Letter to the Editor Received: February 23, 2015 Accepted: February 24, 2015 Published online: May 6, 2015

Cardiology 2015;131:161 DOI: 10.1159/000381179

Authors’ Reply to the Letter by Madias Entitled ‘"Bronchogenic Stress Cardiomyopathy", a subset of Takotsubo Syndrome’ Adil Rajwani Zulfiquar Adam James Anthony Hall Division of Cardiology and Cardiothoracic Surgery, The James Cook University Hospital, Middlesbrough, UK

leads in 50%, high lateral leads in 25%, anterior leads in 25%, and aVR in 25%). We are unable to systematically evaluate for resolution of attenuation, however, as ECGs were not routinely captured at outpatient follow-up. Whether these two ECG criteria can help distinguish stress cardiomyopathy from type I myocardial infarction is an intriguing hypothesis, although myocardial oedema might be expected in both processes. In our series of patients with bronchogenic stress cardiomyopathy, transthoracic echocardiography (TTE) was prompted by an abnormal ECG. It may also be reasonable to consider TTE where clinical suspicion is high despite an ostensibly normal ECG, although registries have documented ECG abnormalities in 99% of cases [4]. However, whether a more frequent and early implementation of TTE is appropriate is less clear. Ten to 30% of patients with apparent chronic obstructive pulmonary disease exacerbation do not respond to treatment [5]. The resource implications of a routine use of TTE in this setting are likely to be substantial and would therefore require demonstration of a clear advantage over simple bedside tests such as ECG.

© 2015 S. Karger AG, Basel 0008–6312/15/1313–0161$39.50/0 E-Mail [email protected] www.karger.com/crd

Conflicts of Interest

The authors report no conflicts of interest.

References 1 Rajwani A, Adam Z, Hall JA: Bronchogenic stress cardiomyopathy: a case series. Cardiology 2015;130:106–111. 2 Madias JE: ‘Bronchogenic stress cardiomyopathy’, a subset of Takotsubo syndrome. Cardiology 2015;131:160. 3 Madias JE: Transient attenuation of the amplitude of the QRS complexes in the diagnosis of Takotsubo syndrome. Eur Heart J Acute Cardiovasc Care 2014;3:28–36. 4 Sharkey SW, Windenburg DC, Lesser JR, Maron MS, Hauser RG, Lesser JN, Haas TS, Hodges JS, Maron BJ: Natural history and expansive clinical profile of stress (tako-tsubo) cardiomyopathy. J Am Coll Cardiol 2010; 55: 333–341. 5 Global Strategy for the Diagnosis, Management and Prevention of COPD. Global Initiative for Chronic Obstructive Lung Disease (GOLD), 2015.

Dr. A. Rajwani Division of Cardiology and Cardiothoracic Surgery The James Cook University Hospital, Marton Road Middlesbrough TS4 3BW (UK) E-Mail adilrajwani @ hotmail.com

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Following our recently reported novel observations concerning COPD exacerbation and stress cardiomyopathy [1], we acknowledge with great interest the observations of Madias [2] with respect to electrocardiographic manifestations of stress cardiomyopathy and possible indicators of myocardial oedema. These comments align with our own impression that the ECG is a key investigation in the detection of bronchogenic stress cardiomyopathy, whose clinical features may be difficult to distinguish from the precipitating bronchospasm. We were able to retrieve all ECGs in 4 out of 5 patients. Low QRS complex voltages, as described by Madias [3], were detectable in all patients in at least one group of leads (inferiorly in 50%, anteriorly in 75%, laterally in 25%, high laterally in 75%, and aVR in 50%). However, in 50% of patients we also noted low QRS complex voltages in ECGs remote in time to the clinical episode. Patient characteristics that might influence QRS voltage such as body habitus and lung hyperinflation may be relevant. Using the qualitative criteria set out by Madias [3], transient attenuation of the QRS voltage during serial ECG analyses was also detectable in all 4 patients (lateral

Authors' Reply to the Letter by Madias Entitled '"Bronchogenic Stress Cardiomyopathy", a subset of Takotsubo Syndrome'.

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