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European Journal of Echocardiography 2007 8(6):413-415; doi:10.1016/j.euje.2007.06.015
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Copyright © 2007, The European Society of Cardiology

Reply to the letter to the editor by F. Tona et al.

P. Meimoun, D. Malaquin and T. Benali

We appreciate the interest of Dr Tona and colleagues in our case report on assessment of serial transthoracic coronary flow reserve (CFR) measurements in a patient with tako-tsubo cardiomyopathy (TTC).1

Because myocardial biopsy or cardiac magnetic resonance imaging (MRI) has not been performed in our patient, they state that the transient impairment of coronary flow reserve (CFR) in parallel to transient wall motion abnormalities (WMA) argue for the diagnosis of myocarditis instead of TTC. We would like to bring additive information in order to dissipate ambiguous deductions.

While the mechanisms of TTC are still unknown, the clinical features of this transient cardiomyopathy have been clearly described in the pervious years in various reports, with uniform used diagnostic criteria.2–5 Myocardial biopsy and cardiac MRI, though they have added for the understanding of this fascinating pathology, have not been used systematically to exclude myocarditis, even by authors of the Mayo Clinic diagnostic criteria.6,7 Indeed, the clinical setting is very important, in order to clarify non-specific symptom such as chest pain or dyspnea or ECG abnormalities. The patients affected by TTC are typically elderly females (as our patient) whereas in myocarditis the patients are younger with no sex predominance.8–10 Furthermore, in the vast majority of patients with TTC, a stressful event precedes the symptoms11,12 as it was described in our patient. It is not the case for patients with myocarditis. Our patient with TTC did not have fever, flu-like syndrome and elevation of inflammatory biomarkers, features usually encountered in patients with myocarditis.8–10 The mid-apical involvement of the LV wall with hyperkinesis of the basal segments is a main characteristic of TTC, giving a balloon like appearance,2–5,11,12 as it was described in our patient. This unique apical ballooning pattern of segmental dysfunction has not been described in studies with biopsy-proven cases of myocarditis. Furthermore, in rats experiencing emotional stress this unique pattern of TTC is reproduced and prevented by adrenoreceptor blockade.13 The WMA are always transient in TTC, resolving spontaneously within a few days or weeks, as it was described in our patient, whereas some patients with myocarditis progress to dilated cardiomyopathy or need specific therapy to improve.8 Myocardial biopsy to exclude myocarditis is not routinely indicated or advisable under the clinical circumstances described above. Because of the important therapeutic implications encountered, the main differential diagnosis of TTC is myocardial infarction, and not myocarditis, and a coronary angiography has to be performed as soon as possible.

In patients with suspected myocarditis, the sensitivity of myocardial biopsy is low.8–10 Indeed, endomyocardial biopsy, already performed in some patients at the acute phase of TTC, did not show any evidence of myocarditis2,3,11 and no virus titers were detected in paired serum examinations of patients affected by TTC.2 It was particularly demonstrative in a recent study performing serial myocardial biopsies in eight patients with TTC, and in all samples, measurements of virus titer, electron microscopy, immunohistochemistry, and the terminal deoxynucleotidyl transferase-mediated nick end-labeling method were used.14 Reversible cellular and structural degeneration, absence of programmed cell death, and no sign of myocarditis were found in that study.14

The improvement of CFR in parallel to the regression of WMA is not synonym of myocarditis. It has already been described in patients with reperfused myocardial infarction,15 and in patients affected by TTC, using nuclear cardiac imaging and invasive Doppler flow wire.16,17 Furthermore, a transient impairment of transthoracic CFR has been shown in patients with TTC who had identical presentation as our case; MRI gadolinium contrast enhancement was performed in some of them and did not show any sign of infiltrative or inflammatory process and absence of delayed hyperenhancement.18

Although a unifying mechanistic explanation is still lacking in TTC, a sudden surge of catecholamine leading to myocardial stunning, and preceded by a stressful event is a plausible scenario.11,13 What are the mechanisms of the transient impairment of CFR in this setting? Do catecholamines (or other mediators) induce a direct microvascular injury, or the impairment of CFR is a consequence of WMA? Following findings, although not answering directly this question should give food for thought. Impaired myocardial perfusion due to abnormal myocardial blood flow seen in patients with TTC correlates with the extent of myocardial injury.7 Mental stress, associated with enhanced sympathetic outflow, induces transient coronary endothelial dysfunction.19 The transient structural alterations seen in myocardial biopsy samples of patients with TTC suggest that catecholamine excess induce both microvascular dysfunction and direct myocyte damage.14 And last but not least, TTC affects electively post-menopausal women, suggesting that the lack of oestrogen plays a role in the setting of TTC, as demonstrated in experimental studies.20 Interestingly, estrogens are sexual hormones that have a positive impact on the coronary microcirculation.21 Transthoracic Doppler echocardiography is a unique tool easily available which assesses simultaneously WMA and CFR at bedside. There is no doubt that it will help to clarify which the chicken is and which the egg is.


   References
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 References
 

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  19. Ghiadoni L., Donald A.E., Cropley M., Mullen M.J., Oakley G., Taylor M., et al. Mental stress induces transient endothelial dysfunction in humans. Circulation (2000) 102:2473–2478.[Abstract/Free Full Text]
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  21. Hirata K., Shimada K., Watanabe H., Muro T., Yoshiyama M., Takeuchi K., et al. Modulation of coronary flow velocity reserve by gender, menstrual cycle and hormone replacement therapy. J Am Coll Cardiol (2001) 38:1885–1887.[Free Full Text]

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