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Electrocardiogram differentiation between acute anterior ST-segment elevation myocardial infarction and Takotsubo syndrome☆
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ScienceDirect Journal of Electrocardiology 47 (2014) 953–955 www.jecgonline.com
Letters to the Editor High V1–V2 electrode placement can indeed cause “Brugada-type” patterns in athletes Dear Dr Wagner: On behalf of my colleagues at the University of North Carolina at Chapel Hill, I thank the authors of the letter for their interest in our article on Brugada-type ECGs in athletes [1]. I also wish to acknowledge their very recent efforts to enhance the diagnostic evaluation of athletes' ECGs [2]. Improving on the interpretation of a possible Brugada ECG is a challenging and common goal that we all share [3,4]. I would agree with the first comment that echocardiography would have been helpful in assessing our patients. While the presence of structural heart disease is not required to make or exclude the diagnosis of Brugada syndrome, we cannot definitively conclude whether or not structural abnormalities played a role in our findings. At this time, echocardiograms are not a standard component of our preparticipation screening and thus are ordered if clinically indicated. That said, in a pilot study of approximately 50 football and basketball players who did undergo limited echos, none of those with an abnormal high lead ECG had any structural abnormalities (unpublished data). In regards to the authors' additional observations: we initiated our study in 2009, and thus we referred to the latest guidelines at the time [5]. Indeed, we initially did not classify our positive ECGs as Brugada-type (preferring “Brugadalike”), and using this broader term, found that up to 32% of athletes had a suspicious ECG [1,6]. At the request of the reviewers, we reclassified all of our ECGs as Brugada-type 2 or 3 or neither and subsequently reported a lower number. The authors' analysis of our published examples was compelling. However, the appearance of the r′ in our cohort is heterogeneous. Indeed, looking at Figure 2 from our paper, the descending limb of r′ is curved: if one takes the tangent of the line, rather than the initial half of the downslope to draw the triangle, then the base is at least 4 mm. As Dr. Postema remarks in his editorial, the Serra et al criterion was not applied to high lead ECGs, and the lack of provocation testing (which we did not perform either) limits the negative predictive value [3]. Nevertheless, the authors in their letter reinforce our overarching message: that the abnormal ECGs we recorded with our high lead ECGs were due to purposeful misplacement of leads and very unlikely due to Brugada 0022-0736/© 2014 Elsevier Inc. All rights reserved.
syndrome. Correct lead placement is fundamental to limit non-diagnostic ECGs.
Eugene H. Chung, MD, FACC, FHRS Division of Cardiology, Cardiac Electrophysiology UNC School of Medicine, 160 Dental Circle, CB 7075 Chapel Hill, NC 27599 E-mail address: [email protected] http://dx.doi.org/10.1016/j.jelectrocard.2014.07.012 References [1] Chung EH, McNeely III DE, Gehi AK, Brickner T, Evans S, Pryski E, et al. Brugada-type patterns are easily observed in high precordial lead ECGs in collegiate athletes. J Electrocardiol 2014;47(1):1–6. [2] Serra G, Baranchuk A, Bayes de Luna A, et al. New electrocardiographic criteria to differentiate type 2 Brugada pattern from ECG of healthy athletes with r′-wave in leads V1/V2. Europace 2014 http://dx. doi.org/10.1093/europace/euu025. [3] Posetema PG. Are we able to predict the diagnosis of Brugada syndrome? Europace 2014 http://dx.doi.org/10.1093/europace/euu029. [4] Chevallier S, Forclaz A, Tenkorang J, et al. New electrocardiographic criteria for discriminating between Brugada types 2 and 3 patterns and incomplete right bundle branch block. J Am Coll Cardiol 2011;58:2290–8. [5] Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of second consensus conference. Heart Rhythm 2005;2:429–40. [6] Chung EH, Evans S, Pryski E, et al. High precordial lead ECGs can easily induce Brugada-like patterns in collegiate athletes undergoing preparticipation screening. Featured poster abstract presentation at Heart Rhythm Society Scientific Sessions; 2012.
Electrocardiogram differentiation between acute anterior ST-segment elevation myocardial infarction and Takotsubo syndrome ☆
To the Editor: I enjoyed very much reading the report by Parkkonen et al., published in the Journal online, ahead of print, on June 14, 2014 [1], about differentiating acute anterior STsegment elevation myocardial infarction (ASTEMI) from Takotsubo syndrome (TTS), using the electrocardiogram (ECG). The authors compared the amplitude of the STsegment elevations (+ ST), T-wave inversions (T↓), Q☆
Conflicts of interest: None.
