IJCA-18054; No of Pages 2 International Journal of Cardiology xxx (2014) xxx–xxx
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy☆ Peter Alter ⁎ University of Marburg, Internal Medicine — Cardiology, Baldingerstrasse, 35033 Marburg, Germany
a r t i c l e
i n f o
Article history: Received 25 March 2014 Accepted 12 April 2014 Available online xxxx Keywords: Takotsubo cardiomyopathy Cardiac magnetic resonance imaging Late enhancement Late gadolinium enhancement Ventricular wall stress Heart failure
We thank Madias for the letter [1] regarding our article on increased left ventricular wall stress in Takotsubo cardiomyopathy as recently published in the Journal [2]. We agree with the pathophysiological considerations raised in the thorough contribution, which support our findings. Increased ventricular wall stress is a crucial causative and prognostic determinant in various types of heart failure. Increased wall stress leads to local ischemia, increased oxygen consumption and an altered energy status and influences the interaction between matrix metalloproteinase activity, adverse remodeling and cardiomyocyte hypertrophy [3]. In chronic heart failure, increased wall stress precedes ventricular hypertrophy as previously shown [4]. Left ventricular (LV) hypertrophy per se has been rated as an unfavorable prognostic determinant in heart failure. Of crucial importance is the extent and type of cardiac growth. Besides the adverse growth of an overloaded heart involving activation of the fetal gene program, also physiological adaptations with beneficial physiological cardiac hypertrophy can occur, e.g. an increase of LV mass counterbalances a raised LV wall stress. Beyond a certain degree of LV dilatation, the ensuing increase of mass is not sufficient to compensate for an increased wall stress resulting in a vicious cycle of ongoing LV dilatation and progression of heart failure [4]. Isostress diagrams were used to derive the extent of load reduction required for restoring normal LV wall stress [5].
In contrast to chronic heart failure, Takotsubo cardiomyopathy typically emerges acutely subsequent to distress disorders. It is suggested in the referenced manuscript [2] that elderly females are more prone to develop Takotsubo cardiomyopathy because of a pre-existing mismatch of LV mass and volumes that aggravates increased LV wall stress during distress hypertension. Whereas a long-term increase of catecholamines, e.g. in pheochromocytoma, can lead to adaptive LV hypertrophy, a rapid increase of cardiac filling pressure and distending forces following an excessive catecholamine liberation apparently cannot be compensated. Thus, various unfavorable consequences occur [1,2,6]. Raised ventricular wall stress is associated with an impaired autonomic tone. In particular, a decreased heart rate variability was found [7], which is known to be linked with a worse outcome in patients with heart failure post myocardial infarction. It is suggested that a pre-existing autonomic impairment further influences the susceptibility to catecholamines. Cardiac magnetic resonance (CMR) imaging allows the calculation of ventricular wall stress based on accurate measurements of ventricular volumes and myocardial mass. Although an echocardiography-based approach is feasible, the extent of LV wall stress can be underrated [5]. Interpretation of CMR late gadolinium enhancement (LGE) in cardiomyopathies seems to require differentiation of a variety of types. Of particular interest is the streaky-like occurrence of LGE at the septal midwall and at the so-called hinge points, which is suggestive of functional or mechanical influences. It was recently shown in 300 patients with dilated cardiomyopathy that LGE correlates with increased LV wall stress [8]. LGE in cardiomyopathies differs from LGE of postinfarct scar in terms of extent, pattern and intensity. In Takotsubo cardiomyopathy, the signal-to-noise ratio of LGE is lower when compared with infarct scar [9] and occurrence of LGE is usually short-term reversible. Taking the collagen degradation time into account [3], it remains debatable whether indeed fibrosis contributes substantially to LGE in Takotsubo syndrome. Other determinants seem to be, at least in part, involved [2,8]. Postcontrast myocardial T1 mapping showed an inverse correlation between T1 times and fibrosis as assessed by histology [10]. It is suggested that CMR methods involving T1 mapping techniques better reflect fibrosis in cardiomyopathies than LGE.
References ☆ Response to the letter by John E. Madias. ⁎ Tel.: +49 6421 5866140; fax: +49 6421 5866141. E-mail address: [email protected].
