST-segment elevation myocardial infarction Grigoris V. Karamasis a,⁎, Antonios N. Pavlidis b a b

Department of Cardiology, Imperial College Healthcare NHS Trust, London, UK Department of Cardiology, Barts Health NHS Trust, London, UK

a r t i c l e

i n f o

Article history: Received 13 September 2014 Accepted 23 September 2014 Available online xxxx Keywords: Hypothermia J wave Myocardial infarction

A 32 year old man who was found unconscious, was transferred by the emergency ambulance service to our institution via the primary percutaneous coronary intervention pathway with the suspicion of an inferolateral ST-segment elevation myocardial infarction (Fig. 1). He was known to have type I diabetes mellitus with poor compliance to his insulin regime, but no other risk factors for coronary artery disease. On arrival to the emergency department he was hypotensive (81/62 mm Hg) and his core temperature was 28 °C (82.4 °F). Arterial blood gas analysis revealed severe metabolic acidosis with a lactate of 3.1 mg/dL, glucose 782 mg/dL and pH 6.67. A repeat ECG demonstrated widespread prominent J waves (Osborn waves) and bedside echocardiogram confirmed normal left ventricular systolic function with no regional wall motion abnormalities (Fig. 2). He was transferred to the intensive care unit where he was re-warmed and received treatment for diabetic ketoacidosis. Once his acidosis and hypothermia were corrected (pH 7.37, core temperature 37.3 °C) a repeat ECG was obtained and this showed complete resolution of the Osborn waves (Fig. 3). Prominent J deflections attributed to hypothermia were first reported by Tomaszewski in 1938 [1] and were named Osborn waves in honor of John Osborn who extensively described them in his landmark paper in 1953 [2]. They appear as positive deflections between the end of the QRS complex and the early portion of the ST segment and can

manifest in all leads or in a number of them [3]. The amplitude of Osborn waves increases as core temperature drops and gradually disappears once core temperature returns back to normal levels. Hypothermiainduced J waves are the result of a marked accentuation of the action potential notch in the epicardium but not in the endocardium, resulting in a transmural voltage gradient [4]. Hypercalcemia, central nervous system lesions, coronary vasospasm, left ventricular hypertrophy, and Brugada and early repolarization syndromes can demonstrate a similar ECG pattern [5]. Edelman and Joynt [6] suggested that core temperature alone cannot account for the presence of Osborn waves and other physiological abnormalities, such as impairment of the blood pH, need to coexist. Nevertheless, previous animal studies have shown that Osborn waves can develop even when blood pH is normal [7]. As shown in our case, early recognition of Osborn waves can prevent misinterpretation of ECG as ischemic and avoid unjustified treatment for suspected acute coronary syndrome. Conflict of interest The authors report no relationships that could be construed as a conflict of interest. References [1] Tomaszewski W. Changements electrocardiographiques observes chez un homme mort de froid. Arch Mal Coer 1938;31:525. [2] Osborn JJ. Experimental hypothermia: respiratory and blood pH changes in relation to cardiac function. Am J Physiol 1953;175:389–98. [3] Antzelevitch C1, Yan GX. J wave syndromes. Heart Rhythm 2010;7(4):549–58. [4] Yan GX, Antzelevitch C. Cellular basis for the electrocardiographic J wave. Circulation 1996;93:372–9. [5] Pavlidis AN, Giannakopoulos A, Manolis AJ. Iatrogenic giant Osborn waves. Circulation 2010;122:1519. [6] Edelman ER, Joynt K. J waves of Osborn revisited. J Am Coll Cardiol 2010;55:2287. [7] Pavlidis AN, Giannakopoulos A, Manolis AJ. Iatrogenic giant Osborn waves. Circulation. 2010;122:1519. Response to letter regarding article, “Iatrogenic giant Osborn waves”. Circulation 2011;123:e391.

⁎ Corresponding author at: Hammersmith Hospital, Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK. Tel.: +44 7955293704. E-mail address: [email protected] (G.V. Karamasis).

http://dx.doi.org/10.1016/j.ijcard.2014.09.125 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.

Please cite this article as: Karamasis GV, Pavlidis AN, Osborn waves masquerading as ST-segment elevation myocardial infarction, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.09.125

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G.V. Karamasis, A.N. Pavlidis / International Journal of Cardiology xxx (2014) xxx–xxx

Fig. 1. ECG performed by the ambulance crew showing inferolateral ST elevation with prominent J waves and shivering artifacts in lead V2.

Fig. 2. ECG performed in the emergency department showing striking widespread Osborn waves.

Fig. 3. ECG performed in the intensive care unit after correction of hypothermia and acidemia showing complete resolution of Osborn waves.

Please cite this article as: Karamasis GV, Pavlidis AN, Osborn waves masquerading as ST-segment elevation myocardial infarction, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.09.125