Hemodynamics | EPFL Graph Search

Hemodynamics or haemodynamics are the dynamics of blood flow. The circulatory system is controlled by homeostatic mechanisms of autoregulation, just as hydraulic circuits are controlled by control systems. The hemodynamic response continuously monitors and adjusts to conditions in the body and its environment. Hemodynamics explains the physical laws that govern the flow of blood in the blood vessels. Blood flow ensures the transportation of nutrients, hormones, metabolic waste products, oxygen, and carbon dioxide throughout the body to maintain cell-level metabolism, the regulation of the pH, osmotic pressure and temperature of the whole body, and the protection from microbial and mechanical harm. Blood is a non-Newtonian fluid, and is most efficiently studied using rheology rather than hydrodynamics. Because blood vessels are not rigid tubes, classic hydrodynamics and fluids mechanics based on the use of classical viscometers are not capable of explaining haemodynamics. The study o

Arterial in vitro remodeling

Gabriela Montorzi Thorell

Vascular remodeling is defined as any enduring change in the size and composition of an adult blood vessel, allowing adaptation or repair. The vascular remodeling response has been shown to depend on a variety of endogenous and environmental factors. Physiological remodeling is a tightly regulated process that mainly occurs in response to long-term changes in hemodynamic conditions. The adaptation to these hemodynamic changes implies the production of mediators that influence structure as well as function. A loss of regulation in the adaptive response underlies the pathogenesis of major cardiovascular diseases, including hypertension, atherosclerosis, restenosis and arterial aneurismal dilatation. Specialized enzymes called matrix metalloproteinases (MMPs) have been shown to have a predominant participation in the reorganization of the vessel structure, through the degradation of the extracellular matrix scaffold. The aim of this thesis is to gain insight in the biological and mechanical processes taking place in the vascular wall as an adaptive response to different biomechanical stimuli such as blood pressure and blood flow. This work proposes a new model for the study of vascular remodeling where physical factors acting on the arterial wall can be dissociated and analyzed, individually, in relation to the biological response. The results are presented in form of an introduction, three scientific papers and a conclusion section. The investigation has been designed around three different approaches: adaptation of a non-uniform artery to an in vitro environment, vascular adaptation to steady and pulsatile pressure and vascular adaptation to unidirectional and oscillatory flow. The adaptive response to each one of the variables chosen has been analyzed through biological and biomechanical remodeling indicators of the arterial wall. The introduction is an overview of the biological and biomechanical characteristics of arterial wall in relation to the remodeling process. The contribution of vascular smooth muscle cells and extracellular matrix to physiological and pathological arterial remodeling is discussed. Paper I assesses the relative remodeling of a non-axisymmetric artery in relation to its environment. The study considers the native circumferential asymmetry of the porcine right common carotid, which results from the non-homogenous mechanical and hemodynamic native environment. The adaptive response of the artery to an in vitro perfusion environment is analyzed. The study shows that in vitro perfusion leads, through remodeling, to a circumferentially uniform scleroprotein distribution and to a change in arterial compliance. This study emphasizes the link between structural changes, the biomechanical response and the enzymatic implication in the adaptive response. In paper II we investigate the role of continuous and cyclic stretch, produced by steady or pulsatile pressure acting on the arterial wall, on the remodeling response. The study shows that exposure to continuous and cyclic stretch differentially affects the relative scleroprotein content and leads to a change in arterial wall stiffness. The adaptive outcome is studied through an integrative approach taking into consideration the geometrical and structural adaptation, the biomechanical behavior and the enzymatic agents implicated in extracellular matrix turnover. Paper III analyzes the influence of different flow patterns on the arterial adaptive response. We investigate the differential effects of oscillatory flow, mimicking a plaque-prone hemodynamic environment, and unidirectional flow, to mimicking a physiologically protective (plaquefree) environment. The effect of these hemodynamic forces on the remodeling response are characterized through the study of endothelial and smooth muscle cell function as well as through assessment of agents influencing extracellular matrix turnover. The conclusions section presents a synthesis of the results and contribution of this thesis and proposes perspectives for future studies.

