Preload, Afterload, E and e′

The stated aim of Taraldsen et al. was to assess the effect of preload augmentation on left ventricular (LV) diastolic parameters in healthy subjects and subjects with cardiac disease [1]. The authors reported that augmented preload (with augmented preload effectively defined as an increase in intravascular volume) did not affect E/e′ in subjects with normal LV filling pressure but increased E/e′ in subjects with elevated LV filling pressure. These findings add to previous evidence that E and e′ responses can be variable and also that these responses remain incompletely understood. I propose that additional insights about E, e′ and E/e′ may be possible from the available data of Taraldsen et al., beginning with the definition of preload and also considering additional measurements. Preload is myocardial stretch and change in myocardial stretch has been assessed in the current study by change in LV end-diastolic volume (LVEDV). LVEDV did not increase with volume change in the elevated LV filling pressure group and therefore preload did not increase in this group. A potential explanation for the increase in E in this group is that LVEDP was elevated and LVEDV could not increase further, but that mean left atrial pressure did increase. More specific for e′ is that LV long-axis preload is long-axis stretch, change of which can be measured by change in LV end-diastolic length (LVEDL). This distinction is potentially important because LVEDL does not necessarily change in parallel with LV short-axis diameter or LVEDV [2]. Afterload effects should also be considered in this study as afterload can affect e′ and indirectly affect preload. Moreover, an increase in LV stroke volume following an increase in preload can increase the blood pressure (BP) and thus afterload. It is therefore a limitation of this study that BP has not been reported. Also relevant to this study is that increases in stroke volume due to saline infusion may not just be due to increases in LVEDV but also to decreases in LV end-systolic volume, the latter likely due to a reduction in afterload via a decrease in blood viscosity [3]. Lastly, a major determinant of e′ is the extent of the preceding LV long-axis contraction and its close relationship with the extent of early diastolic long-axis excursion [4], but in the study of Taraldsen et al., as in most previous studies of e′, long-axis excursion changes during the interventions could have been measured but were not. The data that support the findings of this study are available from the corresponding author upon reasonable request.