International Journal of Cardiology 177 (2014) 167–168
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Myocardial infarction, Takotsubo syndrome, or myocardial infarction/ Takotsubo syndrome? John E. Madias ⁎ The Icahn School of Medicine at Mount Sinai, New York, NY, United States The Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, United States
a r t i c l e
i n f o
Article history: Received 24 August 2014 Accepted 16 September 2014 Available online 28 September 2014 Keywords: Myocardial infraction Type 1 myocardial infraction Type 2 myocardial infraction Takotsubo syndrome Third universal definition of myocardial infarction Myocardial infraction/Takotsubo syndrome
To the Editor: I was delighted to read the contribution by Y-Hassan, published on August 5, 2014 in the Journal ahead of print, regarding the vagaries of distinguishing the diagnoses of type 2, supply/demand (ischemic imbalance), myocardial infarction (MI-2), and surprisingly even type 1, “the conventional type” myocardial infarction (MI-1), from the one of Takotsubo syndrome (TTS) [1]. The logical arguments of the author lead to the sober conclusion that if one applies strictly the criteria of the Third universal definition of myocardial infarction [2] for the diagnoses of MI-2 and MI-1, and the various current diagnostic criteria for TTS, summarized elsewhere [3,4], in the evaluation of patients presenting with symptoms/signs of an acute coronary syndrome (ACS), a given case of a patient presenting in the Emergency Department (ED), or cared for in the Coronary Care Unit (CCU), or even followed-up in the Cardiac Clinic (CC) may be categorized as MI-2, MI-1, or TTS, interchangeably, and this is alarming! Some clinicians may feel that there are major distinguishing features between MI-1 and TTS, and therefore it is unlikely that these 2 clinical entities can be missed for each other, but patients with MI-1, particularly presenting very early or very late in the process or with atypical features, may look surprisingly similar to patients with TTS. Also if one considers the ⁎ Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, United States. Tel.: +1 718 334 5005; fax: +1 718 334 5990. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.09.063 0167-5273/© 2014 Published by Elsevier Ireland Ltd.
triggering of the TTS pathophysiology as a complication, or in the aftermath, of bleeding, left ventricular (LV) outflow tract obstruction, sepsis, chronic obstructive pulmonary diseases with acute respiratory decompensation, the various types of cerebrovascular accidents [1], and in many other acute critical illnesses, TTS may be a very frequent occurrence. The prevalence of TTS may be even higher if one envisages this pathology presenting in its classic form (apical ballooning, midventricular akinesis/dyskinesis, or reverse TTS), less frequently, than in the form of TTS with varying in topography and severity ventricular wall motion abnormalities (VWMAs) affecting the LV and/or right ventricle (RV) [5]. Finally in accordance with the notion that TTS can present as a comorbidity, one can envisage a “TTS component” in the setting of an MI-1, or MI-2 [3,5]. Thus a transient VWMA in a contralateral to the myocardial territory, which has been impacted by an MI-1 or MI-2, may represent a “TTS component” [3,5], and such occurrence may be frequent. If such a complication of MI-1 or MI-2 is mild, in its clinical expression, the diagnosis of a “TTS component” may be problematic. Is there a solution to this conundrum? First, we should accept the possibility that occasionally MI-1, MI-2, and TTS, early in their course may be indistinguishable from each other [1], and clinical characteristics, employment of cardiac catheterization, echocardiography (ECHO), other imaging, and testing for catecholamines and biomarkers, may not always be helpful in their differentiation. Second, we should accept the possibility that occasionally we may need to settle for a delayed, retrospective differential diagnosis of MI-1, MI-2 and TTS, in the CCU, during hospitalization, or even in the CC, employing imaging modalities, particularly ECHO, since this is the most feasible, available, and economical means of repeatedly interrogating for changes in the initially observed VWMAs, and global LV ejection fraction, and RV ejection fraction. A caveat to be considered herein is that such changes (improvement) at follow-up are also witnessed in patients with MI-1 or MI-2. Perhaps the absence of LV remodeling, particularly common in patients with MI-1, may be useful in making retrospectively the diagnosis of TTS. As to the abolishment and/or amelioration of VWMAs at follow-up in patients presenting in a picture of ACS, repeat more sophisticated ECHO evaluation [6], than currently routinely practiced, with ancillary information (e.g., presence, severity, and extend of coronary artery lesions), may be needed for the differentiation among MI-1, MI-2, and TTS. Third, we should accept the possibility that occasionally a “TTS component” may coincide with an MI-1 or MI-2, with one of the latter two acting as the physical/emotional stressful factor(s) triggering it, and in this case such a combination may require
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J.E. Madias / International Journal of Cardiology 177 (2014) 167–168
repeat comparative ECHO, in the CCU, during hospitalization, and at follow-up in the CC, to tease out the “TTS component”, from the ventricular consequences of MI-1, or MI-2. To this end, one should enlist the additional insights provided by real-time 3D ECHO, and longitudinal, circumferential, and radial peak strains 2D, via speckle tracking ECHO, regarding the extent and distribution of the initially observed LV and RV VWMAs [6], in conjunction with the relative extent of delayed gadolinium hyperenhancement, using cardiac magnetic resonance imaging [6], at follow-up during hospitalization, or in the CC. The contribution by Y-Hassan [1], brings to focus a problem which will confront increasingly clinicians in the ER, CCU, and the CC, i.e., the diagnostic differentiation of MI-1, MI-2, and TTS, and even the possible comorbidity of a “TTS component” in the presence of an MI-1, or MI-2. Conflicts of interest None.
