ACE has been identified in aortic sclerotic lesions. 13 Although there is evidence that some ACE may be produced locally, the majority was extracellular and colocalized with apolipoprotein B, a component of retained LDL particles, which suggests that the ACE may be “carried” into the lesion via LDL cholesterol particles. Additionally, angiotensin II, which has been associated with promotion of monocyte infiltration and enhancement of the uptake of modified LDL within atherosclerotic lesions, has been detected in early aortic sclerotic lesions, which implies that the ACE identified was active enzymatically. 13

In the diseased aortic valve, a subset of the normal valve fibroblasts within the fibrosa layer differentiate into myofibroblasts, which possess smooth muscle cell characteristics, with expression of α-actin, vimentin, and desmin. 1, 14 In advanced aortic stenotic valve specimens, angiotensin type-1 receptors have been detected on a subset of the myofibroblasts that express α-actin, which again suggests that the ACE detected is active enzymatically. 13 Further investigations will be required to better define the potential role for the reninangiotensin system and causative pathways in the pathogenesis of calcific aortic valve disease.