The effect of left ventricular contractility on arterial hemodynamics: A model-based investigation.

Stamatia Pagoulatou,Georgios Rovas,Nikolaos Stergiopulos,Vasiliki Bikia,Dionysios Adamopoulos,Nejka Potocnik

doi:10.1371/journal.pone.0255561

Stamatia Pagoulatou, Georgios Rovas + Show 4 more

Open Access

https://doi.org/10.1371/journal.pone.0255561

Copy DOI

Abstract

Ventricular-arterial coupling is a major determinant of cardiovascular performance, however, there are still inherent difficulties in distinguishing ventricular from vascular effects on arterial pulse phenotypes. In the present study, we employed an extensive mathematical model of the cardiovascular system to investigate how sole changes in cardiac contractility might affect hemodynamics. We simulated two physiologically relevant cases of high and low contractility by altering the end-systolic elastance, Ees, (3 versus 1 mmHg/mL) under constant cardiac output and afterload, and subsequently performed pulse wave analysis and wave separation. The aortic forward pressure wave component was steeper for high Ees, which led to the change of the total pressure waveform from the characteristic Type A phenotype to Type C, and the decrease in augmentation index, AIx (-2.4% versus +18.1%). Additionally, the increase in Ees caused the pulse pressure amplification from the aorta to the radial artery to rise drastically (1.86 versus 1.39). Our results show that an increase in cardiac contractility alone, with no concomitant change in arterial properties, alters the shape of the forward pressure wave, which, consequently, changes central and peripheral pulse phenotypes. Indices based on the pressure waveform, like AIx, cannot be assumed to reflect only arterial properties.

Highlights

The arterial blood pressure is the result of the instantaneous interaction between the left ventricle (LV) of the heart and the arterial system
Where end-systolic pressure-volume relationship (ESPVR) is equal to Ees (VLV−Vd), with Ees being the end-systolic elastance and Vd the dead volume [17], and enddiastolic pressure-volume relationship (EDPVR) is equal to P0 exp(β VLV), with P0 being the dead pressure and β a diastolic stiffness parameter
We find that changes in the ESPVR have a major impact on both central and peripheral hemodynamics

Summary

Introduction

The arterial blood pressure is the result of the instantaneous interaction between the left ventricle (LV) of the heart and the arterial system. The ventricular-arterial coupling is a major determinant of left ventricular function and global cardiovascular health [1,2,3]. Several physiological and pathological processes are linked with deleterious alterations in one component of the interaction, which gradually compromise the function and structure of its counterpart. For example, is linked with the stiffening of the arterial tree [4, 5]; the increase in vascular load triggers remodeling of the LV, which leads to further increases in systemic pressure and so on [6].

Methods

Results

Discussion

Conclusion