[1] Madias JE. Ventricular wall stress and late gadolinium enhancement in patients with Takotsubo syndrome: more data worth contemplating about. Int J Cardiol 2014 May 1;173(2):339. http://dx.doi.org/10.1016/j.ijcard.2014.03.038.
http://dx.doi.org/10.1016/j.ijcard.2014.04.153 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: Alter P, Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.04.153
2
P. Alter / International Journal of Cardiology xxx (2014) xxx–xxx
[2] Alter P, Figiel JH, Rominger MB. Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy. Int J Cardiol 2014;172:e184–6. [3] Janicki JS, Brower GL, Gardner JD, Chancey AL, Stewart Jr JA. The dynamic interaction between matrix metalloproteinase activity and adverse myocardial remodeling. Heart Fail Rev 2004;9:33–42. [4] Alter P, Rupp H, Stoll F, et al. Increased end diastolic wall stress precedes left ventricular hypertrophy in dilative heart failure—use of the volume-based wall stress index. Int J Cardiol 2012;157:233–8. [5] Alter P, Rupp H, Rominger MB, et al. B-type natriuretic peptide and wall stress in dilated human heart. Mol Cell Biochem 2008;314:179–91. [6] Redfors B, Shao Y, Ali A, Omerovic E. Are ischemic stunning, conditioning, and “takotsubo” different sides to the same coin? Int J Cardiol 2014;172:490–1. [7] Alter P, Rupp H, Rominger MB, et al. A new method to assess ventricular wall stress in patients with heart failure and its relation to heart rate variability. Int J Cardiol 2010;139:301–3.
[8] Alter P, Rupp H, Adams P, et al. Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non-ischaemic dilated cardiomyopathy. Eur J Heart Fail 2011;13:937–44. [9] Nakamori S, Matsuoka K, Onishi K, et al. Prevalence and signal characteristics of late gadolinium enhancement on contrast-enhanced magnetic resonance imaging in patients with takotsubo cardiomyopathy. Circ J 2012;76:914–21. [10] Sibley CT, Noureldin RA, Gai N, et al. T1 mapping in cardiomyopathy at cardiac MR: comparison with endomyocardial biopsy. Radiology 2012;265:724–32.
Please cite this article as: Alter P, Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.04.153
Contents lists available at ScienceDirect
International Journal of Cardiology journal homepage: www.elsevier.com/locate/ijcard
Letter to the Editor
Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy☆ Peter Alter ⁎ University of Marburg, Internal Medicine — Cardiology, Baldingerstrasse, 35033 Marburg, Germany
a r t i c l e
i n f o
Article history: Received 25 March 2014 Accepted 12 April 2014 Available online xxxx Keywords: Takotsubo cardiomyopathy Cardiac magnetic resonance imaging Late enhancement Late gadolinium enhancement Ventricular wall stress Heart failure
We thank Madias for the letter [1] regarding our article on increased left ventricular wall stress in Takotsubo cardiomyopathy as recently published in the Journal [2]. We agree with the pathophysiological considerations raised in the thorough contribution, which support our findings. Increased ventricular wall stress is a crucial causative and prognostic determinant in various types of heart failure. Increased wall stress leads to local ischemia, increased oxygen consumption and an altered energy status and influences the interaction between matrix metalloproteinase activity, adverse remodeling and cardiomyocyte hypertrophy [3]. In chronic heart failure, increased wall stress precedes ventricular hypertrophy as previously shown [4]. Left ventricular (LV) hypertrophy per se has been rated as an unfavorable prognostic determinant in heart failure. Of crucial importance is the extent and type of cardiac growth. Besides the adverse growth of an overloaded heart involving activation of the fetal gene program, also physiological adaptations with beneficial physiological cardiac hypertrophy can occur, e.g. an increase of LV mass counterbalances a raised LV wall stress. Beyond a certain degree of LV dilatation, the ensuing increase of mass is not sufficient to compensate for an increased wall stress resulting in a vicious cycle of ongoing LV dilatation and progression of heart failure [4]. Isostress diagrams were used to derive the extent of load reduction required for restoring normal LV wall stress [5].
