Left ventricular-arterial coupling in systemic hypertension

The Relationship of Renal Augmented Velocity Index With Ventricular–Arterial Coupling in Comparison to Renal Resistive Index

“…In our study, renal Avi was independently associated with E a and VAC, while there was no correlation between renal Avi and E es . It is expected that E es adapts to the changes in E a in hypertensive patients; however, it does not necessarily mean that incremental response of E es to the increases in E a should provide a fixed coupling ratio due to the heterogeneity in left ventricular response in terms of mass and geometry 13,37,41,42 . Therefore, we suggest that structural and functional disparities in LV remodeling pattern are the underlying reason of the absence of the correlation between renal Avi and E es in our study.…”

“…However, E a is somewhat a matter of debate due to the assumption that it is relatively insensitive to pulsatile component of the arterial load. Concerning this issue, we relied on mathematical models and findings presented by studies that consistently reported the contribution of pulsatile load to E a 11,13–20,37–40,43,44 . Third, we cannot extrapolate our results to disease groups rather than hypertension, but indeed the strict inclusion criteria employed in this study strengthen the validity of the results as well as the absence of antihypertensive drug usage which can interfere with the arterial stiffness and renal RI values of patients 7,8 .…”

“…Previous studies examining VAC in patients with hypertension revealed that E a increased due to structural modifications leading to impaired arterial elastic properties. And as a response to this increase in E a , LV exhibited adaptative mechanisms including the changes in left ventricular mass or geometry which resulted in the rise of E es to preserve the coupling ratio in normal ranges 13,14,19,20,37–41 …”

“…Notably, the present study cannot provide the underlying mechanistic link between E a , VAC, and renal Avi. However, it is noteworthy to say that E a identifies the state of the arterial tree by integrating not only the steady but also the pulsatile components of the arterial load which may become prominent due to hypertension‐related structural modifications such as arterial stiffening that may lead to decreased compliance of the conduit arteries 13,14,17,37–40,43,44 . It is also the case in hypertension that stiffening may compromise the cushioning effect of large arteries, which in turn will result in undamped transmission of central energy to renal vasculature 45,46 .…”

“…Therefore, noninvasive estimation of VAC by transthoracic echocardiography was extensively carried out to assess global CV efficiency in various pathophysiological conditions. It is calculated by the ratio of effective arterial elastance ( E a ) to left ventricular end‐systolic elastance ( E es ), where E a defines the net arterial load imposed to LV and E es indicates the contractile state and stiffness of the myocardium 13–20 …”