To the Editor:
Akashi et al present interesting comments on the role of catecholamines in takotsubo cardiomyopathy patients. Combined α- and β-adrenergic blockade is an intriguing hypothesis; however, the only evidence we are aware of for any benefit is in a rat immobilization stress model. In addition, as the commentators note, several studies have shown that catecholamine levels are not consistently elevated in patients with takotsubo cardiomyopathy. Nevertheless, many patients in our practice are treated on diagnosis with carvedilol and angiotensin-converting enzyme (ACE) inhibitor as with any other nonischemic cardiomyopathy. The duration of treatment varies according to physician preference. None of the patients in our study were on combined α- and β-blockers on presentation. The role of higher doses of β-adrenergic blockers in attenuation or prevention of this syndrome remains to be studied. We have published a case of recurrent takotsubo cardiomyopathy,1 where the recurrence was precipitated by a higher level stressor (cerebrovascular accident) than the first episode, and the patient developed much higher cardiac enzyme levels despite being on low dose β-blocker therapy, suggesting that the severity of the syndrome may to a large extent depend on the level of stressor.
Our study is by no means definitive with regard to the role of adrenergic blockade in the prevention or attenuation of takotsubo cardiomyopathy. Additional studies with higher doses of β-adrenergic blockade and combined α- and β-blockade (although difficult to carry out given the low recurrence rates), would certainly provide additional insight into this question.