(A) CD31-positive fetal valvular endothelial cells (VECs) in the second and third trimesters and VECs in children’s valves consistently expressed nonmuscle myosin produced by embryonic or activated cells (SMemb), matrix metalloproteinase (MMP)-1, MMP-13, and cell adhesion molecules ICAM-1 and VCAM-1, whereas normal adult VECs mostly had negligible expression levels of these proteins. Bar = 50 µm. Magnification 400x. (B) Percent of endothelial cells positive for maker. *Significant differences in protein expression in adult valves (p < 0.001). From Aikawa et al. (1).

Schematic summary of cardiac valve remodeling in fetal valves according to the findings of the present study. Activated/immature cell phenotypes and collagen remodeling in gestation were followed after birth by decreased cell activation and eventually, in adults, by quiescence. These cellular changes were accompanied by increased collagen fiber thickness and alignment. Thin lines = thin, immature collagen fibers; thick lines = thick, mature collagen fibers. From Aikawa et al. (1). Abbreviations as in Figure 1.

Disease frequency was calculated for each parish by comparing the number of native cases of operated calcific aortic valve stenosis (CAVS) to the population living in the village. Population was estimated from the mean of the censuses performed in 1926, 1931, and 1936. This map shows an obvious spatial heterogeneity. Two clusters of high frequency can be described, 1 on the northern part of the map and 1 between the southern part of Nantes and La Roche-sur-Yon and between the Atlantic coast and Cholet, corresponding to a well-known isolate called "vendee-cholletaise." The letters represent parishes in which familial aggregation of the disease has been identified. From Probst et al. (3).

Control valve, degenerative mitral valve (arrow points to hypertrophic chondrocytes), calcified aortic valves (arrow points to positive stain), and bicuspid aortic valve (arrow points to positive stain) (magnification 25x). Insert within each photo is high-power magnification to demonstrate cellular staining (magnification 40x) (A) Bone sialoprotein strain. (B) Osteoponton stain. (C) Osteocalcin stain. From Caira et al. (4).

Control valve, degenerative mitral valve (arrow points to hypertrophic chondrocytes), calcified aortic valves (arrow points to positive stain), and bicuspid aortic valve (arrow points to positive stain) (magnification 25x). Insert within each photo is a high-power magnification to demonstrate cellular staining (magnification 40x). (A) Lipoprotein receptor-related protein 5 stain. (B) Wnt 3 stain. (C) Proliferating cell nuclear antigen strain. From Caira et al. (4).

EF = left ventricular ejection fraction; EFU = ejection fraction units. From Vaquette et al. (18).

(A) Kaplan-Meier event-free survival for asymptomatic patients with mitral valve prolapse; (n = 74) versus flail leaflet (n = 58), p = 0.23. (B) Kaplan-Meier survival free of various events. From Rosenchek et al. (32).

ALP = anterior leaflet prolapse; PLP = posterior leaflet prolapse. From De Bonis et al. (33).

AL = anterior leaflet prolapse; BL = bileaflet prolapse; MR = mitral regurgitation; PL = posterior leaflet prolapse. From David et al. (34).

(A) Aortogram showed no aortic regurgitation. (B) Left ventriculogram showed no mitral regurgitation and no evidence of subaortic stenosis. From Boudjemline et al. (47).