954
Letters to the Editor / Journal of Electrocardiology 47 (2014) 953–955
waves, and QT-interval duration of the admission ECGs of 48 patients with apical TTS, 9 patients with midventricular TTC, and 96 patients, with ASTEMI, and found that the patients with ASTEMI had ST + in lead V1 more often than the patients with the 2 forms of TTS, and that they also had higher ST + in leads V2-V5, than the patients with TTS. They also concluded that the absence of ST + in lead V1, and ST + b 2 mm in amplitude in lead V2 partially distinguishes TTC from ASTEMI, although this ECG criterion cannot be relied upon in clinical practice for a safe differentiation of these 2 conditions. The authors should be commended for bringing up the issue of where the ST + is measured by different authors, and its impact on the calculation of sensitivity, specificity, and predictive value of the various ECG indices employed in the differentiation between ASTEMI and TTS. Recently a report has associated TTS with low voltage ECG (LVECG), or attenuation of the amplitude of QRS complexes (ATTQRS), based on the comparison of 2 ECGs [2]. The present study employed only the admission ECG, and thus only LVECG could be explored; accordingly it would be of interest to evaluate whether LVECG was more common in patient with TTS than in those with ASTEMI in the present study. Also an association with LVECG in leads I and aVL has been noted in patients with mid-ventricular TTS [3], and this could be explored in the 9 patients with this type of TTS of the present study. Finally, it will be of interest to the readers to know about the remarkable finding of the one patient who "had a measured [ejection fraction] (EF) of 0%, suggesting contraction movement in a plane not measurable in 2-dimensional left ventriculography”, and what was the approximate EF by echocardiography, reflecting 3D assessment of left ventricular function.
John E. Madias, MD, FACC, FAHA* Icahn School of Medicine at Mount Sinai, New York, NY, USA Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, USA *Division of Cardiology, Elmhurst Hospital Center, 79–01 Broadway, Elmhurst, NY 11373, USA E-mail address: [email protected] http://dx.doi.10.1016/j.jelectrocard.2014.08.004
References [1] Parkkonen O, Allonen J, Vaara S, Viitasalo M, Nieminen MS, Sinisalo J. Differences in ST-elevation and T-wave amplitudes do not reliably differentiate takotsubo cardiomyopathy from acute anterior myocardial infarction. J Electrocardiol 2014 http://dx.doi.org/ 10.1016/j.jelectrocard.2014.06.006 [pii: S0022-0736(14)00206-4. Epub ahead of print].
[2] 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. [3] Madias JE. Electrocardiogram lead-specific QRS attenuation in an atypical midventricular case of Takotsubo syndrome. J Electrocardiol 2013;46:728–9.
Letter by Di Bella et al. regarding the article “Agreement between ST elevation and late enhancement evaluated by MRI in patients with acute myocarditis” ☆ , ☆☆ To the Editor: We have read with great interest the paper by Gabriela Meléndez-Ramírez et al. [1] about the agreement between ST segment elevation (STE) and late gadolinium enhancement (LGE) evaluated by MRI in patients with acute myocarditis (AM). The authors have enrolled 32 consecutive patients with AM; they have showed a moderate agreement between the localization of STE and LGE only in the inferolateral localization. Recently, we have analyzed the electrocardiographic (ECG) findings of 81 patients with AM, at admission and 48 hours later [2]. The main results of our study were: 1) ST/ T interval changes did not show a close relationship with the areas of ventricular damage detected by MRI; 2) about 1/3 of patients with AM had normal ECG at admission; 3) pericardial involvement (myopericarditis) was a frequent finding (pericardial effusion and pericardial LGE were observed in 60% of patients), and it was more often associated with a normal rather than an abnormal ECG. The heterogeneity of etiology and clinical presentation, along with the complexity of pathophysiology of AM can contribute to understand the reasons why the results observed in our study [2] differ from those reported by Gabriela Meléndez-Ramírez et al. [1]. First of all, AM presents both a systemic phase (flu-like syndrome and viral proliferation) and a phase of myocardial tissue involvement, as a consequence of either a direct viral damage or an immune reaction. Cardiac MRI by LGE is able to identify focal macroscopic myocardial damage, which is usually observed in the epicardial layer of the lateral wall [2]. However, many data suggest that even segments of left ventricular myocardium which do not show LGE on MRI can be involved by AM as well, and therefore this phenomenon may explain the divergence of ECG findings from MRI pattern. An interesting paper by De Cobelli, comparing biopsy versus LGE on MRI, reported a septal biopsy positive for AM in segments which failed to show LGE on MRI [3].
☆ ☆☆
Conflict of interest: none declared. Funding: None.
