Metal Artifact Reduction MRI in the Diagnosis of Periprosthetic Hip Joint Infection.

A 54-year-old woman presented with progressive right hip pain after hip arthroplasty 9 years earlier. The emerging role of metal artifact reduction MRI in the noninvasive diagnosis of infectious synovitis as the surrogate marker for periprosthetic hip joint infection and differentiation from other synovitis types is discussed.

Long-Term Characterization of Cranial Defects After Surgical Correction for Single-Suture Craniosynostosis.

INTRODUCTION: Craniosynostosis is typically corrected surgically within the first year of life through cranial vault reconstruction. These procedures often leave open calvarial defects at the time of surgery, which are anticipated to close over time in a large proportion of cases. However, residual calvarial defects may result as long-term sequelae from cranial vault remodeling. When larger defects are present, they may necessitate further reconstruction for closure.Better understanding of the calvarial osseous healing process may help to identify which defects will resolve or shrink to acceptable size and which will require further surgery. Our study aims to assess the long-term changes in defect size after cranial vault reconstruction for craniosynostosis. METHODS: One-year postoperative and long-term computed tomography scans were retrieved from the craniofacial anomalies archive. Analysis used custom software. All defects above the size of 1 cm were analyzed and tracked for calvarial location, surface area, and circularity. Monte Carlo simulation was performed to model the effect of initial defect size on the rate of defect closure. RESULTS: We analyzed a total of 74 defects. The mean ± SD initial defect surface area was 3.27 ± 3.40 cm. The mean ± SD final defect surface area was 1.71 ± 2.54 cm. The mean ± SD percent decrease was 55.06% ± 28.99%. There was a significant difference in the percentage decrease of defects in the parietal and frontoparietal locations: 68.4% and 43.7%, respectively (P = 0.001). Monte Carlo simulation results suggest that less than 10% of defects above the size of 9 cm will close to the size of 2.5 cm or less. CONCLUSIONS: We describe and make available a novel validated method of measuring cranial defects. We find that the large majority of initial defects greater than 9 cm remain at least 1 in in size (2.5 cm) 1 year postoperatively. In addition, there appear to be regional differences in closure rates across the cranium, with frontoparietal defects closing more slowly than those in the parietal region. This information will aid surgeons in the decision-making process regarding cranioplasty after craniosynostosis correction.

Number of P-wave fragmentations on P-SAECG correlates with infiltrated atrial fat.

BACKGROUND: Although atrial fibrillation (AF) triggers are known, the underlying AF substrate is less well understood. The goal of our study was to explore correlations between electrophysiological and structural characteristics of atria in patients with paroxysmal AF and individuals at AF risk. METHODS: Patients in sinus rhythm (N = 90; age 57 ± 10 year; 55 men [63.2%]) with structural heart disease and paroxysmal AF (n = 12 [13%]), or with AF risk factors and LVEF > 35% (n = 78), underwent SAECG and cardiac magnetic resonance study. Interatrial and epicardial fat was analyzed with a Dark-blood DIR-prepared Fat-Water-separated sequence in the horizontal longitudinal axis. All local P-wave extrema were identified on SAECG leads during sinus rhythm. A P-wave fragmentation (Pf) was defined as an absolute difference between adjacent extrema which was above three standard deviations of noise, and was normalized by the duration of the P wave in the corresponding lead. RESULTS: The Pf was greater on the filtered than on the unfiltered P-SAECG signal (13.1 ± 3.8 vs. 3.4 ± 1.2; P < 0.0001). Pf was the greatest on the Y lead (13.0 ± 3.5 on Y lead vs. 12.1 ± 3.4 on Z lead; P = 0.003. Pf on Z lead correlated with interatrial fat index (r = 0.544; P = 0.001). Epicardial fat significantly correlated with body mass index (BMI; r = 0.302; P = 0.015). After adjustment for BMI, left atrium (LA) size, epicardial fat, and interatrial septum width, interatrial fat independently associated with the Pf on Z lead (ß-coefficient 0.009 [95%CI 0.0003-0.019]; P = 0.043). CONCLUSIONS: Infiltrated atrial fat correlates with discontinuous conduction on posterior LA wall and represents AF early substrate.

Infiltrated atrial fat characterizes underlying atrial fibrillation substrate in patients at risk as defined by the ARIC atrial fibrillation risk score.

BACKGROUND: It is known that expanded epicardial fat is associated with atrial fibrillation (AF). However, infiltrated intraatrial fat has not been previously quantified in individuals at risk as determined by the ARIC AF risk score. METHODS: Patients in sinus rhythm (N=90, age 57 ± 10 years; 55 men [63.2%]), in 3 groups at risk of AF as determined by the ARIC AF risk score [low (≤ 11 points; n=15), moderate (12-18 points; n=40), high (≥ 19 points; n=23) risk of AF], and paroxysmal AF (n=12) underwent cardiac magnetic resonance study. Intraatrial and epicardial fat was analyzed with a Dark-blood DIR-prepared Fat-Water-separated sequence in the horizontal longitudinal axis. OsiriX DICOM viewer (Geneva, Switzerland) was used to quantify the intraatrial fat area. Width of the cephalad portion of the interatrial septum was measured at the level of the fossa ovalis. RESULTS: Intraatrial fat monotonically increased with growing AF risk in study groups (low AF risk 16 ± 4 vs. moderate AF risk 32 ± 18 vs. high AF risk 81 ± 83 mm(2); ANOVA P=0.012). Log-transformed intraatrial fat predicted ARIC AF risk score in multivariate ordered probit regression after adjustment for sex, race, left and right atrial area indices, and body mass index (ß-coefficient 0.50 [95% CI 0.03-0.97]; P=0.037), whereas epicardial fat did not. Interatrial septum width showed similar association (3.0 ± 1.4 vs. 5.0 ± 1.8 vs. 7.1 ± 2.7 mm; ANOVA P<0.001; adjusted ß-coefficient 2.80 [95% CI 1.19-4.41]; P=0.001). CONCLUSIONS: Infiltrated intraatrial fat characterizes evolving substrate in individuals at risk of AF.