Impact of size mismatch and left ventricular function on performance of the St. Jude disc valve after aortic valve replacement

BACKGROUND: The hemodynamic function of the St. Jude valve may change relative to changes in left ventricular function after aortic valve replacement for aortic stenosis. From theoretical reasons one may hypothesize that prosthetic valve hemodynamic function is related to left ventricular failure and mismatch between valve size and patient/ventricular chamber size. METHODS: Forty patients aged 24 to 82 years who survived aortic valve replacement for aortic stenosis with a standard St. Jude disc valve (mean size, 23.5 mm; range, 19 to 29 mm) were followed up prospectively with Doppler echocardiography and radionuclide left ventriculography preoperatively and 9 days, 3 months, and 18 months after the operation with assessment of intravascular hemolysis at 18 months. Follow-up to a maximum of 7.4 years (mean, 6.3 years) was 100% complete. RESULTS: Left ventricular muscle mass index decreased from 198 +/- 62 g.m-2 preoperatively to 153 +/- 53 g.m-2 at 18 months (p < 0.001), paralleled by a significant increase in left ventricular ejection fraction, peak ejection rate, and peak filling rate; only 18% of the patients had normal left ventricular muscle mass index and only 32% normal ventricular function (normal left ventricular ejection fraction, peak ejection rate, peak filling rate, early filling fraction, and late filling fraction during atrial contraction) at 18 months. Prosthetic valve peak Doppler gradient dropped from 20 +/- 6 mm Hg at 9 days to 17 +/- 5 mm Hg at 18 months (p < 0.05). Reduction of left ventricular muscle mass index was unrelated to peak gradient and size of the valve. Peak gradient at 18 months rose with valve orifice diameter of 17 mm or less (by 6 mm Hg), orifice diameter/body surface area of 9 mm.m-2 or less (by 5 mm Hg), left ventricular enddiastolic dimension (by 23 mm Hg per 10 mm increase), and impaired ventricular function (by 3 mm Hg). All but 2 patients (5%) had intravascular hemolysis; none had anemia. Two patients with moderate paravalvular leak had the highest serum lactic dehydrogenase levels; 4 patients with trivial leak had higher serum lactic dehydrogenase levels than those without leak. Serum lactic dehydrogenase levels rose with moderate paravalvular leak, impaired ventricular function, and valve orifice diameter. Six patients with trivial or moderate paravalvular leak had a cumulative 7-year freedom from bleeding and thromboembolism of 44% +/- 22% compared with 87% +/- 5% for those without leak (p < 0.05). CONCLUSIONS: The peak gradient of the St. Jude aortic valve dropped marginally over the first 18 postoperative months in association with incomplete left ventricular hypertrophy regression and marginal improvement of ventricular function. Mismatch between valve size and ventricular cavity size or patient size and impaired function of a dilated ventricle significantly compromised the performance of the St. Jude valve. Probably explained by platelet destruction or activation, paravalvular leak was related to bleeding and thromboembolic complications.     

Increased serum IgD concentrations in children with Henoch-Sch?nlein purpura

Serum IgD concentrations were measured in 39 children with Henoch Schonlein purpura (HSP) and 40 control children by means of radial immunodiffusion. Serum IgG, IgA and IgM concentrations in the HSP patients were measured by nephelometry. The geometric mean IgD concentration in children with HSP (16.7 microg/ml) was significantly higher than in control children (9.1 microg/ml; P=0.03). Serial testing in 10 HSP patients revealed no significant change in IgD concentrations over periods ranging from 1 to 12 months. There was no relationship between IgD and IgA concentrations in the HSP patients. Nineteen of the 39 HSP patients (49%) had nephritis. The mean IgD concentration in patients with nephritis (10.7 microg/ml) did not differ from control values, but was significantly lower than the mean IgD level in the remaining 20 patients who did not have nephritis (25.4 microg/ml; P=0.02). These results indicate that serum IgD levels are increased in children with HSP who did not have nephritis. IgD concentrations in patients with nephritis were similar to levels in control children.     

Ultrastructural analyses of the attachment (bonding) zone between bone and implanted biomaterials

This report presents transmission electron and high voltage transmission electron microscopic observations of bone and associated remodeling tissues directly interfacing with endosteal dental implants. Undecalcified interfacial tissues were serially sectioned from mandibular samples encasing 60 implants placed into 30 dogs. Two-dimensional ultrastructural analyses and three-dimensional stereology showed that osteogenesis adjacent to dental implants is a dynamic interaction of osseous cells and a collagenous fiber matrix. This study showed that the interfacial bone consists of a mineralized collagen fiber matrix associated with an inorganic (hydroxylapatite) matrix. This study suggested that an unmineralized collagen fiber matrix initially is laid down directly at the implant surface, and that this matrix then is mineralized. Osteoblasts interacted with this matrix, eventually becoming encased within developing lacunae during the remodeling process. This process formed the cellular (osteocyte) aspects of the developed bone. Osteocyte processes extended through canaliculi directly to the implant surface. Apparently, these processes also were entrapped within canaliculi during the mineralization events. At times, these processes paralleled the implant surface. The bone-implant interfacial zone was primarily fibrillar (both mineralized and unmineralized) in morphology, with an electron-dense, ruthenium positive deposition. This electron-dense material was approximately 20 to 50 nanometers in thickness, and only this thin layer separated the remodeled mineralized bone from the implant.     

For patients with Dukes'' B (TNM Stage II) colorectal carcinoma, examination of six or fewer lymph nodes is related to poor prognosis

Pulse sequences based on FID signals and projection reconstruction (PR) were investigated for lung MRI at 0.5 T and evaluated for artifacts caused by: (1) k-space mismapping due to either delay or distortion of the readout gradient waveform, (2) cardiac motion and pulsatile flow, and (3) respiratory motion. Nonstructured artifacts were described, simulated, and experimentally confirmed for the first time. Nonstructured artifacts did not impair the demonstration of structures of high signal-to-noise ratio (SNR) but generated quantitative errors in the image intensity analysis over the lung parenchyma. The use of FID-based PR techniques for lung MRI is not justified at 0.5 T.