ScienceDirect Journal of Electrocardiology 47 (2014) 953–955 www.jecgonline.com
Letters to the Editor High V1–V2 electrode placement can indeed cause “Brugada-type” patterns in athletes Dear Dr Wagner: On behalf of my colleagues at the University of North Carolina at Chapel Hill, I thank the authors of the letter for their interest in our article on Brugada-type ECGs in athletes [1]. I also wish to acknowledge their very recent efforts to enhance the diagnostic evaluation of athletes' ECGs [2]. Improving on the interpretation of a possible Brugada ECG is a challenging and common goal that we all share [3,4]. I would agree with the first comment that echocardiography would have been helpful in assessing our patients. While the presence of structural heart disease is not required to make or exclude the diagnosis of Brugada syndrome, we cannot definitively conclude whether or not structural abnormalities played a role in our findings. At this time, echocardiograms are not a standard component of our preparticipation screening and thus are ordered if clinically indicated. That said, in a pilot study of approximately 50 football and basketball players who did undergo limited echos, none of those with an abnormal high lead ECG had any structural abnormalities (unpublished data). In regards to the authors' additional observations: we initiated our study in 2009, and thus we referred to the latest guidelines at the time [5]. Indeed, we initially did not classify our positive ECGs as Brugada-type (preferring “Brugadalike”), and using this broader term, found that up to 32% of athletes had a suspicious ECG [1,6]. At the request of the reviewers, we reclassified all of our ECGs as Brugada-type 2 or 3 or neither and subsequently reported a lower number. The authors' analysis of our published examples was compelling. However, the appearance of the r′ in our cohort is heterogeneous. Indeed, looking at Figure 2 from our paper, the descending limb of r′ is curved: if one takes the tangent of the line, rather than the initial half of the downslope to draw the triangle, then the base is at least 4 mm. As Dr. Postema remarks in his editorial, the Serra et al criterion was not applied to high lead ECGs, and the lack of provocation testing (which we did not perform either) limits the negative predictive value [3]. Nevertheless, the authors in their letter reinforce our overarching message: that the abnormal ECGs we recorded with our high lead ECGs were due to purposeful misplacement of leads and very unlikely due to Brugada 0022-0736/© 2014 Elsevier Inc. All rights reserved.
syndrome. Correct lead placement is fundamental to limit non-diagnostic ECGs.
Eugene H. Chung, MD, FACC, FHRS Division of Cardiology, Cardiac Electrophysiology UNC School of Medicine, 160 Dental Circle, CB 7075 Chapel Hill, NC 27599 E-mail address: [email protected] http://dx.doi.org/10.1016/j.jelectrocard.2014.07.012 References [1] Chung EH, McNeely III DE, Gehi AK, Brickner T, Evans S, Pryski E, et al. Brugada-type patterns are easily observed in high precordial lead ECGs in collegiate athletes. J Electrocardiol 2014;47(1):1–6. [2] Serra G, Baranchuk A, Bayes de Luna A, et al. New electrocardiographic criteria to differentiate type 2 Brugada pattern from ECG of healthy athletes with r′-wave in leads V1/V2. Europace 2014 http://dx. doi.org/10.1093/europace/euu025. [3] Posetema PG. Are we able to predict the diagnosis of Brugada syndrome? Europace 2014 http://dx.doi.org/10.1093/europace/euu029. [4] Chevallier S, Forclaz A, Tenkorang J, et al. New electrocardiographic criteria for discriminating between Brugada types 2 and 3 patterns and incomplete right bundle branch block. J Am Coll Cardiol 2011;58:2290–8. [5] Antzelevitch C, Brugada P, Borggrefe M, et al. Brugada syndrome: report of second consensus conference. Heart Rhythm 2005;2:429–40. [6] Chung EH, Evans S, Pryski E, et al. High precordial lead ECGs can easily induce Brugada-like patterns in collegiate athletes undergoing preparticipation screening. Featured poster abstract presentation at Heart Rhythm Society Scientific Sessions; 2012.
Electrocardiogram differentiation between acute anterior ST-segment elevation myocardial infarction and Takotsubo syndrome ☆
To the Editor: I enjoyed very much reading the report by Parkkonen et al., published in the Journal online, ahead of print, on June 14, 2014 [1], about differentiating acute anterior STsegment elevation myocardial infarction (ASTEMI) from Takotsubo syndrome (TTS), using the electrocardiogram (ECG). The authors compared the amplitude of the STsegment elevations (+ ST), T-wave inversions (T↓), Q☆
Conflicts of interest: None.
