“…Since the majority of CA patients present a midrange EF (z50%) that increases during exercise according to the data presented, 1 this ''maintained'' contractility could be attributed either to a less impaired circumferential strain or to rather preserved torsional dynamics that may compensate for the severe loss of longitudinal function. 4,5 It is quite unfortunate that the authors have not calculated the impact of CA on the other deformation parameters. This kind of analysis could provide additional evidence about the interaction between amyloid deposition and strain impairment patterns in CA, and it could further suggest that it is not only the apex-to-base amyloid deposition gradient, supported by the authors, but also the epi-to endocardium (Figure 1) one that differently affects the myocardial fibers [2][3][4][5] and provides the pathophysiologic basis for the conclusions reached.…”