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The IN VIVO effective orifice areas by valve size of the Mitroflow aortic pericardial bioprosthesis provide the opportunity of avoiding obstructive characteristics for all valve sizes, including optimizing the management of the small aortic annulus.

Exposure to ETS acutely increased LDL accumulation in perfused arteries. Repeated exposure to ETS may represent important early events in atherogenesis.

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Abstract-Current research suggests that estrogen may have primary effects on the artery wall. To investigate the mechanisms of female sex hormone actions in the artery wall, we used an isolated, perfused, rat carotid artery model to examine the effects of estradiol on the rates of accumulation of normal (N-LDL) and minimally modified (MM-LDL) low density lipoprotein in ovariectomized rats. N-LDL, MM-LDL, and oxidized LDL (OX-LDL) were fluorescently labeled and perfused into individual arteries. The rate of LDL accumulation was measured by quantitative fluorescence microscopy before and after treatment with estradiol (1 nmol/L, 272 pg/mL). Estradiol had no effect on the rate of Key Words: artery Ⅲ arteriosclerosis Ⅲ LDL Ⅲ estrogen Ⅲ oxidized LDL Ⅲ endothelium Ⅲ permeability A cardinal characteristic of the development of atherosclerosis is the accumulation of LDL within the arterial wall. 1-3 Sites of relative increase in LDL permeability have been identified in normal arteries 4 and can be induced by injury to the endothelium. 5-9 Alternatively, others have reported increased binding and decreased efflux of LDL from the vascular wall, even under conditions where LDL influx was not affected. 10,11 Therefore, LDL accumulation in the artery wall potentially occurs by several mechanisms, perhaps depending on the stage of atheroma formation.A large body of evidence indicates that modification of LDL in the artery wall promotes atherosclerosis. 12 Recent studies demonstrate evidence of modification of LDL in the blood. [13][14][15][16][17] Furthermore, a previous study showed increased accumulation and degradation of oxidized LDL (OX-LDL) in the artery wall in vivo. 18 These studies suggest that the reason there is increased accumulation and degradation of OX-LDL is because arterial permeability to undegraded, OX-LDL is greater than arterial permeability to native LDL (N-LDL). However, the precise mechanism(s) by which modified LDL (MM-LDL) affects LDL flux in the artery wall, such as increases in permeability to LDL, remains incompletely understood.Modification of LDL (eg, oxidation), either in the circulation or the artery wall, could promote atherosclerosis by increasing LDL accumulation in the artery. Also, alteration of constituents of the artery wall, such as proteoglycans, could influence LDL binding to the artery wall. Furthermore, oxidant-mediated injury of endothelial cell membranes could compromise the endothelial layer barrier to macromolecules in arteries. 5 To counteract oxidant stress effects on LDL and/or the artery wall, a number of potential antioxidants have been examined. In particular, some estrogens (eg, 17␤-estradiol) are known to reduce LDL accumulation in the artery wall 19,20 and to be potent antioxidants. [21][22][23] In addition, estrogens may protect endothelial cells from oxidative damage. 21,22 This action would be expected to prevent increased LDL permeation into the artery wall. Furthermore, estradiol has been shown to inhibit LDL oxidation in vivo at supraphysiological 24 and physiolo...