References [1] Y-Hassan S. In case of strict application, the third universal definition of myocardial infarction will erase takotsubo syndrome as a diagnosis. Int J Cardiol Aug. 5, 2014. http://dx.doi.org/10.1016/j.ijcard.2014.07.220 [pii: S0167-5273(14)01430-2, Epub ahead of print]. [2] Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012;60:1581–98. [3] Madias JE. Why the current diagnostic criteria of Takotsubo syndrome are outmoded: a proposal for new criteria. Int J Cardiol 2014;174:468–70. [4] Redfors B, Shao Y, Lyon AR, Omerovic E. Diagnostic criteria for takotsubo syndrome: a call for consensus. Int J Cardiol 2014;176:274–6. [5] Madias JE. Forme fruste cases of Takotsubo syndrome: a hypothesis. Eur J Intern Med 2014;25:e47. [6] Orii M, Hirata K, Tanimoto T, et al. Two-dimensional speckle tracking echocardiography for the prediction of reversible myocardial dysfunction after acute myocardial infarction: comparison with magnetic resonance imaging. Echocardiography Aug. 11, 2014. http://dx.doi.org/10.1111/echo.12726 [Epub ahead of print].
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Myocardial infarction, Takotsubo syndrome, or myocardial infarction/ Takotsubo syndrome? John E. Madias ⁎ The Icahn School of Medicine at Mount Sinai, New York, NY, United States The Division of Cardiology, Elmhurst Hospital Center, Elmhurst, NY, United States
a r t i c l e
i n f o
Article history: Received 24 August 2014 Accepted 16 September 2014 Available online 28 September 2014 Keywords: Myocardial infraction Type 1 myocardial infraction Type 2 myocardial infraction Takotsubo syndrome Third universal definition of myocardial infarction Myocardial infraction/Takotsubo syndrome
To the Editor: I was delighted to read the contribution by Y-Hassan, published on August 5, 2014 in the Journal ahead of print, regarding the vagaries of distinguishing the diagnoses of type 2, supply/demand (ischemic imbalance), myocardial infarction (MI-2), and surprisingly even type 1, “the conventional type” myocardial infarction (MI-1), from the one of Takotsubo syndrome (TTS) [1]. The logical arguments of the author lead to the sober conclusion that if one applies strictly the criteria of the Third universal definition of myocardial infarction [2] for the diagnoses of MI-2 and MI-1, and the various current diagnostic criteria for TTS, summarized elsewhere [3,4], in the evaluation of patients presenting with symptoms/signs of an acute coronary syndrome (ACS), a given case of a patient presenting in the Emergency Department (ED), or cared for in the Coronary Care Unit (CCU), or even followed-up in the Cardiac Clinic (CC) may be categorized as MI-2, MI-1, or TTS, interchangeably, and this is alarming! Some clinicians may feel that there are major distinguishing features between MI-1 and TTS, and therefore it is unlikely that these 2 clinical entities can be missed for each other, but patients with MI-1, particularly presenting very early or very late in the process or with atypical features, may look surprisingly similar to patients with TTS. Also if one considers the ⁎ Division of Cardiology, Elmhurst Hospital Center, 79-01 Broadway, Elmhurst, NY 11373, United States. Tel.: +1 718 334 5005; fax: +1 718 334 5990. E-mail address: [email protected].
http://dx.doi.org/10.1016/j.ijcard.2014.09.063 0167-5273/© 2014 Published by Elsevier Ireland Ltd.
