Valid and reliable animal models are essential for mechanistic and therapeutic studies of traumatic brain injury (TBI). Therefore, model characterization is a continual and reciprocal process between the experimental laboratory and the clinic. Several excellent experimental models of TBI, including the lateral fluid percussion rat model, are currently in wide use in many neurotrauma laboratories. However, small differences in the position of lateral fluid percussion craniectomy are reported between labs. Additionally, differences in hippocampal cell death have also been reported. Therefore, we hypothesized that small changes in craniectomy position could affect commonly used outcome measures such as vestibulomotor function, Morris water maze (MWM) performance, hippocampal cell loss, and glial fibrillary acidic protein (GFAP) immunoreactivity. Four placements were systematically manipulated: rostral, caudal, medial, and lateral. The medial and caudal placements produced significantly greater impairments in the MWM acquisition task over the lateral and rostral placements. The rostral placement produced diffuse cortical damage but little hippocampal cell loss. In contrast, the medial, lateral, and caudal placements produced more mid-dorsally localized cortical damage and significant cell loss in the CA2/CA3 and hilus ipsilateral to the injury site. Furthermore, reactive astrocytosis was more pronounced in the medial, lateral, and caudal placements than in the rostral placement. All craniectomy position groups had similar durations of traumatic unconsciousness and similar impairment on motor tasks. We conclude that small alterations in craniectomy position produce differences in cognitive performance, hippocampal cell loss, and reactive astrocytosis but not in motor performance nor transient unconsciousness.

We conducted a retrospective analysis of 423 consecutive patients who received an implantable cardioverter defibrillator (ICD) with © 2013 American Heart Association, Inc. and January 19, 2007. A retrospective analysis was performed to evaluate the relationship between post-CRT-D LVEF and ICD therapy for ventricular tachyarrhythmias. A landmark population of 270 patients, with post-CRT-D LVEF measured and no ICD therapy within 1 year of device implantation, was followed for subsequent outcomes. Of these, 22 patients (8.2%) had subsequent appropriate ICD therapy over a median follow-up of 1.5 years. The estimated 2-year risk of appropriate ICD therapy is 3.0% (95% confidence interval [95% CI], 0%-6.3%), 2.1% (95% CI, 0%-5.0%), and 1.5% (95% CI, 0%-3.9%) for post-CRT-D LVEF of 45%, 50%, and 55%, respectively. In patients with a primary prevention indication for CRT-D, the estimated 2-year risk is 3.3% (95% CI, 0%-7.3%), 2.5% (95% CI, 0%-6.1%), and 1.9% (95% CI, 0%-5.1%) for post-CRT-D LVEF of 45%, 50%, and 55%, respectively. Conclusions-When a CRT responder demonstrates near normalization in LVEF to ≥45%, the incidence of ICD therapy for ventricular arrhythmias becomes low. Future studies are needed to determine whether an ICD is still needed in some of these patients at the time of generator replacement. (Circ Arrhythm Electrophysiol. 2013;6:257-264.) Circ Arrhythm Electrophysiol

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