Insights Into Degenerative Aortic Valve Disease
Seth H. Goldbarg, MD,
Sammy Elmariah, MD,
Marc A. Miller, MD and
Valentin Fuster, MD, PhD*
Zena and Michael A. Wiener Cardiovascular Institute and Marie-Josée and Henry R. Kravis Cardiovascular Health Center, The Mount Sinai School of Medicine, New York, New York.
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Figure 4 Diseased Valvular Endothelium
Diseased endothelium exhibits nonlaminar flow, low-density lipoprotein (LDL) deposition, macrophage infiltration, and matrix metalloproteinase (MMP) expression. Differential expression of cytoskeletal elements promotes a valvular phenotype. BMP = bone morphogenic protein. Modified, with permission, from Fuster et al. (18).
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Figure 5 Interplay of Lipids and Inflammation With Genetics on Degenerative Aortic Valve Disease
IL = interleukin; OPG = osteoprotegrin; RANK = receptor activator of nuclear factor kappa B; TNF = tumor necrosis factor; other abbreviations as in Figure 4. Modified, with permission, from O’Brien (21).
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Figure 6 Ex Vivo Confocal Microscopy Performed at 100x Magnification of Apo-E Knockout Murine Aortas
The aortas were incubated with control, nitro-2-1,3-benzoxadiazol-4-yl (NBD)-labeled micelles (green), and NBD-labeled immunomicelles (green) and stained with 4’,6-diamidino-2-phenylindole (blue) and R-phycoerythrin-labeled anti-CD68 (red) that stains for macrophages. Reprinted, with permission, from Lipinski et al. (27).
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Figure 8 ACE in a Human Aortic Valve Lesion
(A) Double immunostaining for macrophages (blue stain) and angiotensin-converting enzyme (ACE) (red stain) demonstrate that the majority of macrophages lack ACE protein (blue stain); most staining is extracellular. A minority of macrophages contain ACE protein (purple stain). (B) Double immunostaining for macrophages (blue stain) and apolipoprotein B (apoB), the primary protein of low-density lipoprotein cholesterol particles (brown stain), demonstrates the presence of extensive extracellular apoB staining, which colocalizes with extracellular ACE. Original magnification x400. Reprinted, with permission, from O’Brien et al. (46).
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Figure 9 HE Staining of Native and Decellularized Porcine Pulmonary Heart Valves
Shown are conduit wall (A) and leaflet (B). Original magnification x400. (C, D) Native (left) and decellularized (right) porcine pulmonary heart valves, staining for collagen I and III (green), elastin (red), and deoxyribonucleic acid (white). Confocal laser scanning microscopy, original magnification x400. Shown are conduit wall (C) and leaflet (D). Reprinted, with permission, from Rieder et al. (56). HE = hematoxylin and eosin.
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Figure 10 Changes in Hemodynamic Function Over 4 Months
Maximum systolic gradient (A), mean gradient (B), and effective orifice area (C) at time of implantation (t = 0) and after 4 months (t = 4) in vivo. Reprinted, with permission, from Sutherland et al. (63).
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Figure 11 Macroscopic Appearance of Tissue-Engineered Semilunar Heart Valve Before Implantation
Valve viewed from below with leaflet free margins apposed in closed position (A) and viewed in profile (B) with arrows outlining 1 sinus of Valsalva. Echocardiograms of implanted valve in short (C) and long (D) axes, in same approximate orientation as macroscopic images (A, B). Reprinted, with permission, from Sutherland et al. (63).
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