Carter, Rickey E

Objectives The aim of this study was to investigate the impact on metal artifacts and dose efficiency of using a tin filter in combination with high-energy threshold (TH) images of a photon-counting detector (PCD) computed tomography (CT) system. Materials and Methods A 3D-printed spine with pedicle screws was scanned on a PCD-CT system with and without tin filtration. Image noise and severity of artifacts were measured for low-energy threshold (TL) and TH images. In a prospective, institutional review board–approved, Health Insurance Portability and Accountability Act-compliant study, 20 patients having a clinical energy-integrating detector (EID) CT were scanned on a PCD-CT system using tin filtration. Images were reviewed by 3 radiologists to evaluate visualization of anatomic structures, diagnostic confidence, and image preference. Artifact severity and image noise were measured. Wilcoxon signed rank was used to test differences between PCD-CT TH and EID-CT images. Results Phantom TH images with tin filtration reduced metal artifacts and had comparable noise (32 HU) to TL images (29 HU) acquired without tin filtration. Visualization scores for the cortex, trabeculae, and implant-trabecular interface from PCD-CT TH images (4.4 ± 0.9, 4.4 ± 1.0, and 4.4 ± 1.0) were significantly higher (P < 0.0001) than EID-CT images (3.3 ± 1.3, 3.3 ± 1.2, and 3.3 ± 1.6). A strong preference was shown for PCD-CT TH images due to improved diagnostic confidence and decreased artifact severity. Noise in PCD-CT TH images (93 ± 41 HU) was significantly lower than that in EID-CT images (133 ± 92 HU, P < 0.05). Conclusions Threshold high images acquired with tin filtration on PCD-CT demonstrated a substantial decrease in metal artifacts and an increase in dose efficiency compared with EID-CT.

Objective: To evaluate the effect of hepatic steatosis on LI-RADS® major features at MRI in patients with non-alcoholic fatty liver disease (NAFLD)-associated hepatocellular carcinoma (HCC). Methods: HCC and liver parenchyma features at MRI from 48 consecutive patients with NAFLD and histology proven HCC (mean ± SD; 4.5 ± 3.4 cm) were independently reviewed by three radiologists. Inter-rater agreement was determined by prevalence/bias-adjusted kappa. Hepatic fat signal fraction (FS%) was independently calculated. HCC features were compared by FS% at MRI using logistic regression analysis and histologic steatosis grade using Cochran-Armitage test for trend, stratified by cirrhotic liver morphology or histologic fibrosis stage. Receiver operating characteristic curves were generated to determine the sensitivity and specificity for major HCC features by FS%. Results: Major HCC features included arterial phase hyperenhancement (APHE) in 45 (93%), portal venous phase washout (PVWO) in 30 (63%), delayed phase washout (DPWO) in 38 (79%) and enhancing “capsule” in 34 (71%). Cirrhotic morphology was present in 22 (46%). Inter-rater agreement was 0.75 for APHE, 0.42–0.58 for PVWO, 0.58–0.71 for DPWO and 0.38–0.67 for enhancing “capsule”. There was an 18%, 14% and 22% increase in the odds of absent PVWO, DPWO and capsule appearance for every 1% increase in hepatic FS% in patients with non-cirrhotic liver morphology (p = 0.011, 0.040 and 0.029, respectively). Hepatic FS% ≥ 14.8% had a sensitivity and specificity of 64 and 100% for absent PVWO and 71 and 90% for absent DPWO in patients with non-cirrhotic liver morphology. Conclusion: Absent washout and capsule appearance are associated with increasing hepatic steatosis in patients with non-cirrhotic, NAFLD-associated HCC. Advances in knowledge: In patients with non-cirrhotic, non-alcoholic fatty liver disease (NAFLD)-associated hepatocellular carcinoma (HCC), absent HCC washout and capsule appearance are associated with increasing hepatic steatosis, thereby potentially impacting the noninvasive imaging diagnosis of HCC in these patients. Lack of washout or capsule appearance in steatotic livers at MRI may require alternative criteria for the diagnosis of HCC in patients with non-cirrhotic NAFLD.

Purpose: The aim of this study was to evaluate the ability of computer-aided detection (CAD) and human readers to detect pulmonary nodules ≥5 mm using 100 kV ultra–low-dose computed tomography (ULDCT) utilizing a tin filter. Materials and Methods: After informed consent, 55 patients prospectively underwent standard-dose chest CT (SDCT) using 120 kV followed by ULDCT using 100 kV/tin. Reference nodules ≥5 mm were identified by a thoracic radiologist using SDCT. Four thoracic radiologists marked detected nodules on SDCT and ULDCT examinations using a dedicated computer workstation. After a 6-month memory extinction, readers were shown the same ULDCT cases with all CAD markings as well as their original detections, and characterized CAD detections as true positive or false positive. Results: Volume CT Dose index (CTDIvol) for SDCT and ULDCT were 5.3±2 and 0.4±0.2 mGy (P<0.0001), respectively. Forty-five reference nodules were detected in 30 patients. Reader sensitivity varied widely but similarly for SDCT (ranging from 45% to 87%) and ULDCT (45% to 83%). CAD sensitivity was 76% (34/45) for SDCT and 71% (32/45) for ULDCT. After CAD, reader sensitivity substantially improved by 19% and 18% for 2 readers, and remained nearly unchanged for the other 2 readers (0% and 2%), despite reader perception that many more nodules were identified with CAD. There was a mean of 2 false-positive CAD detections/case. Conclusions: ULDCT with 100 kV/tin reduced patient dose by over 90% without compromising pulmonary nodule detection sensitivity. CAD can substantially improve nodule detection sensitivity at ULDCT for some readers, maintaining interobserver performance.

