We would like to commend Lyseggen et al for this detailed study 1 and presentation of these fascinating data. The authors confirmed our findings that long-axis ventricular myocardial isovolumic acceleration showed good correlation with dP/dt max , with positive inotropy induced by dobutamine infusion, and its relative preload resistance over a physiological range. 2 We do, however, have some reservations regarding the authors' interpretation of some of their other findings and the conclusions drawn from them.There was a significant decrease in myocardial isovolumic acceleration (IVA) after volume loading, which caused an acute elevation in left ventricular end-diastolic pressure from a baseline of 5.9Ϯ1.3 mm Hg to a nonphysiological value of 19.0Ϯ2.2 mm Hg. First, few indexes of contractile performance could be expected to be resistant to loading change of this magnitude. Furthermore, in Figure 6, the linearity of IVA at more physiological changes in preload is demonstrated. This is in keeping with our conclusion that IVA "is unaffected by preload and afterload changes within a physiological range."With ischemia lasting 1 to 2 minutes, the present study demonstrated changes in motion during the isovolumic contraction period, with marked initial lengthening resulting in a negative velocity spike and the disappearance of a positive IVA spike. The conclusion that IVA is unhelpful during ischemia is in contrast to earlier findings by the same group 3 and those of others 4 demonstrating the added benefit of examining myocardial motion in the isovolumic contraction period. Indeed, although referenced, the differing data in the present study are not discussed in relationship to the group's own previously published data. We think, therefore, that it is premature to dismiss IVA as being unable to "reflect impaired myocardial function during ischemia."Finally, the authors demonstrate maintenance of IVA, despite the lack of a preceding atrial systole. Analysis of the relationship between IVA and the phonocardiogram showed that the onset of IVA coincided with the onset of the low-frequency vibrations of the first heart sound. Most data support the hypothesis that these vibrations are caused by the onset of ventricular myocardial contraction. 5 Because the high-frequency component of the first heart sound occurs late in the isovolumic period, it is not surprising that IVA shows no significant relationship to this event. Furthermore, the classic work of Rushmer clearly demonstrates active asynchronous contraction as the initial stage of long-axis ventricular shortening because it assumes a more spherical shape. 6 The evidence, therefore, for Lyseggen et al concluding that IVA may be "related to late diastolic events" is not clear to us.
ResponseWe have read the comments by Cheung and colleagues about our article in Circulation 1 with interest. The first comment addresses the question of load dependency. Although there may be only minor changes in myocardial isovolumic acceleration (IVA) within a physiological range of fill...
