European Heart Journal Advance Access originally published online on January 31, 2008
European Heart Journal 2008 29(5):681-682; doi:10.1093/eurheartj/ehn001
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A pathophysiological study of tako-tsubo cardiomyopathy with F-18 fluorodeoxyglucose positron emission tomography: reply
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
5-161 Maehata, Tajimi
Gifu 5078522
Japan
Tel: +81 572 22 5311
Fax: +81 572 25 1246
Email: tetsuro-moet{at}nifty.com
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
Tajimi
Japan
Department of Radiology
Kizawa Memorial Hospital
Minokamo
Japan
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
Tajimi
Japan
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
Tajimi
Japan
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
Tajimi
Japan
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
Tajimi
Japan
Department of Cardio-Renal Medicine and Hypertension
Nagoya City University Graduate School of Medical Sciences
Nagoya
Japan
Department of Cardiovascular Medicine
Gifu Prefectual Government Tajimi Hospital
Tajimi
Japan
Department of Cardio-Renal Medicine and
Hypertension
Nagoya City University Graduate School of
Medical Sciences
Nagoya
Japan
We thank Dr Radhakrishnan for his interest in our work. We are pleased to have the opportunity to reply to his constructive comments. Some previous investigators have reported that markedly reduced F18-FDG uptake, relative to perfusion at the cardiac apex, has been observed in this syndrome during the acute phase, which resolved by the time of follow-up.1 This phenomenon may imply a close relationship between the glucose metabolic disorder and the onset of tako-tsubo cardiomyopathy, although we did not evaluate glucose metabolism in patients with tako-tsubo cardiomyopahy during the chronic phase. On the other hand, Wittstein et al.2 reported that sudden elevations in plasma catecholamine levels after emotional or physical stress are possibly involved in the pathogenesis of tako-tsubo cardiomyopathy, although the pathophysiological mechanism underlying the deteriorating effect of catecholamines is not fully understood. In fact, all of our patients had a marked elevation of norepinephrine after the onset of tako-tsubo cardiomyopathy. Another study showed that high doses of catecholamines possibly depress glucose uptake with respect to beta receptor stimulation.3 Additionally, it has been reported that beta adrenergic receptor density in the apical myocardium is greater than that at the base, and increased myocardial responsiveness to adenylate stimulation in the apical myocardium compensates for its sparse sympathetic innervation.4 Therefore, we speculate that the biased localization of adrenergic receptors in the apical myocardium may account for the association between the abnormal catecholamine flux and the glucose metabolic disorder in the myocardium. However, further investigation is required to confirm that the glucose metabolism disorder in the myocardium may reflect the root cause or a secondary response in patients with tako-tsubo cardiomopathy.
We agree with the hypothesis of sex hormones influencing the pathogenesis of tako-tsubo cardiomyopathy because all women in our current study were post-menopausal. However, we have no data concerning the function of sex hormones in patients with tako-tsubo cardiomyopathy. More recently, Ueyama et al.5 suggested that estrogen supplementation partially prevents emotional stress-induced cardiovascular responses, both by indirect action on the nervous system and by direct action on the heart. From this data, a reduction in estrogen levels following menopause may augment the reactivity to stress via the modulation of autonomic functions, resulting in the high incidence of tako-tsubo cardiomyopathy in post-menopausal women. This issue is considered to be very important and interesting. Estrogen supplementation therapy may possibly prevent the onset of tako-tsubo cardiomyopathy in post-menopausal women if we can confirm the effect of sex hormones on this syndrome. In fact, we will try to investigate this issue and clarify the underlying true mechanism.
References
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- Wittstein IS, Thiemann DR, Lima JA, Baughman KL, Schulman SP, Gerstenblith G, Wu KC, Rade JJ, Bivalacqua TJ, Champion HC. Neurohumoral features of myocardial stunning due to sudden emotional stress. N Engl J Med (2005) 352:539–548.
[Abstract/Free Full Text] - Huang MT, Lee CF, Dobson GP. Epinephrine enhances glycogen turnover and depresses glucose uptake in vivo in rat heart. FASEB J (1997) 11:973–980.[Abstract]
- Mori H, Ishikawa S, Kojima S, Hayashi J, Watanabe Y, Hoffman JI, Okino H. Increased responsiveness of left ventricular apical myocardium to adrenergic stimuli. Cardiovasc Res (1993) 27:192–198.
[Abstract/Free Full Text] - Ueyama T, Ishikura F, Matsuda A, Asanuma T, Ueda K, Ichinose M, Kasamatsu K, Hano T, Akasaka T, Tsuruo Y, Morimoto K, Beppu S. Chronic estrogen supplementation following ovariectomy improves the emotional stress-induced cardiovascular responses by indirect action on the nervous system and by direct action on the heart. Circ J (2007) 71:565–573.[CrossRef][Web of Science][Medline]
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