954
Letters to the Editor / Journal of Electrocardiology 47 (2014) 953–955
waves, and QT-interval duration of the admission ECGs of 48 patients with apical TTS, 9 patients with midventricular TTC, and 96 patients, with ASTEMI, and found that the patients with ASTEMI had ST + in lead V1 more often than the patients with the 2 forms of TTS, and that they also had higher ST + in leads V2-V5, than the patients with TTS. They also concluded that the absence of ST + in lead V1, and ST + b 2 mm in amplitude in lead V2 partially distinguishes TTC from ASTEMI, although this ECG criterion cannot be relied upon in clinical practice for a safe differentiation of these 2 conditions. The authors should be commended for bringing up the issue of where the ST + is measured by different authors, and its impact on the calculation of sensitivity, specificity, and predictive value of the various ECG indices employed in the differentiation between ASTEMI and TTS. Recently a report has associated TTS with low voltage ECG (LVECG), or attenuation of the amplitude of QRS complexes (ATTQRS), based on the comparison of 2 ECGs [2]. The present study employed only the admission ECG, and thus only LVECG could be explored; accordingly it would be of interest to evaluate whether LVECG was more common in patient with TTS than in those with ASTEMI in the present study. Also an association with LVECG in leads I and aVL has been noted in patients with mid-ventricular TTS [3], and this could be explored in the 9 patients with this type of TTS of the present study. Finally, it will be of interest to the readers to know about the remarkable finding of the one patient who "had a measured [ejection fraction] (EF) of 0%, suggesting contraction movement in a plane not measurable in 2-dimensional left ventriculography”, and what was the approximate EF by echocardiography, reflecting 3D assessment of left ventricular function.
John E. Madias, MD, FACC, FAHA* Icahn School of Medicine at Mount Sinai, New York, NY, USA Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, USA *Division of Cardiology, Elmhurst Hospital Center, 79–01 Broadway, Elmhurst, NY 11373, USA E-mail address: [email protected] http://dx.doi.10.1016/j.jelectrocard.2014.08.004
References [1] Parkkonen O, Allonen J, Vaara S, Viitasalo M, Nieminen MS, Sinisalo J. Differences in ST-elevation and T-wave amplitudes do not reliably differentiate takotsubo cardiomyopathy from acute anterior myocardial infarction. J Electrocardiol 2014 http://dx.doi.org/ 10.1016/j.jelectrocard.2014.06.006 [pii: S0022-0736(14)00206-4. Epub ahead of print].
[2] 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. [3] Madias JE. Electrocardiogram lead-specific QRS attenuation in an atypical midventricular case of Takotsubo syndrome. J Electrocardiol 2013;46:728–9.
Letter by Di Bella et al. regarding the article “Agreement between ST elevation and late enhancement evaluated by MRI in patients with acute myocarditis” ☆ , ☆☆ To the Editor: We have read with great interest the paper by Gabriela Meléndez-Ramírez et al. [1] about the agreement between ST segment elevation (STE) and late gadolinium enhancement (LGE) evaluated by MRI in patients with acute myocarditis (AM). The authors have enrolled 32 consecutive patients with AM; they have showed a moderate agreement between the localization of STE and LGE only in the inferolateral localization. Recently, we have analyzed the electrocardiographic (ECG) findings of 81 patients with AM, at admission and 48 hours later [2]. The main results of our study were: 1) ST/ T interval changes did not show a close relationship with the areas of ventricular damage detected by MRI; 2) about 1/3 of patients with AM had normal ECG at admission; 3) pericardial involvement (myopericarditis) was a frequent finding (pericardial effusion and pericardial LGE were observed in 60% of patients), and it was more often associated with a normal rather than an abnormal ECG. The heterogeneity of etiology and clinical presentation, along with the complexity of pathophysiology of AM can contribute to understand the reasons why the results observed in our study [2] differ from those reported by Gabriela Meléndez-Ramírez et al. [1]. First of all, AM presents both a systemic phase (flu-like syndrome and viral proliferation) and a phase of myocardial tissue involvement, as a consequence of either a direct viral damage or an immune reaction. Cardiac MRI by LGE is able to identify focal macroscopic myocardial damage, which is usually observed in the epicardial layer of the lateral wall [2]. However, many data suggest that even segments of left ventricular myocardium which do not show LGE on MRI can be involved by AM as well, and therefore this phenomenon may explain the divergence of ECG findings from MRI pattern. An interesting paper by De Cobelli, comparing biopsy versus LGE on MRI, reported a septal biopsy positive for AM in segments which failed to show LGE on MRI [3].
☆ ☆☆
Conflict of interest: none declared. Funding: None.