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Takotsubo cardiomyopathy and microvascular dysfunction
International Journal of Cardiology 196 (2015) 107
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Takotsubo cardiomyopathy and microvascular dysfunction☆ Lovely Chhabra a,⁎, Pooja Sareen b a b
Dept. of Cardiovascular Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT 06102, USA Dept. of Medicine, Baystate Medical Center, Springfield, MA 01107, USA
a r t i c l e
i n f o
Article history: Received 20 May 2015 Accepted 27 May 2015 Available online 6 June 2015 Keywords: Takotsubo cardiomyopathy Microvascular dysfunction Q-waves Myopericarditis
We read with great interest the work by Khalid et al. which investigated the role of TIMI frame count (TFC) in Takotsubo cardiomyopathy (TC) [1]. The authors found a TFC prolongation in the left anterior descending artery in patients with TC as compared to the control population, suggesting evidence of possible microvascular dysfunction in TC. Despite abundant research work and awareness about TC, the exact pathogenesis of this disorder till date remains elusive. The three most common proposed mechanisms include catecholamine-mediated myocardial stunning, multivessel coronary vasospasm and coronary microvascular dysfunction. The current study adds to the body of evidence that microvascular dysfunction may play a role in the pathogenesis of TC. Prior literature suggests several reportings that favor this causal association. The presence of predominantly reversible anterior/ anteroseptal or diffuse precordial Q-waves in patients with TC and more recent reports suggesting an association between viral myopericarditis and TC seem to support the hypothesis of microvascular dysfunction and extended epicardial inflammation in the pathogenesis of TC [2–4]. One of the prior landmark studies on this subject also demonstrated prolonged TFCs in the left anterior descending and left circumflex coronary arteries in patients with TC as compared to the control population [5]. The mean TFC prolongation was however only modest in that study (5 and 7 counts in LAD and LCx arteries respectively), suggesting that microvascular dysfunction plays only a minor role in the pathogenesis of TC [5]. Even in the current study, TFC prolongation
☆ Funding: None. ⁎ Corresponding author at: 80 Seymour Street, Hartford, CT 06102, USA. E-mail address: [email protected] (L. Chhabra).
http://dx.doi.org/10.1016/j.ijcard.2015.05.161 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
in LAD was quite small (3 counts) which again suggests that microvascular dysfunction may only be a small contributor to the pathogenesis of TC among the myriad of other contributing mechanisms [1]. A few facts in the current study however need some clarification. The data shown in Table 2 and the text description are contradicting, namely the prevalence of diabetes mellitus and hypertension in TC patients and controls [1]. This clarification would indeed be valuable for the readership, as there has been some recent literature evidence to suggest that prevalence of diabetes in TC patients is indeed quite low and this is thought to be related to diabetes mellitus-induced autonomic neuropathy which leads to a brain–heart disconnection [6]. Future large controlled investigations on this subject will be able to shed more light on the pathogenesis of TC and strengthen our understanding further on this subject. Conflict of interest None. References [1] N. Khalid, I. Iqbal, R. Coram, T. Raza, I. Fahsah, S. Ikram, Thrombolysis in myocardial infarction frame count in takotsubo cardiomyopathy, Int. J. Cardiol. 191 (2015) 107–108. [2] R.P. Vivo, S.R. Krim, J. Hodgson, It's a trap! Clinical similarities and subtle ECG differences between takotsubo cardiomyopathy and myocardial infarction, J. Gen. Intern. Med. 23 (11) (2008) 1909–1913. [3] L. Chhabra, Myopericarditis and takotsubo cardiomyopathy association, Int. J. Cardiol. 186 (2015) 143. [4] L. Galiuto, A.R. De Caterina, A. Porfidia, L. Paraggio, S. Barchetta, G. Locorotondo, A.G. Rebuzzi, F. Crea, Reversible coronary microvascular dysfunction: a common pathogenetic mechanism in Apical Ballooning or Tako-Tsubo Syndrome, Eur. Heart J. 31 (11) (2010) 1319–1327. [5] S.W. Sharkey, J.R. Lesser, M. Menon, M. Parpart, M.S. Maron, B.J. Maron, Spectrum and significance of electrocardiographic patterns, troponin levels, and thrombolysis in myocardial infarction frame count in patients with stress (tako-tsubo) cardiomyopathy and comparison to those in patients with ST-elevation anterior wall myocardial infarction, Am. J. Cardiol. 101 (12) (2008) 1723–1728. [6] J.E. Madias, Low prevalence of diabetes mellitus in patients with Takotsubo syndrome: a plausible 'protective' effect with pathophysiologic connotations, Eur. Heart J. Acute Cardiovasc. Care (Feb 11 2015) (pii: 2048872615570761, PMID: 25673782, Epub ahead of print).
