Vertebral body tethering compared to posterior spinal fusion for skeletally immature adolescent idiopathic scoliosis patients: preliminary results from a matched case-control study.

PURPOSE: Direct comparisons between vertebral body tethering (VBT) and posterior spinal fusion (PSF) for adolescent idiopathic scoliosis (AIS) are limited. We aimed to evaluate 2-year results of VBT and PSF to report comparative outcomes. METHODS: 26 prospectively enrolled VBT patients were matched 1:1 by age, gender, Risser sign and major curve magnitude with PSF patients. At a minimum 2-year follow-up, surgical results and radiographic outcomes were reviewed. RESULTS: Operative time, anesthesia time, blood loss, and length of stay were significantly lower in the VBT group (< 0.001, p = 0.003, p < 0.001, p < 0.001, respectively). The major curve at 2 years was corrected by 46% in the VBT group vs. 66% in the PSF (p = 0.0004). Success following VBT, defined as no fusion surgery and Cobb angle < 35° at the 2-year follow-up, was seen in 20 VBT patients (77%) (p = 0.0003) and correlated with mean Cobb angle of < 35° on 3-month imaging. 12 VBT patients (46%) showed curve improvement over time, and those patients had significantly lower mean Cobb angle on the 3-month radiograph than non-modulators (23° vs 31°, p = 0.014). At 2 years, cord breakage occurred in five patients (19%). By 2 years, three VBT patients developed complications (2 pleural effusion and 1 overcorrection needing return to OR). In contrast to PSF, growth continued at T1-T12 (mean 13 mm) and over the instrumented levels (mean 10 mm) following VBT, compared to no growth over instrumented segments in the fusion cohort (p = 0.011, p = 0.0001). CONCLUSION: In Sanders stages 3 and 4 patients treated in the USA, Cobb angle < 35° on 3-month imaging was associated with success at the 2-year follow-up. Curve correction was superior in the PSF group with 96% achieving curve correction to < 35° vs. 77% of the VBT patients. Cord breakage was noted in 19% of VBT patients at the 2-year follow-up. Three patients developed complications in both the VBT and PSF cohorts. LEVEL OF EVIDENCE: Level II (prospective study with matched retrospective comparison group).

Management of Isolated, Congenital Anterior Mitral Valve Cleft.

Background: Isolated anterior mitral valve clefts (MVC) are rare congenital heart defects, and data are limited regarding the natural history and surgical outcomes for such isolated MVCs. Methods: We conducted a retrospective review of patients with congenital MVC who were evaluated at Mayo Clinic in Rochester, Minnesota between 1993 and 2020. Patients were separated into two cohorts: those who underwent surgical repair of the MVC and those who had not yet undergone repair. Baseline and postoperative clinical and echocardiographic data were analyzed. Results: Fourteen patients were included in the nonsurgical cohort and eight patients in the surgical cohort. Surgical repair was via primary median sternotomy (n = 6) or robot-assisted, minimally invasive (n = 2). All cleft repairs were performed by simple suture closure. Intraoperative evaluation of the clefts did not reveal additional structural factors that could account for the mitral regurgitation (MR). At latest follow-up of the surgical cohort, the median grade of MR was 1 (range 0-1), and median left ventricular ejection fraction was 65% (IQR 59%-67%), both similar to the immediate postoperative result. At latest follow-up, all patients in the nonsurgical cohort were NYHA Class 1, and median MR grade was 1. All patients were asymptomatic (NYHA Class 1). Conclusions: Our findings corroborate prior reports that MVC repair is safe and successful and is followed by a low rate of recurrent mitral valve dysfunction. Durable surgical repair of isolated, congenital MVC can be performed safely in select patients. The decision to intervene should be based on the severity of mitral regurgitation and patient symptoms rather than the presence of the MVC alone.

Pyridine-pyrimidine amides that prevent HGF-induced epithelial scattering by two distinct mechanisms.

Stimulation of cultured epithelial cells with scatter factor/hepatocyte growth factor (HGF) results in individual cells detaching and assuming a migratory and invasive phenotype. Epithelial scattering recapitulates cancer progression and studies have implicated HGF signaling as a driver of cancer metastasis. Inhibitors of HGF signaling have been proposed to act as anti-cancer agents. We previously screened a small molecule library for compounds that block HGF-induced epithelial scattering. Most hits identified in this screen exhibit anti-mitotic properties. Here we assess the biological mechanism of a compound that blocks HGF-induced scattering with limited anti-mitotic activity. Analogs of this compound have one of two distinct activities: inhibiting either cell migration or cell proliferation with cell cycle arrest in G2/M. Each activity bears unique structure-activity relationships. The mechanism of action of anti-mitotic compounds is by inhibition of microtubule polymerization; these compounds entropically and enthalpically bind tubulin in the colchicine binding site, generating a conformational change in the tubulin dimer.