Figure 4.
Schematic illustrating the potential roles for mechanical forces in the initiation of valvular pathologies. The inflow surface experiences high-magnitude pulsatile shear stresses and is the predominant location for thrombotic/bacterial endocarditis (A–G). The outflow surface experiences much lower, oscillatory shear stresses and is the predominant location for sclerotic/calcific lesion formation (1–6).
