Late posterior hip instability after lumbar spinopelvic fusion.

The kinematic relationship between the hip and the axial skeleton is dynamic and can be variable based on individual anatomy. It has been shown [1] that pelvic incidence (sacral slope + pelvic tilt) can be used as a proxy to determine the ability of the pelvis to accommodate changes in sagittal balance. Individuals have varied pelvic incidence and thus may adapt differently degenerative and/or iatrrogenic to changes that occur in the axial spine. This is a case report in which surgical changes to the lumbopelvic spine resulted in chronic posterior periprosthetic hip instability. The focus of this discussion reflects the intimate relationship between the hip and spine and highlights the role between sagittal balance and acetabular version, specifically as it pertains to total hip arthroplasty.

Unicortical PEEK inset locking fixation for metacarpal fractures: a biomechanical study.

PURPOSE: There are numerous constructs employed in the treatment of metacarpal fractures with varying degrees of success. While plate fixation commonly involves dorsal application of a bicortical non-locking plate, there has been recent exploration of other fixation options including unicortical locked plating. The purpose of this study was to evaluate the biomechanical integrity of a polyetheretherketone (PEEK) inset locking plate and, in doing so, compare it to standard plate fixation (utilizing a clinically proven bicortical non-locking titanium plate) in a simulated porcine metacarpal fracture model. METHODS: Reproducible mid-shaft fractures were created in porcine second metacarpals. The fractured specimens were reduced and plated with either a bicortical non-locking plate or a unicortical locking plate with a PEEK locking design. Constructs were then loaded to failure in the same fashion as performed to create the fracture. Peak load was measured as the apex on the load-to-failure deflection curve. Stiffness was calculated as the linear slope on the load-to-failure deflection curve. Data were analyzed via Student's t test. RESULTS: Unicortical locking constructs failed at 344 ± 119 N, while bicortical non-locking constructs were found to fail at 277 ± 101 N (p = 0.19). The unicortical locking constructs demonstrated a stiffness of 80 ± 36 N/mm compared with the bicortical non-locking constructs (69 ± 36 N/mm) although again the difference was not found to be statistically different (p = 0.49). CONCLUSION: Based on this study, a locked plating construct using a polymer mechanism provides an interesting new locking fixation method for small bone fractures and with our limited number of specimens tested, provided at least a similar strength and rigidity profile in comparison with bicortical fixation in the treatment of metacarpal fractures.

Sildenafil (Viagra) attenuates ischemic cardiomyopathy and improves left ventricular function in mice.

We tested the hypothesis that chronic treatment with sildenafil attenuates myocardial infarction (MI)-induced heart failure. Sildenafil has potent protective effects against necrosis and apoptosis following ischemia-reperfusion in the intact heart and cardiomyocytes. ICR mice underwent MI by left anterior descending coronary artery ligation and were treated with sildenafil (0.71 mg/kg bid) or saline for 4 wk. Infarct size (IS) was measured 24 h postinfarction, and apoptosis was measured by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling. Left ventricular end-diastolic diameter (LVEDD) and fractional shortening (FS) were measured by echocardiography. Sildenafil reduced IS (40.0 +/- 4.6%) compared with that in saline (69.6 +/- 4.1%, P < 0.05). NG-nitro-l-arginine methyl ester, a nitric oxide synthase (NOS) inhibitor (15 mg/kg bid), blocked the protective effect of sildenafil (IS, 60.2 +/- 1.6%, P < 0.05 vs. sildenafil). Western blot analysis revealed a significant increase in endothelial NOS/inducible NOS proteins 24 h post-MI after treatment with sildenafil versus saline. Apoptosis decreased from 2.4 +/- 0.3% with saline to 1.2 +/- 0.1% with sildenafil (P < 0.05) on day 7 and from 2.0 +/- 0.2% with saline to 1.2 +/- 0.1% with sildenafil on day 28 (P < 0.05), which was associated with an early increase in the Bcl-2-to-Bax ratio. LVEDD increased from baseline value of 3.6 +/- 0.1 to 5.2 +/- 0.2 and to 5.5 +/- 0.1 mm on days 7 and 28, respectively, with saline (P < 0.05) but was attenuated to 4.4 +/- 0.2 and 4.4 +/- 0.1 mm following sildenafil treatment on days 7 and 28, respectively (P > 0.05 vs. baseline). FS significantly improved post-MI with sildenafil. A marked decline in cardiac hypertrophy was observed with sildenafil, which paralleled a reduction in pulmonary edema. Survival rate was lower with saline (36%) compared with sildenafil (93%, P < 0.05). Sildenafil attenuates ischemic cardiomyopathy in mice by limiting necrosis and apoptosis and by preserving left ventricular function possibly through a nitric oxide-dependent pathway.