PubMed · 8413402
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
P Bloomfield, D J Wheatley, H C Miller. 1993-10-21. Outcomes after heart-valve replacement.. https://doi.org/10.1056/nejm199310213291717
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
OBJECTIVES: The objective of this study was to compare stentless bioprostheses with stented bioprostheses with regard to their hemodynamic behavior during exercise. BACKGROUND: Stentless aortic bioprostheses have better hemodynamic performances at rest than stented bioprostheses, but very few comparisons were performed during exercise. METHODS: Thirty-eight patients with normally functioning stentless (n = 19) or stented (n = 19) bioprostheses were submitted to a maximal ramp upright bicycle exercise test. Valve effective orifice area and mean transvalvular pressure gradient at rest and during peak exercise were successfully measured using Doppler echocardiography in 30 of the 38 patients. RESULTS: At peak exercise, the mean gradient increased significantly less in stentless than in stented bioprostheses (+5 +/- 3 vs. +12 +/- 8 mm Hg; p = 0.002) despite similar increases in mean flow rates (+137 +/- 58 vs. +125 +/- 65 ml/s; p = 0.58); valve area also increased but with no significant difference between groups. Despite this hemodynamic difference, exercise capacity was not significantly different, but left ventricular (LV) mass and function were closer to normal in stentless bioprostheses. Overall, there was a strong inverse relation between the mean gradient during peak exercise and the indexed valve area at rest (r = 0.90). CONCLUSIONS: Hemodynamics during exercise are better in stentless than stented bioprostheses due to the larger resting indexed valve area of stentless bioprostheses. This is associated with beneficial effects with regard to LV mass and function. The relation found between the resting indexed valve area and the gradient during exercise can be used to project the hemodynamic behavior of these bioprostheses at the time of operation. It should thus be useful to select the optimal prosthesis given the patient's body surface area and level of physical activity.
Previous studies have shown that vascular grafts were prone to inducing an atherosclerosis-like phenomenon, thus possibly jeopardizing their performance. Furthermore, lipid retention, observed in most synthetic arterial prostheses explanted from humans, appears to have an important role in the progression of this atherosclerotic process, therefore hindering the healing process and neo-intima formation of these synthetic conduits. The current study examined lipid concentration profiles across prosthesis membranes exposed to lipid dispersion under various transmural pressures, flow rates, and durations of exposure. It was demonstrated that the lipids rapidly permeated the prosthesis membrane, as lipid advection increased to a maximum, then steadily decreased until the membrane became completely impermeable to the fluid. The concentration of lipids within the grafts was monitored using FT-IR microspectroscopy, then correlated as a function of time in order to evaluate the mass transfer coefficients and lipid saturation concentration. Lipid sorption, as a function of time, was described by a mechanism taking into account two first-order kinetic models. The lipids were first rapidly adsorbed onto the Teflon(R), potentially influenced by the strong affinity of these lipids for the highly hydrophobic polytetrafluoroethylene polymer. This affinity then enhanced the germination of the lipid deposits that filled in the prosthesis wall. For lipid retention as a function of the transmural pressure and flow rate, no clear tendency was established.
Implant surface roughness influences osteoblast proliferation, differentiation, and local factor production. Moreover, the responsiveness of osteoblasts to systemic hormones such as 1, 25-(OH)(2)D(3) is altered by the effects of surface roughness; on the roughest Ti surfaces the effects of roughness and 1, 25-(OH)(2)D(3) are synergistic. Prostaglandin E(2) (PGE(2)) appears to be involved in mediating the effects of surface roughness on the cells, as well as in the response to 1,25-(OH)(2)D(3). However, it is not yet known through which signaling pathways surface roughness exerts its effects on the response of osteoblasts to 1, 25-(OH)(2)D(3). The present study examined the potential role of protein kinase A (PKA), phospholipase A(2)(PLA(2)), and protein kinase C (PKC) in this process. MG63 osteoblast-like human osteosarcoma cells were cultured on cpTi disks with R(a) values of 0. 54 microm (PT), 4.14 microm (SLA), or 4.92 microm (TPS). PKA was inhibited by adding H8 to the cultures; similarly, PLA(2) was inhibited with quinacrine or activated with melittin, and PKC was inhibited with chelerythrine. Inhibitors or activators were included in the culture media through the entire culture period or for the last 24 h of culture. In addition, cultures were treated for 24 h with inhibitors or activators in the presence of 1,25-(OH)(2)D(3). The effects on cell number and alkaline phosphatase specific activity were determined after 24 h; PKC activity was determined after 9 min and at 24 h. Cell number was reduced on rough surfaces, and alkaline phosphatase activity was increased. 1,25-(OH)(2)D(3) had a synergistic effect with surface roughness on alkaline phosphatase. However, neither surface roughness nor 1,25-(OH)(2)D(3) had an effect on PKC. H8 treatment for 24 h inhibited cell number and alkaline phosphatase on all surfaces; however, when it was present throughout the culture period, the PKA inhibitor had no effect on cell number, but decreased alkaline phosphatase-specific activity. H8 reduced the 1,25-(OH)(2)D(3)-mediated effect on cell number and alkaline phosphatase. Quinacrine inhibited cell proliferation and alkaline phosphatase on all surfaces and further reduced the 1,25-(OH)(2)D(3)-dependent decreases in both parameters. Melittin had no effect when applied for 24 h and did not modify the 1,25-(OH)(2)D(3) effect; however, when present throughout the culture period, it caused a decrease in proliferation and an increase in enzyme activity. Chelerythrine, the PKC inhibitor, only inhibited cell proliferation when it was present throughout the entire culture period. However, it decreased alkaline phosphatase in cultures treated for 24 h, but increased enzyme activity when it was present for the entire culture period. The results indicate that surface roughness and 1,25-(OH)(2)D(3) both mediate their effects through PLA(2) which catalyzes the rate-limiting step in PGE(2) production. Further downstream, PGE(2) activates PKA. Surface roughness-dependent effects are also mediated through PKC, but only after the cells have reached confluence and are undergoing phenotypic maturation. The effect of surface roughness on responsiveness to 1,25-(OH)(2)D(3) is mediated through PLA(2)/PKA and not through PKC.