Chong CR et al. Clin Cardiol. 2013. doi: 10.1002/clc.22129.
Letters to the Editor
Article first published online: 14 JUN 2013
© 2013 Wiley Periodicals, Inc.
Volume 36, Issue 8, page 492, August 2013
Madias, J. E. (2013), Response to Dissociation Between Severity of Takotsubo Cardiomyopathy and Presentation With Shock or Hypotension. Clin Cardiol, 36: 492. doi: 10.1002/clc.22162
To the Editor:
I read with interest the study of Chong et al, describing 80 patients with Takotsubo syndrome (TTS), which focused primarily on hypotension (HYP), its clinical impact, and its possible determinants (left ventricular [LV] dysfunction and the neurohormonal profile). The authors were primarily interested in the relationship of HYP on the day of admission of patients with LV dysfunction. Although there was an inverse correlation of N-terminal pro-brain natriuretic peptide (NT-proBNP) with pulmonary artery saturation—a measure of cardiac output—there was no significant relationship found between normetanephrine release and systolic blood pressure (SBP).
Multivariate analyses did not disclose a significant relationship between SBP and wall motion score index (WMSI), myocardial edema assessed by cardiac magnetic resonance imaging, or peak NT-proBNP. The authors concluded that HYP and shock found in TTS are multifactorial in origin, probably due to LV inotropic dysfunction and vasodilatation. The authors appeared to be puzzled by HYP in the presence of the catecholamine surge characteristic of TTS, stating that “marked release of catecholamine should theoretically protect against HYP via both pressor and positive inotropic effects.” However, HYP is not surprising considering recent pathophysiological insights from the animal laboratory showing that TTS is primarily due to an epinephrine-mediated myocardial stunning (affecting mainly the LV apex and to a smaller degree the midventricular wall), and engendered by a reversible change from a β2-adrenergic receptor/Gs-dependent cardiostimulatory to a β2-adrenergic receptor/Gi-dependent cardioinhibitory functionality.[2, 3]
Surprisingly, the authors did not provide information about the LV ejection fraction (LVEF) of their patients, in addition to the data on WMSI based on echocardiograms (ECHO) performed within the first 48 hours following admission, as done in the bulk of reports currently published (see PubMed article search on takotsubo: http://www.ncbi.nlm.nih.gov/pubmed/?term=takotsubo).4 An analysis of the relationship between SBP and LVEF would have been of interest.
Finally, there was no information provided about a plausible determinant in patients with TTS and HYP, that of ECHO-based intraventricular pressure gradient, found early in the clinical course of TTS. Such gradients, which are transient, may not be detected by ECHO if performed on the second day after admission of patients with TTS. HYP and/or shock may be associated with a low LVEF and a midventricular pressure gradient. Do the authors have data on these 2 plausible determinants of HYP and/or shock?
John E. Madias, MD, FACC, FAHA
Division of Cardiology, Elmhurst Hospital
Elmhurst, New York
Icahn School of Medicine at Mount Sinai
New York University
New York, New York