18F-sodium fluoride uptake is a marker of active calcification and disease progression in patients with aortic stenosis.

BACKGROUND: 18F-Sodium fluoride (18F-NaF) and 18F-fluorodeoxyglucose (18F-FDG) are promising novel biomarkers of disease activity in aortic stenosis. We compared 18F-NaF and 18F-FDG uptake with histological characterization of the aortic valve and assessed whether they predicted disease progression. METHODS AND RESULTS: Thirty patients with aortic stenosis underwent combined positron emission and computed tomography using 18F-NaF and 18F-FDG radiotracers. In 12 patients undergoing aortic valve replacement surgery (10 for each tracer), radiotracer uptake (mean tissue/ BACKGROUND: =0.65; P=0.04) and osteocalcin (r=0.68; P=0.03) immunohistochemistry. There was no significant correlation between 18F-FDG uptake and CD68 staining (r=-0.43; P=0.22). After 1 year, aortic valve calcification increased from 314 (193-540) to 365 (207-934) AU (P<0.01). Baseline 18F-NaF uptake correlated closely with the change in calcium score (r=0.66; P<0.01), and this improved further (r=0.75; P<0.01) when 18F-NaF uptake overlying computed tomography-defined macrocalcification was excluded. No significant correlation was noted between valvular 18F-FDG uptake and change in calcium score (r=-0.11; P=0.66). CONCLUSIONS: 18F-NaF uptake identifies active tissue calcification and predicts disease progression in patients with calcific aortic stenosis. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01358513.

Anterior shoulder instability associated with coracoid nonunion in patients with a seizure disorder.

BACKGROUND: An association between coracoid fracture and glenohumeral instability with both a seizure disorder and the subsequent development of coracoid nonunion has not previously been recognized. This is clinically important as patients with a seizure disorder and glenohumeral instability frequently require a primary osseous reconstructive procedure, such as coracoid osteotomy and transfer to the anterior glenoid rim (the Bristow-Latarjet procedure), to address glenoid osseous deficiency. We report on coracoid fracture nonunion in five patients with a seizure disorder and anterior glenohumeral instability and discuss the implications for surgical treatment. METHODS: Coracoid fracture was specifically sought on three-dimensional reconstructions of computed tomography scans in a consecutive series of 234 patients presenting to our unit with recurrent anterior instability. In addition to demographic data, we specifically sought information on any history of shoulder injury, the mechanism of injury, or previous seizure activity in these patients. In patients with a coracoid fracture or nonunion viewed to be at high risk of failure with a soft-tissue procedure, an open osseous reconstructive procedure was performed. The type of operative procedure was determined by the location of the nonunion. RESULTS: We identified six coracoid fracture nonunions in association with anterior glenohumeral instability in five patients (mean age, 26.8 years; range, twenty-four to thirty years). All patients had instability occurring in association with seizures. In the four shoulders with the anatomic location of the coracoid nonunion at its so-called elbow, a standard Bristow-Latarjet procedure was performed. In the two shoulders in which the nonunion was more distal, an Eden-Hybbinette procedure was performed. CONCLUSIONS: We recommend having a high index of suspicion of coracoid fracture when treating patients with a seizure disorder who have anterior glenohumeral instability. In these patients, preoperative computed tomographic images allow the diagnosis of a coracoid nonunion to be made prior to surgery and help to determine whether there is sufficient intact coracoid bone to allow a Bristow-Latarjet procedure to be performed.