**1. Introduction**

The central role of biomechanics in the pathogenesis of atheroma is supported by a body of circumstantial evidence [1]: atherosclerotic plaque is not laid down uniformly on the inner lining of arteries but at the junctions of branch vessels, at points where the external wall of the artery is fixed to surrounding structures and at kinks and bends where mechanical strain and flow turbulence occur. It is susceptible to the effects of blood pressure [2]. It is not seen in veins except when these are used as arterial grafts [3]. Blood pressure is a well-established risk factor for coronary artery disease [4]. Atherosclerosis occurs prematurely in situations where arterial wall stiffness is increased such as diabetes, pseudoxanthoma elasticum and progeria syndromes [5–7]. Blood viscosity, which contributes to the transmission of shear strain to the endothelium, is an independent risk factor for ischaemic heart disease [8]. Lastly, experimental and computer modelling studies have demonstrated an association between atherosclerosis-prone areas of the arterial tree and conditions of local blood flow characterised by high strain-low shear, and oscillatory reverse flow [9, 10].

There are two postulated mechanisms whereby such mechanical strain acting on the inner arterial wall might give rise to the development of atherosclerosis and explain its focal localisation within the arterial tree: firstly, the endothelium might be damaged directly by forces stripping it from the underlying intima or causing ultrastructural changes to the intercellular junctions thus exposing the underlying collagen network of the intima to blood components giving rise to collagen-platelet and collagen-fibrin interactions and the development of plaque according to the incrustation theory of atherogenesis. Such endothelial damage has been shown to give rise to atheroma-like lesions in experimental animals [11], and the attachment of the endothelium to underlying collagen is less strong in animals that are atheroma-prone compared to those that are resistant [12]. Direct mechanical damage to the endothelium would tend to occur at sites where there was maximum lifting and shear stress and this might explain its focal distribution. Secondly, endothelial cells are highly mechano-sensitive and certain conditions of shear stress and pulse waveform have been shown to provoke a stress response in endothelial cells favouring platelet and white cell adherence, translocation of white cells and expression of inflammatory mediators, processes that have been linked to the development of atherosclerosis [10, 13–16].

Experiments related to this latter mechanism have hitherto concentrated on the effect of shear stress, which may be likened to the aerodynamic equivalent of drag acting on the endothelial surface. Little work by contrast has been done on the inward "lift" effect in inducing stress acting at right angles to the endothelial surface, tending to lift the endothelium off the underlying substrate, and inducing conformational change on the inner wall of the artery. Conformational change in the inner arterial wall resulting from this lifting effect would tend to give rise to the boundary layer separation and local oscillatory flow reversal at low flow rate that appear to induce a proatherogenic endothelial cell phenotype in the tissue culture experiments [10, 15, 16].

*Role of Arterial Pressure, Wall Stiffness, Pulse Pressure and Waveform in Arterial Wall… DOI: http://dx.doi.org/10.5772/intechopen.100048*

The study of the factors affecting the inward stress/strain relationship to the arterial wall is consequently of interest both in relation to the initial development of atherosclerosis but also in relation to the stresses causing the developed atherosclerotic plaque to separate and thus cause clinical harm.

The aim of the present work was to examine directly the factors giving rise to transmural stress/strain and to their possible interactions. A bench-based test rig was employed similar to that described by Giussaniani et al. [17] modified to provide continuous pulsatile flow within fresh pig arteries.
