International Journal of Cardiology 196 (2015) 36–37
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Takotsubo cardiomyopathy — Everything's illuminated? L. Christian Napp a,⁎, Jelena-Rima Ghadri b, Johann Bauersachs a, Christian Templin b a b
Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany University Heart Center, Department of Cardiology, University Hospital Zurich, Zurich, Switzerland
a r t i c l e
i n f o
Article history: Received 21 May 2015 Accepted 29 May 2015 Available online 30 May 2015 Keywords: Takotsubo cardiomyopathy Acute coronary syndrome Coronary artery disease Regional wall motion abnormality Post-ischemic myocardial stunning
We are grateful for the attention and comments [1] Dr. Y-Hassan gave to our manuscript [2]. With his letter Dr. Y-Hassan raises two important points to which we want to respond. Presence of TTCM in patients with ACS. Indeed, there are reports on patients simultaneously suffering from ACS and TTCM [3]. While it is virtually impossible to discriminate whether ACS or TTCM was first, it appears likely that the one may have triggered the second. In cases of a TTCM pattern with a coronary lesion distant to the wall motion abnormality, e.g. plaque rupture in the RCA and apical ballooning, the coexistence is easy to appreciate. In contrast, a much bigger challenge is the clinical evaluation of ACS patients with a significant coronary lesion and a TTCM pattern fully matching the perfusion territory of the stenosed vessel. Neither biomarkers nor imaging modalities (angiography, echocardiography, MRI, nuclear imaging) would be able to exclude coexisting TTCM in such cases. Notwithstanding, our second patient demonstrated markedly elevated biomarker levels on admission, STsegment elevations congruent with the LAD territory, a subtotal lesion in the LAD and a full perfusion-contraction overlap, strongly suggesting that STE-ACS was the correct diagnosis. As stated correctly by Dr. YHassan, we cannot completely exclude that she had TTCM in addition to and precipitated by ACS. Of note, while of interest for pathophysiological considerations, the question whether TTCM was additionally present appeared not relevant for treatment: The decision for or against PCI did not depend on the diagnosis of coexisting TTCM. However, in selected cases of TTCM with coexisting CAD, where angiography cannot determine the significance of the coronary lesion, additional imaging ⁎ Corresponding author at: Department of Cardiology and Angiology OE 6880, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. E-mail address: [email protected] (L.C. Napp).
http://dx.doi.org/10.1016/j.ijcard.2015.05.169 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
tools such as intracoronary diagnostics (e.g. optical coherence tomography) or MRI may be indicated for making a therapeutic decision. TTCM is proposed to be a form of post-ischemic myocardial stunning. We thank Dr. Y-Hassan for this important comment, which emphasizes the need for future mechanistic research in the TTCM field. Until today the pathophysiology of TTCM is incompletely understood. While lots of theories and associations were described, e.g. coronary spasms, catecholamine spillover, spontaneously resolved intracoronary thrombus, and β-receptor heterogeneity, a clear-cut demonstration of pathogenesis reaching unified acceptance is still lacking. As comprehensively outlined by Dr. Y-Hassan, stunning in TTCM indeed shares many features with post-ischemic myocardial stunning (PIMS) [1,4]. However, one important difference is that PIMS requires ischemia as a trigger. Microvascular perfusion abnormalities during TTCM probably represent the consequence but not the cause of stunning in the majority of patients. Coronary (macrovascular) perfusion abnormalities appear unlikely to be the cause of TTCM, as the peculiar wall motion abnormalities – in particular in its midventricular and basal form – obviously do not relate to a coronary territory. Dr. Y-Hassan further mentioned that dobutamine may improve contractility also in TTCM. In light of many publications reporting the development of TTCM after dobutamine administration, there are very few studies on the effect of dobutamine for treatment of TTCM, with controversial results [5,6]. Of note, dobutamine significantly increases the risk for developing a dynamic left ventricular outflow tract obstruction (DLVOTO) already in healthy people [7,8]. Importantly, DLVOTO is a frequent complication during TTCM [9], especially in its apical form. Therefore, as long as guidelines on TTCM treatment do not exist, the use of dobutamine should be considered with caution. Taken together, the field eagerly awaits novel approaches to mechanistically study the pathogenesis of TTCM, a disease we only begin to understand. Sources of funding None. Conflict of interest None declared. Acknowledgments None.