triggering of the TTS pathophysiology as a complication, or in the aftermath, of bleeding, left ventricular (LV) outflow tract obstruction, sepsis, chronic obstructive pulmonary diseases with acute respiratory decompensation, the various types of cerebrovascular accidents [1], and in many other acute critical illnesses, TTS may be a very frequent occurrence. The prevalence of TTS may be even higher if one envisages this pathology presenting in its classic form (apical ballooning, midventricular akinesis/dyskinesis, or reverse TTS), less frequently, than in the form of TTS with varying in topography and severity ventricular wall motion abnormalities (VWMAs) affecting the LV and/or right ventricle (RV) [5]. Finally in accordance with the notion that TTS can present as a comorbidity, one can envisage a “TTS component” in the setting of an MI-1, or MI-2 [3,5]. Thus a transient VWMA in a contralateral to the myocardial territory, which has been impacted by an MI-1 or MI-2, may represent a “TTS component” [3,5], and such occurrence may be frequent. If such a complication of MI-1 or MI-2 is mild, in its clinical expression, the diagnosis of a “TTS component” may be problematic. Is there a solution to this conundrum? First, we should accept the possibility that occasionally MI-1, MI-2, and TTS, early in their course may be indistinguishable from each other [1], and clinical characteristics, employment of cardiac catheterization, echocardiography (ECHO), other imaging, and testing for catecholamines and biomarkers, may not always be helpful in their differentiation. Second, we should accept the possibility that occasionally we may need to settle for a delayed, retrospective differential diagnosis of MI-1, MI-2 and TTS, in the CCU, during hospitalization, or even in the CC, employing imaging modalities, particularly ECHO, since this is the most feasible, available, and economical means of repeatedly interrogating for changes in the initially observed VWMAs, and global LV ejection fraction, and RV ejection fraction. A caveat to be considered herein is that such changes (improvement) at follow-up are also witnessed in patients with MI-1 or MI-2. Perhaps the absence of LV remodeling, particularly common in patients with MI-1, may be useful in making retrospectively the diagnosis of TTS. As to the abolishment and/or amelioration of VWMAs at follow-up in patients presenting in a picture of ACS, repeat more sophisticated ECHO evaluation [6], than currently routinely practiced, with ancillary information (e.g., presence, severity, and extend of coronary artery lesions), may be needed for the differentiation among MI-1, MI-2, and TTS. Third, we should accept the possibility that occasionally a “TTS component” may coincide with an MI-1 or MI-2, with one of the latter two acting as the physical/emotional stressful factor(s) triggering it, and in this case such a combination may require
168
J.E. Madias / International Journal of Cardiology 177 (2014) 167–168
repeat comparative ECHO, in the CCU, during hospitalization, and at follow-up in the CC, to tease out the “TTS component”, from the ventricular consequences of MI-1, or MI-2. To this end, one should enlist the additional insights provided by real-time 3D ECHO, and longitudinal, circumferential, and radial peak strains 2D, via speckle tracking ECHO, regarding the extent and distribution of the initially observed LV and RV VWMAs [6], in conjunction with the relative extent of delayed gadolinium hyperenhancement, using cardiac magnetic resonance imaging [6], at follow-up during hospitalization, or in the CC. The contribution by Y-Hassan [1], brings to focus a problem which will confront increasingly clinicians in the ER, CCU, and the CC, i.e., the diagnostic differentiation of MI-1, MI-2, and TTS, and even the possible comorbidity of a “TTS component” in the presence of an MI-1, or MI-2. Conflicts of interest None.
References [1] Y-Hassan S. In case of strict application, the third universal definition of myocardial infarction will erase takotsubo syndrome as a diagnosis. Int J Cardiol Aug. 5, 2014. http://dx.doi.org/10.1016/j.ijcard.2014.07.220 [pii: S0167-5273(14)01430-2, Epub ahead of print]. [2] Thygesen K, Alpert JS, Jaffe AS, et al. Third universal definition of myocardial infarction. J Am Coll Cardiol 2012;60:1581–98. [3] Madias JE. Why the current diagnostic criteria of Takotsubo syndrome are outmoded: a proposal for new criteria. Int J Cardiol 2014;174:468–70. [4] Redfors B, Shao Y, Lyon AR, Omerovic E. Diagnostic criteria for takotsubo syndrome: a call for consensus. Int J Cardiol 2014;176:274–6. [5] Madias JE. Forme fruste cases of Takotsubo syndrome: a hypothesis. Eur J Intern Med 2014;25:e47. [6] Orii M, Hirata K, Tanimoto T, et al. Two-dimensional speckle tracking echocardiography for the prediction of reversible myocardial dysfunction after acute myocardial infarction: comparison with magnetic resonance imaging. Echocardiography Aug. 11, 2014. http://dx.doi.org/10.1111/echo.12726 [Epub ahead of print].
