Prognostic Factors in Open Triangular Fibrocartilage Complex (TFCC) Repair

Purpose: Patients with triangular fibrocartilage complex (TFCC) injury report ulnar-sided wrist pain and impaired function. Open TFCC repair aims to improve the condition of these patients. Patients have shown reduction in pain and improvement in function at 12 months after surgery; however, results are highly variable. The purpose of this study was to relate patient (eg, age and sex), disease (eg, trauma history and arthroscopic findings), and surgery factors (type of bone anchor) associated with pain and functional outcomes at 12 months after surgery. Methods: This study included patients who underwent an open TFCC repair between December 2011 and December 2018 in various Xpert Clinics in the Netherlands. All patients were asked to complete Patient-Rated Wrist Evaluation (PRWE) questionnaires at baseline as well as at 12 months after surgery. Patient, disease, and surgery factors were extracted from digital patient records. All factors were analyzed by performing a multivariable hierarchical linear regression. Results: We included 274 patients who had received open TFCC repair and completed PRWE questionnaires. Every extra month of symptoms before surgery was correlated with an increase of 0.14 points on the PRWE total score at 12 months after surgery. In addition, an increase of 0.28 points in the PRWE total score at 12 months was seen per extra point of PRWE total score at baseline. Conclusions: Increased preoperative pain, less preoperative function, and a longer duration of complaints are factors that were associated with more pain and less function at 12 months after open surgery for TFCC. This study arms surgeons with data to predict outcomes for patients undergoing open TFCC repair. Type of study/level of evidence: Prognostic II.</p

Factors associated with return to work after open reinsertion of the triangular fibrocartilage

The aim of this study was to assess return to work (RTW) after open Triangular Fibrocartilage Complex (TFCC) reinsertion. RTW after open surgery for TFCC injury was assessed by questionnaires at 6 weeks, 3 months, 6 months, and 12 months post-operatively. Median RTW time was assessed on inverted Kaplan–Meier curves and hazard ratios were calculated with Cox regression models. 310 patients with a mean age of 38 years were included. By 1 year, 91% of the patients had returned to work, at a median 12 weeks (25%–75%: 6–20 weeks). Light physical labor (HR 3.74) was associated with RTW within the first 15 weeks; this association altered from 23 weeks onward: light (HR 0.59) or moderate physical labor (HR 0.25) was associated with lower RTW rates. Patients with poorer preoperative Patient-Rated Wrist Evaluation (PRWE) total score returned to work later (HR 0.91 per 10 points). Overall cost of loss of productivity per patient was €13,588. In the first year after open TFCC reinsertion, 91% of the patients returned to work, including 50% within 12 weeks. Factors associated with RTW were age, gender, work intensity, and PRWE score at baseline

Multi-ancestry genome-wide study identifies effector genes and druggable pathways for coronary artery calcification

Coronary artery calcification (CAC), a measure of subclinical atherosclerosis, predicts future symptomatic coronary artery disease (CAD). Identifying genetic risk factors for CAC may point to new therapeutic avenues for prevention. Currently, there are only four known risk loci for CAC identified from genome-wide association studies (GWAS) in the general population. Here we conducted the largest multi-ancestry GWAS meta-analysis of CAC to date, which comprised 26,909 individuals of European ancestry and 8,867 individuals of African ancestry. We identified 11 independent risk loci, of which eight were new for CAC and five had not been reported for CAD. These new CAC loci are related to bone mineralization, phosphate catabolism and hormone metabolic pathways. Several new loci harbor candidate causal genes supported by multiple lines of functional evidence and are regulators of smooth muscle cell-mediated calcification ex vivo and in vitro. Together, these findings help refine the genetic architecture of CAC and extend our understanding of the biological and potential druggable pathways underlying CAC.</p