Franklin Open (Dec 2024)
Reconceptualizing the ventricular-arterial interaction for non-invasive damping modelling: Application in young soccer players and ballet dancers
Abstract
Introduction: The left ventricle (LV) serves as the primary source of mechanical energy in circulation, subsequently converted into kinetic energy throughout the arterial system (AS). Analyzing the specific area within an LV pressure-volume (PV) loop helps characterize the function of the cardiac pump. Simultaneously, the AS functions as a blood reservoir, receiving the blood ejected by the LV. The enclosed area in the AS PV-loop is linked to an energy dissipation process (where not all pressure work is regained), attributed to the viscous function of smooth muscle cells. Objective: The main objective of this work was to investigate wall energy dissipation in the vascular bed in terms of LV and AS PV-loop evaluation, to determine if different types of training could lead to differentiated levels of wall energy dissipation. The ‘coupling concept’ is proposed to be conceived from LV and AS loop energy interaction, quantified by a ‘ventricular-arterial damping factor’ (VADF). Material and Methods: Data from subjects with different kinds of training (soccer players and ballet dancers) were collected noninvasively and compared with a control group of untrained individuals to analyze the differentiating characteristics of the subjects, especially in terms of Stroke Work Dissipation (WDIS). To this end, a lumped parameters Windkessel (WK) model was proposed for the assessment of LV and AS loops, through an interactive process. Changes in wall energy dissipation were observed under training routines. Both soccer players and ballet dancers showed increased WDIS and VADF compared to the untrained individuals (p<0.05). However, elastic work (WEL), defined as the difference between LV stroke work and WDIS, was found to remain constant in ballet dancers, unlike in soccer players. Conclusion: The WK model enabled the simulation of the interaction between LV and AS based on a ventricular-arterial coupling framework. The findings suggest that higher WDIS values, together with the preservation of WEL, may indicate an enhanced protective effect by vascular smooth muscle cells and other wall components, involved in the AS dissipation phenomenon.