Abstract Context A better understanding of nocturnal regulation of glucose homeostasis will provide the framework for designing rational therapeutic strategies to improve the management of overnight glucose in patients with type 2 diabetes (T2D). Objective To establish the nocturnal pattern and regulation of glucose production (EGP) in humans and to determine whether the pattern is dysregulated in people with T2D. Design Subjects were infused with [3-3H] glucose overnight. Arterial blood samples were drawn for hormones and analytes to estimate EGP throughout the night. Deuterium-labeled water was provided to measure gluconeogenesis (GNG) using the hexamethylenetetramine method of Landau. Setting Mayo Clinic Clinical Research Trials Unit, Rochester, MN, USA. Participants and Interventions A total of 43 subjects [23 subjects with T2D and 20 nondiabetic (ND) subjects comparable for age and body mass index] were included in this study. Main Outcome(s) Measure(s) Glucose and EGP. Results Plasma glucose, C-peptide, and glucagon concentrations were higher throughout the night, whereas insulin concentrations were higher in subjects with T2D vs ND subjects at 1:00 and 4:00 am but similar at 7:00 am. EGP was higher in the subjects with T2D than in the ND subjects throughout the night (P &lt; 0.001). Glycogenolysis (GGL) fell and GNG rose, resulting in significantly higher (P &lt; 0.001) rates of GNG at 4:00 and 7:00 am and significantly (P &lt; 0.001) higher rates of GGL at 1:00, 4:00, and 7:00 am in T2D as compared with ND. Conclusions These data imply that optimal therapies for T2D for nocturnal/fasting glucose control should target not only the absolute rates of EGP but also the contributing pathways of GGL and GNG sequentially.

BACKGROUND: Patients who develop ARDS from medical or traumatic causes typically present after the inciting event has already occurred. Postoperative ARDS is unique in that the inciting insult potentially responsible for ARDS is known ahead of time, which provides an opportunity to study the early pathophysiology of ARDS. The objective of this study was to better understand the early pathophysiology of postoperative ARDS through a temporal analysis of key biomarkers of interest. METHODS: We performed a case-control study of adults undergoing elective thoracic, aortic vascular, or cardiac surgery, which placed them at increased risk of developing postoperative ARDS. Biomarkers were measured at baseline, 2 h, and 6 h after the key intraoperative event believed to be responsible for ARDS. RESULTS: Of the 467 subjects enrolled, 26 developed ARDS and were matched to non-ARDS controls 1:2 based on age, sex, surgical procedure, and surgical lung injury prediction score. Patients with ARDS were more likely to have lower preoperative albumin ( P = .029), longer surgery ( P = .007), larger amounts of intraoperative fluid ( P = .036), and higher intraoperative peak inspiratory pressures ( P = .006). Baseline plasminogen activator inhibitor-1 levels were higher in the ARDS group ( P = .03). Changes in postoperative biomarker levels from baseline were greater in the ARDS group for interleukin-8 (baseline to 6 h, P = .02) and surfactant protein-D (baseline to 2 h, P = .009). CONCLUSIONS: Our study supported the hypothesis that dysregulated coagulation, inflammation, and epithelial injury are pathophysiologic features of early postoperative ARDS. Interleukin-8, plasminogen activator-1, and surfactant protein-D may help predict development of postoperative ARDS.

Background: Diagnosis of heart failure with preserved ejection fraction (HFpEF) is challenging in euvolemic patients with dyspnea, and no evidence-based criteria are available. We sought to develop and then validate noninvasive diagnostic criteria that could be used to estimate the likelihood that HFpEF is present among patients with unexplained dyspnea to guide further testing. Methods: Consecutive patients with unexplained dyspnea referred for invasive hemodynamic exercise testing were retrospectively evaluated. Diagnosis of HFpEF (case) or noncardiac dyspnea (control) was ascertained by invasive hemodynamic exercise testing. Logistic regression was performed to evaluate the ability of clinical findings to discriminate cases from controls. A scoring system was developed and then validated in a separate test cohort. Results: The derivation cohort included 414 consecutive patients (267 cases with HFpEF and 147 controls; HFpEF prevalence, 64%). The test cohort included 100 consecutive patients (61 with HFpEF; prevalence, 61%). Obesity, atrial fibrillation, age >60 years, treatment with ≥2 antihypertensives, echocardiographic E/e’ ratio >9, and echocardiographic pulmonary artery systolic pressure >35 mm Hg were selected as the final set of predictive variables. A weighted score based on these 6 variables was used to create a composite score (H 2 FPEF score) ranging from 0 to 9. The odds of HFpEF doubled for each 1-unit score increase (odds ratio, 1.98; 95% CI, 1.74–2.30; P <0.0001), with an area under the curve of 0.841 ( P <0.0001). The H 2 FPEF score was superior to a currently used algorithm based on expert consensus (increase in area under the curve of 0.169; 95% CI, 0.120–0.217; P <0.0001). Performance in the independent test cohort was maintained (area under the curve, 0.886; P <0.0001). Conclusions: The H 2 FPEF score, which relies on simple clinical characteristics and echocardiography, enables discrimination of HFpEF from noncardiac causes of dyspnea and can assist in determination of the need for further diagnostic testing in the evaluation of patients with unexplained exertional dyspnea.