Growth and Remodeling: Coronary Arteries

Blood vessels are subjected to pulsatile mechanical loading of blood pressure and flow throughout the cardiac cycle. The vessels undergo structural and mechanical adaptations in response to changes in the local hemodynamic conditions. For example, changes in blood flow cause changes in fluid wall shear stress (WSS), which is a tractive frictional force exerted by flowing blood on the inner layer of the vessel wall that elicits a wide range of biochemical and physiological responses that have been demonstrated in both experimental (Wang and Prewitt 1991) and clinical studies (Green et al. 2004; Joannides et al. 1995). Studies have also shown that a sudden increase in blood flow initiates an enlargement of the arterial lumen that progresses for months as the WSS tends to a homeostatic or normal level (Kamiya and Togawa 1980; Kassab et al. 2002). A gradual increase in blood flow is reported to result in an outward hypertrophic remodeling of resistance (Buus et al. 2001; Pourageaud and DeMey 1997; Tulis et al. 1998; Tuttle et al. 2001; Wesselman et al. 2004) and conductance arteries (Kassab et al. 2002; London and Safar 1996; Lu et al. 2001). The flow-induced remodeling may attempt to maintain mechanical homeostasis (Kassab and Fung 1995; Chap. 1 ). When blood flow is elevated in a vessel, the endothelium responds to restore WSS toward homeostatic levels by changing vascular tone, increasing the lumen diameter (Tulis et al. 1998), and potentially altering the function and mechanical properties of the vessel wall. Changes in the mechanical loading and hence in the internal stresses and strains lead to an adaptive process in molecules, cells, structure, material properties, and possibly function.