Limited Health Literacy Among Patients With Orthopedic Injuries: A Cross-sectional Survey of Patients Who Underwent Orthopedic Trauma Surgery in a County Hospital Setting.

BACKGROUND: Patients with limited health literacy have difficulty understanding their injuries and postoperative treatment, which can negatively affect their outcomes. MATERIALS AND METHODS: This cross-sectional questionnaire-based study of 103 adult patients sought to quantify patients' health literacy at a single county hospital's orthopedic trauma clinic and to examine their ability to understand injuries and treatment plans. Demographics, Newest Vital Sign (NVS) health literacy assessment, and knowledge scores were used to assess patients' comprehension of their injuries and treatment plan. Patients were grouped by NVS score (NVS <4: limited health literacy). Fisher's exact tests and t tests were used to compare demographic and comprehension scores. Multivariate logistic regression analysis was used to examine the association among low health literacy, sociodemographic variables, and knowledge scores. RESULTS: Of the 103 patients, 75% were determined to have limited health literacy. Patients younger than 30 years were more likely to have adequate literacy (50% vs 23%, P=.01). Patients who spoke Spanish as their primary language were 8.77 times more likely to have limited health literacy with respect to sociodemographic factors (odds ratio, 8.77; 95% CI, 1.03-76.92; P=.04). Low health literacy was 3.52 and 4.14 times more likely to predict discordance in answers to specific bone fractures and the narcotics prescribed (P=.04 and P=.02, respectively). CONCLUSION: Spanish-speaking patients have demonstrated limited health literacy and difficulty understanding their injuries and postoperative treatment plans compared with English-speaking patients. Patients with low health literacy are more likely to be unsure regarding which bone they fractured or their prescribed opiates. [Orthopedics. 202x;4x(x):xx-xx.].

Patterns of Misdiagnosis and Discordance in Detecting Osteoporosis: A Comparison of Dual-energy X-ray Absorptiometry and Lumbar Computed Tomography Hounsfield Units.

STUDY DESIGN: This was a retrospective chart review. OBJECTIVE: This study aims to identify the prevalence of osteoporosis (OP) by lumbar computed tomography (CT) Hounsfield units (HUs) in patients who have normal or osteopenic bone determined by dual-energy x-ray absorptiometry (DEXA). SUMMARY OF BACKGROUND DATA: OP is a critical issue in the postmenopausal and aging population. Bone mineral density assessment by DEXA has been described as insensitive for diagnosing OP in the lumbar spine. Improving the detection of OP can bring more patients to treatment and reduce the risks associated with low bone mineral density. PATIENTS AND METHODS: We retrospectively reviewed all patients with DEXA scans and noncontrast CTs of the lumbar spine over a 15-year period. Patients were diagnosed as non-OP if they had a normal DEXA T -score (≥ -1) or osteopenic DEXA T -score (between -1.1 and -2.4). Patients in this cohort were considered osteoporotic by CT if L1-HU ≤110. Demographics and lumbar HUs were compared between these stratified groups. RESULTS: A total of 74 patients were included for analysis. All patients were demographically, similar, and the average patient age was 70 years. The prevalence of OP determined by CT L1-HU ≤110 was 46% (normal DEXA: 9%, osteopenic DEXA: 63%). A significant number of males in our study were considered osteoporotic by L1-HU ≤110 (74%, P = 0.03). All individual axial and sagittal lumbar HU measurements including L1-L5 average lumbar HUs were statistically significant among non-OP and OP groups except for the lower lumbar levels ( P > 0.05 for L4 axial HUs, and L4-L5 sagittal HUs). CONCLUSIONS: The prevalence of OP in patients with normal or osteopenic T -scores is high. Among those with osteopenia by DEXA, more than 50% may lack appropriate medical treatment. The DEXA scan may be particularly insensitive to male bone quality making the CT HU the diagnostic method of choice for detecting OP. LEVEL OF EVIDENCE: Level III.

Patient physiology influences the MRI-based vertebral bone quality score.

