Journal of Cardiac Failure Vol. 21 No. 1 2015
Letters to the Editor Dobutamine Stress Echocardiography, Diastolic Function, and Myocardial Performance Index in Patients With History of Takotsubo Syndrome
referring to the data from the Stockholm Myocardial Infarction With Normal Coronaries study, estimate that “TTS constitutes around one-third or more of all such patients,”1 and one wonders if many of the rest, except for myocarditis or hypertrophic cardiomyopathy, have milder forms of TTS.9
To the Editor: Disclosures 1
The report by Collste et al, published ahead of print on September 26, 2014, in the Journal, about the response of 22 patients with takotsubo syndrome (TTS) to dobutamine stress echocardiography (DSE) compared with 22 control subjects, showed that the patients with TTS are not vulnerable to sympathetic stress 6 months after their index episode of TTS; in addition, the TTS patients had similar diastolic function, and myocardial performance index (MPI) during DSE but higher MPI at rest than the control subjects of similar age and sex. The authors appropriately attributed the myocardial dysfunction at rest of the TTS patients in part to their higher rate of risk factors for coronary artery disease compared with the control subjects. Those results corroborate earlier information from the same group revealing nonpersistence of sympathetic vulnerability to mental stress, heart rate variability, and salivary cortisol in the same 44 patients.2 I would greatly appreciate the response of the authors to the following remarks/questions about their article: 1) although magnetic resonance imaging, performed during hospitalization in these patients, is reported as normal (presumably implying absence of scar), one wonders about the presence of myocardial edema (ME), which often persists for a long time during convalescence from TTS,3 and its causative role in subtle myocardial dysfunction; 2) ME is associated with persistent T-wave inversions and QTc interval prolongation, and therefore inquiry about such changes in these patients at 6 months is relevant; 3) the authors seem to equate “stress” with DSE, but vulnerability to DSE triggering TTS has been demonstrated in only a few patients,4 and it is conceivable that had the 22 patients undergone DSE before the time of their presentation with TTS, only a few or none of them would have shown vulnerability to DSE; 4) in connection with the above, vulnerability to TTStriggering catecholamines (adrenaline, noradrenaline, isoperanaline, or dobutamine) is drug specific in patients4 and nonhuman animals5e7; 5) it is conceivable that TTS is followed by lingering augmented activity in the brain representations of the autonomic nervous system,8 which could probably engender lingering cardiac dysfunction for many months after the index TTS episode; 6) the authors,
None. John E. Madias, MD, FACC, FAHA Icahn School of Medicine at Mount Sinai New York, New York Division of Cardiology, Elmhurst Hospital Center Elmhurst, New York E-mail: [email protected]
References 1. Collste O, Alam M, Sundqvist M, Olson J, Wardell J, Tornvall P, et al. Vulnerability to sympathetic stress does not persist in Takotsubo stress cardiomyopathy. J Card Fail 2014 http://dx.doi.org/10.1016/j.cardfail.2014.09.008. € Alam M, Frick M. No myocardial 2. Collste O, Tornvall P, Sundin O, vulnerability to mental stress in Takotsubo stress cardiomyopathy. PLoS One 2014;9:e93697. 3. Perazzolo Marra M, Zorzi A, Corbetti F, De Lazzari M, Migliore F, Tona F, et al. Apicobasal gradient of left ventricular myocardial edema underlies transient T-wave inversion and QT interval prolongation (Wellens’ ECG pattern) in tako-tsubo cardiomyopathy. Heart Rhythm 2013;10:70e7. 4. Available at: www.ncbi.nlm.nih.gov/pubmed/?term5takotsubo. Accessed October 4, 2014. 5. Redfors B, Ali A, Shao Y, Lundgren J, Gan LM, Omerovic E. Different catecholamines induce different patterns of takotsubo-like cardiac dysfunction in an apparently afterload dependent manner. Int J Cardiol 2014;174:330e6. 6. Paur H, Wright PT, Sikkel MB, Tranter MH, Mansfield C, O’Gara P, et al. High levels of circulating epinephrine trigger apical cardiodepression in a b2-adrenergic receptor/Gi-dependent manner: a new model of takotsubo cardiomyopathy. Circulation 2012;126: 697e706. 7. Shao Y, Redfors B, Scharin T€ang M, M€ollmann H, Troidl C, Szardien S, et al. Novel rat model reveals important roles of b-adrenoreceptors in stress-induced cardiomyopathy. Int J Cardiol 2013; 168:1943e50. 8. Suzuki H, Matsumoto Y, Kaneta T, Sugimura K, Takahashi J, Fukumoto Y, et al. Evidence for brain activation in patients with Takotsubo cardiomyopathy. Circ J 2014;78:256e8. 9. Madias JE. Forme fruste cases of takotsubo syndrome: a hypothesis. Eur J Intern Med 2014;25:e47. http://dx.doi.org/10.1016/j.cardfail.2014.10.009
