Dynamic left ventricular outflow tract obstruction and acute heart failure in tako-tsubo cardiomyopathy.

favorable prognosis with respect to malignant arrhythmia, a finding supported by other studies (4,5). As wall stress also is increased in advanced cardiomyopathy, the association between LGE and wall stress referred to by the authors is not surprising, because LGE also is a feature of advanced cardiomyopathy (4,5). One would expect that if increased wall stress is the underlying mechanism of myocardial contrast enhancement, it is likely to be diffuse rather than the focal process observed with LGE. Diffuse contrast enhancement cannot be detected with the technique of LGE, because this method requires the presence of apparently normal adjacent myocardium without contrast enhancement. However, because shortened post-contrast myocardial T1 times have been shown to correlate with histological fibrosis (6) in patients with cardiomyopathy, wall stress as the underlying mechanism of contrast enhancement seems unlikely. Interestingly, recent research in hypertensive patients revealed an absence of LGE despite increased wall stress compared with controls (7). To determine conclusively that wall stress contributes to the presence of LGE in nonischemic cardiomyopathy independently of regional fibrosis would require contemporaneous measurement of LGE and wall stress coupled with histological examination of areas of myocardium in which LGE is present. To our knowledge, this has not been performed, and given the lack of invasive pressure measurement along with the unavailability of histological samples, such analysis is not possible from our study population.