BACKGROUND CONTEXT: Osteoporosis is a critical issue affecting postmenopausal women and the aging population. A novel magnetic resonance imaging (MRI)-based vertebral bone quality (VBQ) score has been proposed as a method to identify poor bone quality and predict fragility fractures. The diagnostic accuracy of this tool is not well understood. PURPOSE: To examine the ability of VBQ to predict osteoporosis and osteopenia, its correlation with dual-energy x-ray absorptiometry (DEXA), and the influence of patient-specific factors upon the score. STUDY DESIGN: Retrospective cohort study. PATIENT SAMPLE: Patients over the age of 18 with a DEXA scan and noncontrast, T1-weighted MRI of the lumbar spine completed within a 2-year period. OUTCOME MEASURES: Area-under-curve (AUC) values of the VBQ score predicting osteopenia and osteoporosis when controlling for patient characteristics. METHODS: Patients with noncontrast, T1-weighted MRIs of the lumbar spine and DEXA scans completed within a 2-year time frame were retrospectively reviewed. Patient demographics and medical risk factors for osteoporosis were identified and compared. VBQ scores were measured by two trained researchers and interrater reliability was calculated. Patients were separated into three groups defined by lowest DEXA T-score: Healthy Bone, Osteopenia, and Osteoporosis. analysis of variance, Kruskal-Wallis test, chi-square, t tests, Mann-Whitney U tests, and multivariate linear regression were performed to examine the relationship between patient characteristics, DEXA t-scores, and VBQ scores. Receiver operating characteristic analysis and AUC values were generated for the prediction of osteopenia and osteoporosis. RESULTS: A total of 156 patients were included for analysis. Sufficient inter-rater reliability was determined for VBQ measures (intraclass correlation coefficient: 0.81). Most patients were female (83%), postmenopausal (81%), and had hyperlipidemia (64%). Patients with hyperlipidemia and healthy bone density by DEXA had elevated baseline VBQ scores (p<.001) reflective of values seen in osteopenia and osteoporosis. The AUC of the VBQ score predicting osteopenia and osteoporosis changed to be more concordant with DEXA results after controlling for hyperlipidemia (AUC=0.72, 0.70 vs. AUC=0.88, 0.89; p<.001). Sub-analysis of hyperlipidemia subtypes revealed that elevated high-density lipoprotein is associated with elevated VBQ scores. CONCLUSIONS: Hyperlipidemia increased the MRI-based VBQ score in our healthy bone population. The high signal intensities resembled values seen in osteopenia and osteoporosis, suggesting that physiologic variables which impact bone composition may influence the VBQ score. Specifically, elevated high-density lipoprotein may contribute to this. The microarchitectural changes and the clinical implications of these factors need further exploration.

The effect of low preoperative platelet count on adverse outcomes following lumbar microdiscectomy.

Background: Low preoperative platelet count, or thrombocytopenia, has previously been associated with increased complications in elective spine surgeries. No other study has investigated the effects of abnormal coagulation profiles on postoperative outcomes specific to lumbar microdiscectomy (MLD) using a propensity matched cohort. Methods: Patient data was retrospectively retrieved from the National Surgical Quality Improvement Program database using Current Procedural Terminology (CPT) code 63030 to isolate patients who solely underwent MLD. Data was collected from 2010 to 2019 and included preoperative, perioperative, and 30-day postoperative variables. Patients were grouped into four platelet categories for ANOVA analysis and pairwise comparisons: Severe Thrombocytopenia (≤100), Thrombocytopenia (101-150), Moderate (151-199), and Normal (200-450). Variables that were significant in the univariate analysis were used in the multivariate analysis to determine the likelihood of experiencing adverse postoperative events - unplanned return to the operating room and surgical site infection. A propensity matched analysis was performed to control for confounding variables. Results: A total of 64,747 patients were identified within the 10-year period. The results of the multivariate analysis and the propensity matched analysis showed no significant differences in low preoperative platelet count as an independent predictor of experiencing a return to the operating room or surgical site infection. Furthermore, patients who had diabetes, history of smoking, or had emergency cases were associated with a high likelihood of experiencing these negative adverse events. Conclusion: Thrombocytopenia does not appear to independently predict return to the operating room or postoperative infection following MLD. Proper preoperative management strategies should be implemented to monitor comorbidity burden which would otherwise influence adverse outcomes in patients with thrombocytopenia undergoing MLD.