In contrast to chronic heart failure, Takotsubo cardiomyopathy typically emerges acutely subsequent to distress disorders. It is suggested in the referenced manuscript [2] that elderly females are more prone to develop Takotsubo cardiomyopathy because of a pre-existing mismatch of LV mass and volumes that aggravates increased LV wall stress during distress hypertension. Whereas a long-term increase of catecholamines, e.g. in pheochromocytoma, can lead to adaptive LV hypertrophy, a rapid increase of cardiac filling pressure and distending forces following an excessive catecholamine liberation apparently cannot be compensated. Thus, various unfavorable consequences occur [1,2,6]. Raised ventricular wall stress is associated with an impaired autonomic tone. In particular, a decreased heart rate variability was found [7], which is known to be linked with a worse outcome in patients with heart failure post myocardial infarction. It is suggested that a pre-existing autonomic impairment further influences the susceptibility to catecholamines. Cardiac magnetic resonance (CMR) imaging allows the calculation of ventricular wall stress based on accurate measurements of ventricular volumes and myocardial mass. Although an echocardiography-based approach is feasible, the extent of LV wall stress can be underrated [5]. Interpretation of CMR late gadolinium enhancement (LGE) in cardiomyopathies seems to require differentiation of a variety of types. Of particular interest is the streaky-like occurrence of LGE at the septal midwall and at the so-called hinge points, which is suggestive of functional or mechanical influences. It was recently shown in 300 patients with dilated cardiomyopathy that LGE correlates with increased LV wall stress [8]. LGE in cardiomyopathies differs from LGE of postinfarct scar in terms of extent, pattern and intensity. In Takotsubo cardiomyopathy, the signal-to-noise ratio of LGE is lower when compared with infarct scar [9] and occurrence of LGE is usually short-term reversible. Taking the collagen degradation time into account [3], it remains debatable whether indeed fibrosis contributes substantially to LGE in Takotsubo syndrome. Other determinants seem to be, at least in part, involved [2,8]. Postcontrast myocardial T1 mapping showed an inverse correlation between T1 times and fibrosis as assessed by histology [10]. It is suggested that CMR methods involving T1 mapping techniques better reflect fibrosis in cardiomyopathies than LGE.
References ☆ Response to the letter by John E. Madias. ⁎ Tel.: +49 6421 5866140; fax: +49 6421 5866141. E-mail address: [email protected].
[1] Madias JE. Ventricular wall stress and late gadolinium enhancement in patients with Takotsubo syndrome: more data worth contemplating about. Int J Cardiol 2014 May 1;173(2):339. http://dx.doi.org/10.1016/j.ijcard.2014.03.038.
http://dx.doi.org/10.1016/j.ijcard.2014.04.153 0167-5273/© 2014 Elsevier Ireland Ltd. All rights reserved.
Please cite this article as: Alter P, Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.04.153
2
P. Alter / International Journal of Cardiology xxx (2014) xxx–xxx
[2] Alter P, Figiel JH, Rominger MB. Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy. Int J Cardiol 2014;172:e184–6. [3] Janicki JS, Brower GL, Gardner JD, Chancey AL, Stewart Jr JA. The dynamic interaction between matrix metalloproteinase activity and adverse myocardial remodeling. Heart Fail Rev 2004;9:33–42. [4] Alter P, Rupp H, Stoll F, et al. Increased end diastolic wall stress precedes left ventricular hypertrophy in dilative heart failure—use of the volume-based wall stress index. Int J Cardiol 2012;157:233–8. [5] Alter P, Rupp H, Rominger MB, et al. B-type natriuretic peptide and wall stress in dilated human heart. Mol Cell Biochem 2008;314:179–91. [6] Redfors B, Shao Y, Ali A, Omerovic E. Are ischemic stunning, conditioning, and “takotsubo” different sides to the same coin? Int J Cardiol 2014;172:490–1. [7] Alter P, Rupp H, Rominger MB, et al. A new method to assess ventricular wall stress in patients with heart failure and its relation to heart rate variability. Int J Cardiol 2010;139:301–3.
[8] Alter P, Rupp H, Adams P, et al. Occurrence of late gadolinium enhancement is associated with increased left ventricular wall stress and mass in patients with non-ischaemic dilated cardiomyopathy. Eur J Heart Fail 2011;13:937–44. [9] Nakamori S, Matsuoka K, Onishi K, et al. Prevalence and signal characteristics of late gadolinium enhancement on contrast-enhanced magnetic resonance imaging in patients with takotsubo cardiomyopathy. Circ J 2012;76:914–21. [10] Sibley CT, Noureldin RA, Gai N, et al. T1 mapping in cardiomyopathy at cardiac MR: comparison with endomyocardial biopsy. Radiology 2012;265:724–32.
Please cite this article as: Alter P, Increased ventricular wall stress and late gadolinium enhancement in Takotsubo cardiomyopathy, Int J Cardiol (2014), http://dx.doi.org/10.1016/j.ijcard.2014.04.153
