The focal distribution and compositional variation of atherosclerotic plaques along the coronary tree suggest local differences in susceptibility to atherosclerosis [[1], [2], [3]]. Biomechanical factors are among the local risk factors that play a crucial role in the onset, progression, and compositional change of atherosclerotic plaques [4].

Two important biomechanical factors effective in arterial circulation are blood flow-induced wall shear stress (WSS) and blood pressure-induced mechanical wall stress (MWS) [4]. WSS is the biomechanical stress due to the frictional force exerted by the blood flow on the endothelial cells, parallel to the arterial lumen surface. The sensitivity of endothelial cells to changes in WSS levels can result in the activation of inflammatory pathways [5], such as the downregulation of nitric oxide, leading to plaque initiation [6]. Moreover, non-physiological WSS has been shown to correlate with plaque growth and destabilization [[7], [8], [9], [10]].

The other biomechanical factor, MWS, is the structural stress inside the arterial wall due to the blood pressure and is greatly affected by the local arterial geometry [11,12]. MWS causes the stretch and expansion of the arterial wall and the endothelial cells [13]. In respect of atherosclerosis, MWS has mainly been studied in relation to plaque rupture [[14], [15], [16], [17], [18]]. However, the association of MWS with plaque formation and development has received limited attention although high MWS is known to activate numerous inflammatory pathways and promote extracellular matrix synthesis in the arterial wall, by local Angiotensin II production, causing wall thickening under hypertensive conditions [19,20].

To have a more comprehensive understanding of the involvement of biomechanics in coronary atherosclerosis, we studied the individual and combined effects of MWS and WSS in plaque-free and plaque sectors of atherosclerotic coronaries. Artery-specific computational models of human coronary arteries were constructed to assess MWS and WSS, which are in the end used to examine their influence on coronary atherosclerosis.