EPFL2004

Hemodynamics of ageing, ventricular-arterial coupling and noninvasive assessment of key hemodynamical and cardiac quantities

Stamatia Zoi Pagoulatou

Ageing is a natural process that affects both the anatomical and functional properties of the cardiovascular system and alters the coupling characteristics between the heart and the aorta. These alterations may predispose the cardiovascular system in the development and progression of cardiovascular diseases (CVD), such as hypertension and left ventricular (LV) hypertrophy. CVDs are currently the leading cause of morbidity and mortality globally, and with the population of elderly steadily increasing, they are expected to become socio-economic burden in the near future. Accordingly, the presented body of research aimed at providing novel insights into the evolution of hemodynamics with ageing (Part I) and the physiology of the ventricular-arterial interaction (Part II) by leveraging the potential of a state-of-the-art one-dimensional (1D) model of the systemic circulation. A major goal of this dissertation was also the development, implementation and validation of novel noninvasive tools for monitoring biomarkers of importance (Part III), as well as the evaluation of existing or novel techniques to derive aortic biomechanical properties (Part IV). In Part I, we presented a validated 1D model of the systemic circulation that was adjusted to account for the effects of ageing, as reported by previous literature. The ageing model was found highly consistent with published data from large-scale studies. Examination of the wave reflection profile revealed an increase in the forward wave amplitude over time, which constitutes the principal determinant of the age-induced increase in systolic pressure. Additionally, we highlighted the importance of considering the heterogeneous effects of ageing on the arterial distensibility when adapting the properties of the arterial tree model, in order to predict correctly central hemodynamics. In Part II, we focused on the effect of cardiac systolic function on central and peripheral hemodynamics under physiological and pathological conditions. By means of our computational 1D model, we showed that a physiological increase in cardiac contractility leads to a steeper forward pressure wave pumped by the heart, which, subsequently, drastically alters central and peripheral hemodynamics. These computational results were in good agreement with our subsequent in vivo study, conducted in a group of aortic valve stenosis patients subjected to Transcatheter Aortic Valve Replacement. Part III of this thesis was devoted to the design, development, testing and validation of a method to achieve cardiac and hemodynamic monitoring based on simple, readily available, noninvasive measurements. The concept is based on the personalization of the parameters of the mathematical model of the cardiovascular system according to patient data, and the subsequent derivation of cardiovascular properties in a reverse-engineering approach. Finally, in Part IV, we evaluated existing and novel methods for the assessment of the biomechanical properties of the aorta. We first investigated whether local aortic area compliance, measured as lumen area changes over pulse pressure, is an appropriate index of volume compliance or distensibility when applied to the proximal aorta. In a second analysis, we focused our attention on measures of regional aortic compliance. More specifically, we examined the potential of using compressed-sensing 4D Flow MRI to reliably estimate aortic pulse wave velocity.

EPFL2020

Estimation of Left Ventricular End-Systolic Elastance From Brachial Pressure Waveform via Deep Learning

Vasiliki Bikia, Marija Lazaroska, Stamatia Zoi Pagoulatou, Georgios Rovas, Nikolaos Stergiopulos

Determination of left ventricular (LV) end-systolic elastance (E- es ) is of utmost importance for assessing the cardiac systolic function and hemodynamical state in humans. Yet, the clinical use of E- es is not established due to the invasive nature and high costs of the existing measuring techniques. The objective of this study is to introduce a method to assess cardiac contractility, using as a sole measurement an arterial blood pressure (BP) waveform. Particularly, we aim to provide evidence on the potential in using the morphology of the brachial BP waveform and its time derivative for predicting LV E- es via convolution neural networks (CNNs). The requirement of a broad training dataset is addressed by the use of an in silico dataset (n = 3,748) which is generated by a validated one-dimensional mathematical model of the cardiovasculature. We evaluated two CNN configurations: 1) a one-channel CNN (CNN1) with only the raw brachial BP signal as an input, and 2) a two-channel CNN (CNN2) using as inputs both the brachial BP wave and its time derivative. Accurate predictions were yielded using both CNN configurations. For CNN1, Pearson's correlation coefficient (r) and RMSE were equal to 0.86 and 0.27 mmHg/ml, respectively. The performance was found to be greatly improved for CNN2 (r = 0.97 and RMSE = 0.13 mmHg/ml). Moreover, all absolute errors from CNN2 were found to be less than 0.5 mmHg/ml. Importantly, the brachial BP wave appeared to be a promising source of information for estimating E- es . Predictions were found to be in good agreement with the reference E- es values over an extensive range of LV contractility values and loading conditions. Therefore, the proposed methodology could be easily transferred to the bedside and potentially facilitate the clinical use of E- es for monitoring the contractile state of the heart in the real-life setting.

FRONTIERS MEDIA SA2021