Aneurysm of the mitral valve occurs most commonly in association with infective endocarditis of the aortic valve. The probable mechanism of its formation is destruction of the aortic valve which results in a regurgitant jet that strikes the anterior leaflet of the mitral valve, creating a secondary site of infection leading to the development of an aneurysm. Perforation of these aneurysms may occur, resulting in mitral regurgitation and pulmonary edema from a ventricle already volume overloaded from aortic regurgitation. This report describes the clinical and echocardiographic-pathologic findings in five patients with pathologically proven aneurysm of the mitral valve. There are no clinical features that appear specific for this abnormality. The two-dimensional echocardiographic feature that is helpful in the diagnosis is a bulge of the mitral valve leaflet toward the left atrium that persists throughout the cardiac cycle. Preoperative diagnosis is important because a mitral valve aneurysm may produce serious complications and is frequently overlooked during surgery. Repair of the aneurysm may be feasible; otherwise, valve replacement becomes necessary. Careful two-dimensional echocardiographic examination should be done in patients with left-sided infective endocarditis to detect an aneurysm of the mitral valve.
A Bayesian method for monitoring vancomycin concentrations and adjusting regimens in patients with unstable renal function by using a two-compartment population model was evaluated with a personal computer. The population model was derived from data from 12 cardiac outpatients who received single doses of vancomycin. The performance of the method was then tested in 27 acutely ill patients who received multiple doses of vancomycin. Significant renal impairment was observed in 15 patients. Renal function changed in 15 patients. The vancomycin concentrations in the patients with changing renal function were not at steady state during the observation times. Two concentrations in serum (peak and then trough, or trough and then peak) were fitted along with the population model to individualize the parameter values for each patient. All the subsequent concentrations in serum for each patient were then predicted by using the parameter values for each patient. Future concentrations of 118 serum samples were predicted. The mean absolute prediction error was 3.6 ± 4.5 ,Lg/ml, and the mean prediction error was -0.7 ± 5.3 ,Ig/ml. These results confirm that a two-compartment pharmacokinetic model can be sufficiently individualized with the knowledge of just two concentrations of drug in patient serum; it is possible to predict closely subsequent concentrations in serum, and dosing regimens for individual patients can be well adjusted to achieve the chosen therapeutic goals.Three favorable characteristics of vancomycin are the bactericidal effect, the sustained concentrations in serum achieved compared with those achieved with beta-lactam antibiotics, and the rare development of bacterial resistance (4). These traits, along with the current rise in methicillinresistant staphylococcal infections and the increasing use of prosthetic devices requiring antibiotic prophylaxis (1), have stimulated new interest in vancomycin use. In addition, the availability of more precise methods of measuring vancomycin concentrations in serum and the availability of sophisticated computer software for analyzing drug concentrationin-serum data (7, 14) now make it possible to individualize vancomycin dosage regimens that are more clinically effective, safe, and cost-effective. These factors have led to a growing demand to monitor vancomycin therapy and to interpret the meaning of its concentrations in serum.The (2,4,11,17,18,21). The controversy stems from the fact that the concentration-time profile of vancomycin in serum is not described by a monoexponential decay, as reflected by the one-compartment pharmacokinetic model used in many earlier clinical studies (3,10,18). At least two compartments are required to describe vancomycin pharmacokinetics adequately: a central serum compartment and a peripheral compartment (nonserum) (5,13,16
Thrombus formation and tissue overgrowth were observed in nine Björk-Shiley aortic prostheses recovered six months or longer after implantation. These pathologic findings may be attributed to the flow characteristics of the prosthesis. The open disc of the valve separates the flow into two unequal regions. Varying degrees of thrombus formation were observed in the minor outflow region, including the depression in the aortic face of the disc and the metal strut bridging this area. Tissue overgrowth was noted along the perimeter of the prosthesis adjacent to the minor outflow region. That overgrowth further reduced the available cross section for flow in this already constrained area. In vitro velocity measurements with a laser-Doppler anemometer identified a zone of stagnation about 20 mm wide near the aortic face of the disc. The average velocities in the major and minor outflow regions were around 100 and 25 cm/sec, respectively, and the corresponding peak-shear stresses were approximately 700 and 150 dynes/cm2. There is reason, then, to attribute the thrombus formation and tissue overgrowth to the stagnation zone and the low shear in the minor outflow region.
The flow downstream from the St Jude valve prosthesis is studied in vitro in both steady and pulsatile flow. Conditions for the pulsatile flow studies approximate the in vivo resting state. Laser-Doppler anemometry (LDA) is used to measure instantaneous point velocities at numerous locations pre-selected to conform to a systematic, flow-mapping measurement methodology. Overall, the results for the St Jude valve indicate a relatively undisturbed forward flow through the prosthesis. The acceleration ratios, defined as the maximum mean axial velocity for the St Jude valve divided by that for no valve obstructing the flow, are small, being 1.2 and 1.4 for steady and pulsatile flow, respectively. Both the secondary flow structure and the flow disturbance produced by this valve are minimal. Maximum mean velocities in the radial and azimuthal directions are only about 5-10 per cent of that in the axial direction. There is. however, notable evidence of flow wakes generated by the valve's opened leaflets. Velocity defects caused by these wakes are found to be as much as 50 per cent. The bulk flow through this valve is in this sense quite unlike that reported by others for the natural aortic valve studied in vitro.
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