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Letters to the Editor Dobutamine Stress Echocardiography, Diastolic Function, and Myocardial Performance Index in Patients With History of Takotsubo Syndrome
referring to the data from the Stockholm Myocardial Infarction With Normal Coronaries study, estimate that “TTS constitutes around one-third or more of all such patients,”1 and one wonders if many of the rest, except for myocarditis or hypertrophic cardiomyopathy, have milder forms of TTS.9
To the Editor: Disclosures 1
The report by Collste et al, published ahead of print on September 26, 2014, in the Journal, about the response of 22 patients with takotsubo syndrome (TTS) to dobutamine stress echocardiography (DSE) compared with 22 control subjects, showed that the patients with TTS are not vulnerable to sympathetic stress 6 months after their index episode of TTS; in addition, the TTS patients had similar diastolic function, and myocardial performance index (MPI) during DSE but higher MPI at rest than the control subjects of similar age and sex. The authors appropriately attributed the myocardial dysfunction at rest of the TTS patients in part to their higher rate of risk factors for coronary artery disease compared with the control subjects. Those results corroborate earlier information from the same group revealing nonpersistence of sympathetic vulnerability to mental stress, heart rate variability, and salivary cortisol in the same 44 patients.2 I would greatly appreciate the response of the authors to the following remarks/questions about their article: 1) although magnetic resonance imaging, performed during hospitalization in these patients, is reported as normal (presumably implying absence of scar), one wonders about the presence of myocardial edema (ME), which often persists for a long time during convalescence from TTS,3 and its causative role in subtle myocardial dysfunction; 2) ME is associated with persistent T-wave inversions and QTc interval prolongation, and therefore inquiry about such changes in these patients at 6 months is relevant; 3) the authors seem to equate “stress” with DSE, but vulnerability to DSE triggering TTS has been demonstrated in only a few patients,4 and it is conceivable that had the 22 patients undergone DSE before the time of their presentation with TTS, only a few or none of them would have shown vulnerability to DSE; 4) in connection with the above, vulnerability to TTStriggering catecholamines (adrenaline, noradrenaline, isoperanaline, or dobutamine) is drug specific in patients4 and nonhuman animals5e7; 5) it is conceivable that TTS is followed by lingering augmented activity in the brain representations of the autonomic nervous system,8 which could probably engender lingering cardiac dysfunction for many months after the index TTS episode; 6) the authors,
None. John E. Madias, MD, FACC, FAHA Icahn School of Medicine at Mount Sinai New York, New York Division of Cardiology, Elmhurst Hospital Center Elmhurst, New York E-mail: [email protected]
References 1. Collste O, Alam M, Sundqvist M, Olson J, Wardell J, Tornvall P, et al. Vulnerability to sympathetic stress does not persist in Takotsubo stress cardiomyopathy. J Card Fail 2014 http://dx.doi.org/10.1016/j.cardfail.2014.09.008. € Alam M, Frick M. No myocardial 2. Collste O, Tornvall P, Sundin O, vulnerability to mental stress in Takotsubo stress cardiomyopathy. PLoS One 2014;9:e93697. 3. Perazzolo Marra M, Zorzi A, Corbetti F, De Lazzari M, Migliore F, Tona F, et al. Apicobasal gradient of left ventricular myocardial edema underlies transient T-wave inversion and QT interval prolongation (Wellens’ ECG pattern) in tako-tsubo cardiomyopathy. Heart Rhythm 2013;10:70e7. 4. Available at: www.ncbi.nlm.nih.gov/pubmed/?term5takotsubo. Accessed October 4, 2014. 5. Redfors B, Ali A, Shao Y, Lundgren J, Gan LM, Omerovic E. Different catecholamines induce different patterns of takotsubo-like cardiac dysfunction in an apparently afterload dependent manner. Int J Cardiol 2014;174:330e6. 6. Paur H, Wright PT, Sikkel MB, Tranter MH, Mansfield C, O’Gara P, et al. High levels of circulating epinephrine trigger apical cardiodepression in a b2-adrenergic receptor/Gi-dependent manner: a new model of takotsubo cardiomyopathy. Circulation 2012;126: 697e706. 7. Shao Y, Redfors B, Scharin T€ang M, M€ollmann H, Troidl C, Szardien S, et al. Novel rat model reveals important roles of b-adrenoreceptors in stress-induced cardiomyopathy. Int J Cardiol 2013; 168:1943e50. 8. Suzuki H, Matsumoto Y, Kaneta T, Sugimura K, Takahashi J, Fukumoto Y, et al. Evidence for brain activation in patients with Takotsubo cardiomyopathy. Circ J 2014;78:256e8. 9. Madias JE. Forme fruste cases of takotsubo syndrome: a hypothesis. Eur J Intern Med 2014;25:e47. http://dx.doi.org/10.1016/j.cardfail.2014.10.009
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