Letter Regarding Article by Lyseggen et al, “Myocardial Acceleration During Isovolumic Contraction: Relationship to Contractility”
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To the Editor:
We would like to commend Lyseggen et al for this detailed study1 and presentation of these fascinating data. The authors confirmed our findings that long-axis ventricular myocardial isovolumic acceleration showed good correlation with dP/dtmax, 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 5.9±1.3 mm Hg to a nonphysiological value of 19.0±2.2 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 …