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Takotsubo cardiomyopathy and microvascular dysfunction☆ Lovely Chhabra a,⁎, Pooja Sareen b a b
Dept. of Cardiovascular Medicine, Hartford Hospital, University of Connecticut School of Medicine, Hartford, CT 06102, USA Dept. of Medicine, Baystate Medical Center, Springfield, MA 01107, USA
a r t i c l e
i n f o
Article history: Received 20 May 2015 Accepted 27 May 2015 Available online 6 June 2015 Keywords: Takotsubo cardiomyopathy Microvascular dysfunction Q-waves Myopericarditis
We read with great interest the work by Khalid et al. which investigated the role of TIMI frame count (TFC) in Takotsubo cardiomyopathy (TC) [1]. The authors found a TFC prolongation in the left anterior descending artery in patients with TC as compared to the control population, suggesting evidence of possible microvascular dysfunction in TC. Despite abundant research work and awareness about TC, the exact pathogenesis of this disorder till date remains elusive. The three most common proposed mechanisms include catecholamine-mediated myocardial stunning, multivessel coronary vasospasm and coronary microvascular dysfunction. The current study adds to the body of evidence that microvascular dysfunction may play a role in the pathogenesis of TC. Prior literature suggests several reportings that favor this causal association. The presence of predominantly reversible anterior/ anteroseptal or diffuse precordial Q-waves in patients with TC and more recent reports suggesting an association between viral myopericarditis and TC seem to support the hypothesis of microvascular dysfunction and extended epicardial inflammation in the pathogenesis of TC [2–4]. One of the prior landmark studies on this subject also demonstrated prolonged TFCs in the left anterior descending and left circumflex coronary arteries in patients with TC as compared to the control population [5]. The mean TFC prolongation was however only modest in that study (5 and 7 counts in LAD and LCx arteries respectively), suggesting that microvascular dysfunction plays only a minor role in the pathogenesis of TC [5]. Even in the current study, TFC prolongation
☆ Funding: None. ⁎ Corresponding author at: 80 Seymour Street, Hartford, CT 06102, USA. E-mail address: [email protected] (L. Chhabra).
http://dx.doi.org/10.1016/j.ijcard.2015.05.161 0167-5273/© 2015 Elsevier Ireland Ltd. All rights reserved.
in LAD was quite small (3 counts) which again suggests that microvascular dysfunction may only be a small contributor to the pathogenesis of TC among the myriad of other contributing mechanisms [1]. A few facts in the current study however need some clarification. The data shown in Table 2 and the text description are contradicting, namely the prevalence of diabetes mellitus and hypertension in TC patients and controls [1]. This clarification would indeed be valuable for the readership, as there has been some recent literature evidence to suggest that prevalence of diabetes in TC patients is indeed quite low and this is thought to be related to diabetes mellitus-induced autonomic neuropathy which leads to a brain–heart disconnection [6]. Future large controlled investigations on this subject will be able to shed more light on the pathogenesis of TC and strengthen our understanding further on this subject. Conflict of interest None. References [1] N. Khalid, I. Iqbal, R. Coram, T. Raza, I. Fahsah, S. Ikram, Thrombolysis in myocardial infarction frame count in takotsubo cardiomyopathy, Int. J. Cardiol. 191 (2015) 107–108. [2] R.P. Vivo, S.R. Krim, J. Hodgson, It's a trap! Clinical similarities and subtle ECG differences between takotsubo cardiomyopathy and myocardial infarction, J. Gen. Intern. Med. 23 (11) (2008) 1909–1913. [3] L. Chhabra, Myopericarditis and takotsubo cardiomyopathy association, Int. J. Cardiol. 186 (2015) 143. [4] L. Galiuto, A.R. De Caterina, A. Porfidia, L. Paraggio, S. Barchetta, G. Locorotondo, A.G. Rebuzzi, F. Crea, Reversible coronary microvascular dysfunction: a common pathogenetic mechanism in Apical Ballooning or Tako-Tsubo Syndrome, Eur. Heart J. 31 (11) (2010) 1319–1327. [5] S.W. Sharkey, J.R. Lesser, M. Menon, M. Parpart, M.S. Maron, B.J. Maron, Spectrum and significance of electrocardiographic patterns, troponin levels, and thrombolysis in myocardial infarction frame count in patients with stress (tako-tsubo) cardiomyopathy and comparison to those in patients with ST-elevation anterior wall myocardial infarction, Am. J. Cardiol. 101 (12) (2008) 1723–1728. [6] J.E. Madias, Low prevalence of diabetes mellitus in patients with Takotsubo syndrome: a plausible 'protective' effect with pathophysiologic connotations, Eur. Heart J. Acute Cardiovasc. Care (Feb 11 2015) (pii: 2048872615570761, PMID: 25673782, Epub ahead of print).