L.C. Napp et al. / International Journal of Cardiology 196 (2015) 36–37
References [1] S. Y-Hassan, Acute coronary syndrome or takotsubo syndrome: most probably both of them, the first has triggered the second, Int. J. Cardiol. 190 (2015) 367–368. [2] L.C. Napp, J.R. Ghadri, J. Bauersachs, C. Templin, Acute coronary syndrome or takotsubo cardiomyopathy: the suspect may not always be the culprit, Int. J. Cardiol. 187 (2015) 116–119. [3] F. Tota, M. Ruggiero, M. Sassara, N. Locuratolo, L. Sublimi Saponetti, G. Frasso, et al., Subacute stent thrombosis and stress-induced cardiomyopathy: trigger or consequence? Am. J. Cardiovasc. Dis. 3 (2013) 175–179. [4] E. Braunwald, R.A. Kloner, The stunned myocardium: prolonged, postischemic ventricular dysfunction, Circulation 66 (1982) 1146–1149. [5] B. Uznanska, M. Plewka, K. Wierzbowska-Drabik, L. Chrzanowski, J.D. Kasprzak, Early prediction of ventricular recovery in takotsubo syndrome using stress and contrast echocardiography, Med. Sci. Monit. 15 (2009) CS89–CS94.
37
[6] S. Fujiwara, Y. Takeishi, S. Isoyama, G. Aono, K. Takizawa, H. Honda, et al., Responsiveness to dobutamine stimulation in patients with left ventricular apical ballooning syndrome, Am. J. Cardiol. 100 (2007) 1600–1603. [7] L.C. Napp, U. Bavendiek, J. Tongers, J. Bauersachs, P. Roentgen, Dynamic left ventricular outflow tract obstruction: hemodynamic pitfall ahead, Acute Card. Care 15 (2013) 76–77. [8] P. Meimoun, T. Benali, S. Sayah, A. Luycx-Bore, B. Maitre, C. Tribouilloy, Significance of systolic anterior motion of the mitral valve during dobutamine stress echocardiography, J. Am. Soc. Echocardiogr. 18 (2005) 49–56. [9] O. De Backer, P. Debonnaire, S. Gevaert, L. Missault, P. Gheeraert, L. Muyldermans, Prevalence, associated factors and management implications of left ventricular outflow tract obstruction in takotsubo cardiomyopathy: a two-year, two-center experience, BMC Cardiovasc. Disord. 14 (2014) 147.
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Takotsubo cardiomyopathy — Everything's illuminated? L. Christian Napp a,⁎, Jelena-Rima Ghadri b, Johann Bauersachs a, Christian Templin b a b
Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany University Heart Center, Department of Cardiology, University Hospital Zurich, Zurich, Switzerland
a r t i c l e
i n f o
Article history: Received 21 May 2015 Accepted 29 May 2015 Available online 30 May 2015 Keywords: Takotsubo cardiomyopathy Acute coronary syndrome Coronary artery disease Regional wall motion abnormality Post-ischemic myocardial stunning
We are grateful for the attention and comments [1] Dr. Y-Hassan gave to our manuscript [2]. With his letter Dr. Y-Hassan raises two important points to which we want to respond. Presence of TTCM in patients with ACS. Indeed, there are reports on patients simultaneously suffering from ACS and TTCM [3]. While it is virtually impossible to discriminate whether ACS or TTCM was first, it appears likely that the one may have triggered the second. In cases of a TTCM pattern with a coronary lesion distant to the wall motion abnormality, e.g. plaque rupture in the RCA and apical ballooning, the coexistence is easy to appreciate. In contrast, a much bigger challenge is the clinical evaluation of ACS patients with a significant coronary lesion and a TTCM pattern fully matching the perfusion territory of the stenosed vessel. Neither biomarkers nor imaging modalities (angiography, echocardiography, MRI, nuclear imaging) would be able to exclude coexisting TTCM in such cases. Notwithstanding, our second patient demonstrated markedly elevated biomarker levels on admission, STsegment elevations congruent with the LAD territory, a subtotal lesion in the LAD and a full perfusion-contraction overlap, strongly suggesting that STE-ACS was the correct diagnosis. As stated correctly by Dr. YHassan, we cannot completely exclude that she had TTCM in addition to and precipitated by ACS. Of note, while of interest for pathophysiological considerations, the question whether TTCM was additionally present appeared not relevant for treatment: The decision for or against PCI did not depend on the diagnosis of coexisting TTCM. However, in selected cases of TTCM with coexisting CAD, where angiography cannot determine the significance of the coronary lesion, additional imaging ⁎ Corresponding author at: Department of Cardiology and Angiology OE 6880, Hannover Medical School, Carl-Neuberg-Str. 1, D-30625 Hannover, Germany. E-mail address: [email protected] (L.C. Napp).
