Authors Reply:
We thank Dr. Yalcinkaya and his colleagues for their interest in our analysis of factors underlying the development of hypotension and shock in takotsubo cardiomyopathy (TTC).1 When designing our evaluation, we were initially conscious of the potential interactions of changes within the myocardium (inflammation and regional negative inotropy), potential mechanical issues (outflow tract obstruction, mitral regurgitation, and possibly diastolic ventricular interaction), and disparate peripheral vasomotor stimuli (catecholamine and brain natriuretic peptide release). Our conclusion was that the development of hypotension/shock reflected complex interactions among these factors, rather than easily identifiable individual parameters. Furthermore, it might also be argued that the balance between β1‐ to β2‐adrenoceptor stimulation in individual patients might also be relevant.2
The right ventricle (RV) is frequently involved in TTC.3, 4 In our series, approximately 30% of TTC patients had detectable RV involvement on transthoracic echocardiography. However, both echocardiographic and cardiac magnetic resonance imaging assessment suggested that in most cases this involvement was limited to apical hypokinesis rather than extensive RV dysfunction. In the minority of patients with more extensive (echocardiographic) RV dysfunction, no multivariate correlation with hypotension emerged. It is, of course, possible that in some cases echocardiography was performed after hemodynamic status had improved, so we agree that we may have underestimated the role of RV involvement (assuming that the RV recovers rapidly). We also agree that in theory, TTC is likely to involve the whole RV in an acute inflammatory process.5
We also agree that there is a case for the utilization of T1 mapping in detection of myocardial edema. However, our methodology utilizing T2‐weighted signal ratio was relatively reproducible and permitted quantitation of extent of overall left ventricular edema.5 Detection per se of edema was not a relevant issue here. However, in the context of Dr. Yalcinkaya's interest in the RV, it would indeed be desirable for such methodology to be applicable to both ventricles.
Cher‐Rin Chong, B Pharm Christopher J. Neil, MBBS Thanh H. Nguyen, MD, PhD Kuljit Singh, MBBS John D. Horowitz, MBBS, PhD Clinical Pharmacology and Cardiology Department Queen Elizabeth Hospital Discipline of Medicine University of Adelaide Adelaide Australia
References
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