Acute Genetic Ablation of Cardiac Sodium/Calcium Exchange in Adult Mice: Implications for Cardiomyocyte Calcium Regulation, Cardioprotection, and Arrhythmia.

Background Sodium-calcium (Ca2+) exchanger isoform 1 (NCX1) is the dominant Ca2+ efflux mechanism in cardiomyocytes and is critical to maintaining Ca2+ homeostasis during excitation-contraction coupling. NCX1 activity has been implicated in the pathogenesis of cardiovascular diseases, but a lack of specific NCX1 blockers complicates experimental interpretation. Our aim was to develop a tamoxifen-inducible NCX1 knockout (KO) mouse to investigate compensatory adaptations of acute ablation of NCX1 on excitation-contraction coupling and intracellular Ca2+ regulation, and to examine whether acute KO of NCX1 confers resistance to triggered arrhythmia and ischemia/reperfusion injury. Methods and Results We used the α-myosin heavy chain promoter (Myh6)-MerCreMer promoter to create a tamoxifen-inducible cardiac-specific NCX1 KO mouse. Within 1 week of tamoxifen injection, NCX1 protein expression and current were dramatically reduced. Diastolic Ca2+ increased despite adaptive reductions in Ca2+ current and action potential duration and compensatory increases in excitation-contraction coupling gain, sarcoplasmic reticulum Ca2+ ATPase 2 and plasma membrane Ca2+ ATPase. As these adaptations progressed over 4 weeks, diastolic Ca2+ normalized and SR Ca2+ load increased. Left ventricular function remained normal, but mild fibrosis and hypertrophy developed. Transcriptomics revealed modification of cardiovascular-related gene networks including cell growth and fibrosis. NCX1 KO reduced spontaneous action potentials triggered by delayed afterdepolarizations and reduced scar size in response to ischemia/reperfusion. Conclusions Tamoxifen-inducible NCX1 KO mice adapt to acute genetic ablation of NCX1 by reducing Ca2+ influx, increasing alternative Ca2+ efflux pathways, and increasing excitation-contraction coupling gain to maintain contractility at the cost of mild Ca2+-activated hypertrophy and fibrosis and decreased survival. Nevertheless, KO myocytes are protected against spontaneous action potentials and ischemia/reperfusion injury.

Distinct features of calcium handling and ß-adrenergic sensitivity in heart failure with preserved versus reduced ejection fraction.

KEY POINTS: Heart failure (HF), the leading cause of death in developed countries, occurs in the setting of reduced (HFrEF) or preserved (HFpEF) ejection fraction. Unlike HFrEF, there are no effective treatments for HFpEF, which accounts for ∼50% of heart failure. Abnormal intracellular calcium dynamics in cardiomyocytes have major implications for contractility and rhythm, but compared to HFrEF, very little is known about calcium cycling in HFpEF. We used rat models of HFpEF and HFrEF to reveal distinct differences in intracellular calcium regulation and excitation-contraction (EC) coupling. While HFrEF is characterized by defective EC coupling at baseline, HFpEF exhibits enhanced coupling fidelity, further aggravated by a reduction in ß-adrenergic sensitivity. These differences in EC coupling and ß-adrenergic sensitivity may help explain why therapies that work in HFrEF are ineffective in HFpEF. ABSTRACT: Heart failure with reduced or preserved ejection fraction (respectively, HFrEF and HFpEF) is the leading cause of death in developed countries. Although numerous therapies improve outcomes in HFrEF, there are no effective treatments for HFpEF. We studied phenotypically verified rat models of HFrEF and HFpEF to compare excitation-contraction (EC) coupling and protein expression in these two forms of heart failure. Dahl salt-sensitive rats were fed a high-salt diet (8% NaCl) from 7 weeks of age to induce HFpEF. Impaired diastolic relaxation and preserved ejection fraction were confirmed in each animal echocardiographically, and clinical signs of heart failure were documented. To generate HFrEF, Sprague-Dawley (SD) rats underwent permanent left anterior descending coronary artery ligation which, 8-10 weeks later, led to systolic dysfunction (verified echocardiographically) and clinical signs of heart failure. Calcium (Ca2+ ) transients were measured in isolated cardiomyocytes under field stimulation or patch clamp. Ultra-high-speed laser scanning confocal imaging captured Ca2+ sparks evoked by voltage steps. Western blotting and PCR were used to assay changes in EC coupling protein and RNA expression. Cardiomyocytes from rats with HFrEF exhibited impaired EC coupling, including decreased Ca2+ transient (CaT) amplitude and defective couplon recruitment, associated with transverse (t)-tubule disruption. In stark contrast, HFpEF cardiomyocytes showed saturated EC coupling (increased ICa , high probability of couplon recruitment with greater Ca2+ release synchrony, increased CaT) and preserved t-tubule integrity. ß-Adrenergic stimulation of HFpEF myocytes with isoprenaline (isoproterenol) failed to elicit robust increases in ICa or CaT and relaxation kinetics. Fundamental differences in EC coupling distinguish HFrEF from HFpEF.