http://dx.doi.org/10.1016/j.ijcard.2015.05.169 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
tools such as intracoronary diagnostics (e.g. optical coherence tomography) or MRI may be indicated for making a therapeutic decision. TTCM is proposed to be a form of post-ischemic myocardial stunning. We thank Dr. Y-Hassan for this important comment, which emphasizes the need for future mechanistic research in the TTCM field. Until today the pathophysiology of TTCM is incompletely understood. While lots of theories and associations were described, e.g. coronary spasms, catecholamine spillover, spontaneously resolved intracoronary thrombus, and β-receptor heterogeneity, a clear-cut demonstration of pathogenesis reaching unified acceptance is still lacking. As comprehensively outlined by Dr. Y-Hassan, stunning in TTCM indeed shares many features with post-ischemic myocardial stunning (PIMS) [1,4]. However, one important difference is that PIMS requires ischemia as a trigger. Microvascular perfusion abnormalities during TTCM probably represent the consequence but not the cause of stunning in the majority of patients. Coronary (macrovascular) perfusion abnormalities appear unlikely to be the cause of TTCM, as the peculiar wall motion abnormalities – in particular in its midventricular and basal form – obviously do not relate to a coronary territory. Dr. Y-Hassan further mentioned that dobutamine may improve contractility also in TTCM. In light of many publications reporting the development of TTCM after dobutamine administration, there are very few studies on the effect of dobutamine for treatment of TTCM, with controversial results [5,6]. Of note, dobutamine significantly increases the risk for developing a dynamic left ventricular outflow tract obstruction (DLVOTO) already in healthy people [7,8]. Importantly, DLVOTO is a frequent complication during TTCM [9], especially in its apical form. Therefore, as long as guidelines on TTCM treatment do not exist, the use of dobutamine should be considered with caution. Taken together, the field eagerly awaits novel approaches to mechanistically study the pathogenesis of TTCM, a disease we only begin to understand. Sources of funding None. Conflict of interest None declared. Acknowledgments None.
L.C. Napp et al. / International Journal of Cardiology 196 (2015) 36–37
References [1] S. Y-Hassan, Acute coronary syndrome or takotsubo syndrome: most probably both of them, the first has triggered the second, Int. J. Cardiol. 190 (2015) 367–368. [2] L.C. Napp, J.R. Ghadri, J. Bauersachs, C. Templin, Acute coronary syndrome or takotsubo cardiomyopathy: the suspect may not always be the culprit, Int. J. Cardiol. 187 (2015) 116–119. [3] F. Tota, M. Ruggiero, M. Sassara, N. Locuratolo, L. Sublimi Saponetti, G. Frasso, et al., Subacute stent thrombosis and stress-induced cardiomyopathy: trigger or consequence? Am. J. Cardiovasc. Dis. 3 (2013) 175–179. [4] E. Braunwald, R.A. Kloner, The stunned myocardium: prolonged, postischemic ventricular dysfunction, Circulation 66 (1982) 1146–1149. [5] B. Uznanska, M. Plewka, K. Wierzbowska-Drabik, L. Chrzanowski, J.D. Kasprzak, Early prediction of ventricular recovery in takotsubo syndrome using stress and contrast echocardiography, Med. Sci. Monit. 15 (2009) CS89–CS94.
37
[6] S. Fujiwara, Y. Takeishi, S. Isoyama, G. Aono, K. Takizawa, H. Honda, et al., Responsiveness to dobutamine stimulation in patients with left ventricular apical ballooning syndrome, Am. J. Cardiol. 100 (2007) 1600–1603. [7] L.C. Napp, U. Bavendiek, J. Tongers, J. Bauersachs, P. Roentgen, Dynamic left ventricular outflow tract obstruction: hemodynamic pitfall ahead, Acute Card. Care 15 (2013) 76–77. [8] P. Meimoun, T. Benali, S. Sayah, A. Luycx-Bore, B. Maitre, C. Tribouilloy, Significance of systolic anterior motion of the mitral valve during dobutamine stress echocardiography, J. Am. Soc. Echocardiogr. 18 (2005) 49–56. [9] O. De Backer, P. Debonnaire, S. Gevaert, L. Missault, P. Gheeraert, L. Muyldermans, Prevalence, associated factors and management implications of left ventricular outflow tract obstruction in takotsubo cardiomyopathy: a two-year, two-center experience, BMC Cardiovasc. Disord. 14 (2014) 147.
