The influence of haemodynamics on the mechanics of atherosclerosis growth
Creators: name: Gabriel, Sargon
Publisher: name: RMIT University
Year: 2024
Subjects: classificationCode: 400303
subject: Biomechanical engineering
classificationCode: 401204
subject: Computational methods in fluid flow, heat and mass transfer (incl. computational fluid dynamics)
classificationCode: 490102
subject: Biological mathematics

description: Atherosclerosis is a focal inflammatory disease of the cardiovascular system that locally degenerates arteries. It is characterised by the development of inflammatory lesions within the arterial wall that if left untreated, may develop to critically impede blood-flow or else risk rupture of the arterial vessel itself. Both scenarios result in complications that may lead to potentially life-threatening cardiovascular diseases, such as cerebrovascular disease (causing stroke) and coronary artery disease (causing a heart attack). Preventative medical treatment of these diseases can often be achieved by the control and maintenance of their common precursor, atherosclerosis, generally via stenting the diseased artery or via drug administration. Yet though such treatments have become standard, there is a limit to the degree of foresight that standard medical practice can provide for individual patient response to treatment. The next step forward is the realisation of patient-specific medication via the development of models that are uniquely tailored to individual patient conditions. Computational modelling provides a viable framework to achieve this, wherein physiological processes are expressed by mathematical models that are computationally resolved. The objective of this being, to construct a virtual template for physiological processes, which may be used as a platform to explore medical treatment options for individual patients. To achieve this for atherosclerosis, it is first necessary that its underlying mechanics be expressed mathematically. Indeed, there is at present a variety of mathematical models that attempt to do this. However, the mechanics of atherosclerosis involve a complex amalgamation of coupled processes that operate on multiple length and time scales. There is hence inherent modelling difficulty associated with a wholistic description of atherosclerosis, which current models are yet to completely resolve. In the present research, some of the longstanding modelling difficulties that have withstood resolution are investigated. A review of current atherosclerosis models is made and it is noted that though substantial progress has been made to capture the inflammatory process of biochemical species involved in atherosclerosis, the influence of flow pulsatility on species transport is not well integrated. Therefore, for the present study, a central research question is constructed to investigate the mechanics associated with pulsatile blood flow and its influence on the transport of blood-borne species. It is observed that two dominant time scales are inherent to the progression of atherosclerosis within arteries; a short time scale associated with the blood flow's period of oscillation (order of 1 second) and a long time scale associated with growth and remodelling of the arterial wall (order of months/years). As a consequence of the large difference between the respective sizes of the two time scales, it is generally computationally prohibitive to explicitly resolve both. In models of atherosclerosis, this difficulty is often bypassed by removing the time-scale associated with the oscillating flow; either by representing the flow field with its period-average or its steady-equivalent. It is shown that so-called oscillatory flow disturbances are inherent to a pulsatile flow field, causing variations to emerge between its period-average and steady-equivalent representation. To quantify the significance of these disturbances and hence measure their influence on the flow, the Oscillatory Kinetic Energy Index (OKEI) and Oscillatory Flow Index (OFI) are developed. Oscillatory flow disturbances are also demonstrated to influence the transport of blood-borne species, causing variations to emerge between their period-average and steady-equivalent distributions. The need for integrating the influence of oscillatory flow disturbances in steady models of species transport is hence shown to be necessary, and a model is developed to resolve this.