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A randomized prospective trial was undertaken to compare the hemodynamic performance and left ventricular regression after aortic valve replacement with the Toronto SPV stentless bioprosthesis and the Carpentier Edwards SAV (CE) bioprosthesis. Forty patients were randomized after the annular and sinotubular diameters had been measured. Early hemodynamic measurements were made with a thermodilution cardiac output catheter, and echocardiography was used thereafter. Left ventricular mass was assessed using magnetic resonance imaging (MRI) at 1 week, 6 months, and 32 months. The mean annular size was 25.3+/-2.2 mm (CE) and 25.5+/-1.5 mm (Toronto), although it was possible to implant valves with a mean diameter 3 mm larger in the stentless group (26.0+/-1.7 mm cf. 23.0+/-1.7 mm). Hemodynamic performance in the first 24 hours showed no significant difference between the groups, but there was a trend for shorter ventilation time and shorter stays in the intensive therapy unit in the stentless group. Echocardiography showed superior transvalvular gradients in the stentless group at 1 week (mean 5.5+/-3.1 mm Hg cf. 8.9+/-2.5 mm Hg), and this difference was maintained at a mean follow-up time of 32 months (3.5+/-0.6 mm Hg cf. 6.3+/-0.6 mm Hg). Similar regression of left ventricular mass was seen in both groups at 6 months, but at 32 months, measurement in diastole showed a reduction of 38% (P<.01) in the stentless group compared with 20% (P = ns) in the stented group, and measurements in systole showed a 23% (P<.01) and 13% (P = ns) reduction, respectively. This study confirms that a larger stentless valve can be implanted into a given size of aortic annulus with superior residual aortic valve gradients. These lower gradients seem to result in improved long-term regression of left ventricular mass as measured by MRI.

Tumor development and progression in the nervous system are poorly understood. Consequently, even though there seems to be little possibility of major advances in existing clinical modalities used to treat malignant brain tumors, no targeted molecular therapies have risen to take their place. The variability and plasticity of brain neoplasms make them an illusive target for study and therapeutic intervention. Further complicated by infiltration of vital nervous tissue, clinical studies have serious practical limitations and the ability to assess tumor progression in vivo is still a developing technology. Evaluation of potential new therapies for brain tumors is heavily dependent on the development of more informative and cognate experimental models. To develop and validate new models, it is particularly important to integrate clinical, pathological, and cell biological characterizations of malignant brain tumors. This discussion provides an overview of developments in tumor cell culture and the impact of animal models on brain tumor research. Studies of malignant glial neoplasms associated with a dismal prognosis in patients receive particular attention.