LETTER
Is This Right Ventricular Infarction or Brugada Syndrome? To the Editor: Yamagami et al1 present a case of septic shock from a decubitus-related abscess complicated by deep vein thrombosis of the leg as well as bilateral pulmonary embolism. The challenge that presented in their case was the presence of ST-segment elevation in the precordial leads of the electrocardiogram (ECG). The authors describe incomplete right bundle branch block with ST-segment elevation in leads V1-V4, and they report in the beginning of their article, “even though no acute coronary occlusion existed,” although it is unclear if this was evidence obtained from a coronary catheterization. We believe the explanation by the authors that the ST-segment elevation was “the result of a right ventricular infarction due to pulmonary embolism” is unlikely. The authors need to consider the diagnosis of fever-induced Brugada syndrome. The Brugada ECG pattern is often dynamic and concealed. It can be unmasked by drugs (like cocaine, propranolol), certain disease states (like hyperkalemia), and fever.2,3 Studies have noted that the cardiac sodium channel mutations as seen in patients with Brugada syndrome can result in temperature-gated channels whose potential for arrhythmogenicity increases with higher temperatures.4 Because the resolution of the ST-segment elevation occurred over the course of 4 days, we wonder if the authors can correlate this clinically to the patient’s defervescence. With regard to the ECG, there are several issues that bother us. The right chest leads were not provided (V1RV6R). The ST elevation should be greater in lead V1 (V2R)
Funding: None. Conflict of Interest: None. Authorship: Both authors had access to the data and played a role in writing this manuscript.
0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved.
than in V2 (V1R) in right ventricular infarction and not V2>V1, as in this patient. There are no reciprocal changes of ischemia/injury in the inferior wall as would be seen with an anterior wall myocardial infarction. It is unclear if the only evidence the authors used to make a diagnosis of a right ventricular infarct was the echocardiogram. The creatine kinase-MB isoenzyme was normal. An explanation for the right ventricular dysfunction with positive troponin is the right heart strain caused by the massive pulmonary embolism. It is unlikely for the pulmonary embolism to result in a right ventricular infarction unless the patient was markedly hypotensive with significant right coronary artery disease. This patient would require cardiac catheterization to confirm this. Overall, we think the clinical scenario and ECG are more consistent with Brugada syndrome, and we suggest that the authors include this in their differential diagnosis. Sandhya Manohar, MDa Bernard Gitler, MDa,b a Department of Medicine Montefiore New Rochelle Hospital New Rochelle, NY b Division of Cardiology Montefiore New Rochelle Hospital New Rochelle, NY
http://dx.doi.org/10.1016/j.amjmed.2014.10.048
References 1. Yamagami F, Mizuno A, Shirai T, Niwa K. A savage sequence: STsegment elevations with pulmonary embolism. Am J Med. 2014;127(9):820-822. 2. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the Second Consensus Conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation. 2005;111(5):659-670. 3. ECG Response: October 7, 2014. Circulation. 2014;130(15):1299. 4. Dumaine R, Towbin JA, Brugada P, et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res. 1999;85(9):803-809.
Is This Right Ventricular Infarction or Brugada Syndrome? To the Editor: Yamagami et al1 present a case of septic shock from a decubitus-related abscess complicated by deep vein thrombosis of the leg as well as bilateral pulmonary embolism. The challenge that presented in their case was the presence of ST-segment elevation in the precordial leads of the electrocardiogram (ECG). The authors describe incomplete right bundle branch block with ST-segment elevation in leads V1-V4, and they report in the beginning of their article, “even though no acute coronary occlusion existed,” although it is unclear if this was evidence obtained from a coronary catheterization. We believe the explanation by the authors that the ST-segment elevation was “the result of a right ventricular infarction due to pulmonary embolism” is unlikely. The authors need to consider the diagnosis of fever-induced Brugada syndrome. The Brugada ECG pattern is often dynamic and concealed. It can be unmasked by drugs (like cocaine, propranolol), certain disease states (like hyperkalemia), and fever.2,3 Studies have noted that the cardiac sodium channel mutations as seen in patients with Brugada syndrome can result in temperature-gated channels whose potential for arrhythmogenicity increases with higher temperatures.4 Because the resolution of the ST-segment elevation occurred over the course of 4 days, we wonder if the authors can correlate this clinically to the patient’s defervescence. With regard to the ECG, there are several issues that bother us. The right chest leads were not provided (V1RV6R). The ST elevation should be greater in lead V1 (V2R)
Funding: None. Conflict of Interest: None. Authorship: Both authors had access to the data and played a role in writing this manuscript.
0002-9343/$ -see front matter Ó 2015 Elsevier Inc. All rights reserved.
than in V2 (V1R) in right ventricular infarction and not V2>V1, as in this patient. There are no reciprocal changes of ischemia/injury in the inferior wall as would be seen with an anterior wall myocardial infarction. It is unclear if the only evidence the authors used to make a diagnosis of a right ventricular infarct was the echocardiogram. The creatine kinase-MB isoenzyme was normal. An explanation for the right ventricular dysfunction with positive troponin is the right heart strain caused by the massive pulmonary embolism. It is unlikely for the pulmonary embolism to result in a right ventricular infarction unless the patient was markedly hypotensive with significant right coronary artery disease. This patient would require cardiac catheterization to confirm this. Overall, we think the clinical scenario and ECG are more consistent with Brugada syndrome, and we suggest that the authors include this in their differential diagnosis. Sandhya Manohar, MDa Bernard Gitler, MDa,b a Department of Medicine Montefiore New Rochelle Hospital New Rochelle, NY b Division of Cardiology Montefiore New Rochelle Hospital New Rochelle, NY
http://dx.doi.org/10.1016/j.amjmed.2014.10.048
References 1. Yamagami F, Mizuno A, Shirai T, Niwa K. A savage sequence: STsegment elevations with pulmonary embolism. Am J Med. 2014;127(9):820-822. 2. Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of the Second Consensus Conference: endorsed by the Heart Rhythm Society and the European Heart Rhythm Association. Circulation. 2005;111(5):659-670. 3. ECG Response: October 7, 2014. Circulation. 2014;130(15):1299. 4. Dumaine R, Towbin JA, Brugada P, et al. Ionic mechanisms responsible for the electrocardiographic phenotype of the Brugada syndrome are temperature dependent. Circ Res. 1999;85(9):803-809.
