Transient left ventricular hypocontraction induced by emotional stress with immobilization: an animal model of tako-tsubo cardiomyopathy in humans?

To the Editor: I read with great interest the article by Ueyama et al in the Circulation Journal1 in which they demonstrated that emotional stress with immobilization in the rat induced reversible left ventricular apical ballooning that was normalized by pretreatment with adrenoceptor blockade. They had previously demonstrated the same stress-induced ST segment elevation, which returned to pre stress basal levels after removal of the stress. 2 From those studies, they proposed activation of cardiac adrenoceptors in the absence of ischemia – reperfusion as the primary cause of takotsubo cardiomyopathy. Because this study was published as a Rapid Communication and therefore limited in length, I would like more detailed information about their study. Recent clinical studies, including a multicenter study3 and my group’s study, 4 have demonstrated the predominance of female, elderly patients with tako-tsubo cardiomyopathy, and its precise mechanism remains to be investigated. In addition, few people develop tako-tsubo cardiomyopathy when undergoing mental stress in the clinical setting, suggesting that there are individual differences in the development of this condition. The authors need to state what proportion of rats generally develop left ventricular dysfunction associated with emotional stress with immobilization, and whether there is a predominance of female and elderly subjects, even in this model. In addition, the recent clinical study by my group demonstrated that the circulating norepinephrine concentration was normal or slightly elevated during the early phase of tako-tsubo cardiomyopathy, 4 which seems to be a discrepancy between their result and ours. I would like to know how high was the concentration of circulating, urinary or tissue norepinephrine in the rat.