Ventricular Arrhythmias Underlie Sudden Death in Rats With Heart Failure and Preserved Ejection Fraction.

BACKGROUND: Heart failure (HF) with preserved ejection fraction (HFpEF) is increasingly common clinically, now rivaling or exceeding HF with reduced ejection fraction . Sudden death is the leading mode of exodus in patients with HFpEF, but the underlying causes are largely unknown. Using ambulatory recordings in a rat model, we test the hypothesis that ventricular arrhythmias (VA) underlie sudden death in HFpEF. METHODS: Dahl salt-sensitive rats (7 weeks of age) were fed a high-salt diet to induce HFpEF (n=13) or a normal-salt diet (controls, n=9). Transthoracic echocardiography was performed to check systolic and diastolic function at 14 to 18 weeks of age. Telemetric electrocardiographic recordings were analyzed for QT interval duration, burden of premature ventricular contractions, spontaneous VA, and heart rate variability. Survival was monitored twice daily. RESULTS: High-salt-fed rats with clear diastolic dysfunction, preserved ejection fraction, and HF signs were diagnosed with HFpEF at 14 to 15 weeks of age. QT and QTc intervals were prolonged in HFpEF rats compared with controls. Heart rate variability was reduced in HFpEF rats compared with controls. Spontaneous VA were more prevalent in HFpEF rats (6/13=46.1% versus 0/9=0% in controls; P<0.05), and sudden death was observed in 4 of 13 HFpEF rats. Three of the 4 sudden deaths were associated with VA as the terminal rhythm. CONCLUSIONS: In this rat model with phenotypically verified HFpEF, sudden death was common and generally associated with VA. Further clinical studies are warranted to determine whether these insights translate to sudden death in HFpEF patients.

Distinct regions of the intrinsically disordered protein MUT-16 mediate assembly of a small RNA amplification complex and promote phase separation of Mutator foci.

In C. elegans, efficient RNA silencing requires small RNA amplification mediated by RNA-dependent RNA polymerases (RdRPs). RRF-1, an RdRP, and other Mutator complex proteins localize to Mutator foci, which are perinuclear germline foci that associate with nuclear pores and P granules to facilitate small RNA amplification. The Mutator complex protein MUT-16 is critical for Mutator foci assembly. By analyzing small deletions of MUT-16, we identify specific regions of the protein that recruit other Mutator complex components and demonstrate that it acts as a scaffolding protein. We further determine that the C-terminal region of MUT-16, a portion of which contains predicted intrinsic disorder, is necessary and sufficient to promote Mutator foci formation. Finally, we establish that MUT-16 foci have many properties consistent with a phase-separated condensate and propose that Mutator foci form through liquid-liquid phase separation of MUT-16. P granules, which contain additional RNA silencing proteins, have previously been shown to have liquid-like properties. Thus, RNA silencing in C. elegans germ cells may rely on multiple phase-separated compartments through which sorting, processing, and silencing of mRNAs occurs.