EDUCATE: An international, randomized controlled trial for teaching electrocardiography.

INTRODUCTION: Despite the critical role of electrocardiograms (ECGs) in patient care, evident gaps exist in ECG interpretation competency among healthcare professionals across various medical disciplines and training levels. Currently, no practical, evidence-based, and easily accessible ECG learning solution is available for healthcare professionals. The aim of this study was to assess the effectiveness of web-based, learner-directed interventions in improving ECG interpretation skills in a diverse group of healthcare professionals. METHODS: In an international, prospective, randomized controlled trial, 1206 healthcare professionals from various disciplines and training levels were enrolled. They underwent a pre-intervention test featuring 30 12-lead ECGs with common urgent and non-urgent findings. Participants were randomly assigned to four groups: (i) practice ECG interpretation question bank (question bank), (ii) lecture-based learning resource (lectures), (iii) hybrid question- and lecture-based learning resource (hybrid), or (iv) no ECG learning resources (control). After four months, a post-intervention test was administered. The primary outcome was the overall change in ECG interpretation performance, with secondary outcomes including changes in interpretation time, self-reported confidence, and accuracy for specific ECG findings. Both unadjusted and adjusted scores were used for performance assessment. RESULTS: Among 1206 participants, 863 (72 %) completed the trial. Following the intervention, the question bank, lectures, and hybrid intervention groups each exhibited significant improvements, with average unadjusted score increases of 11.4 % (95 % CI, 9.1 to 13.7; P<0.01), 9.8 % (95 % CI, 7.8 to 11.9; P<0.01), and 11.0 % (95 % CI, 9.2 to 12.9; P<0.01), respectively. In contrast, the control group demonstrated a non-significant improvement of 0.8 % (95 % CI, -1.2 to 2.8; P=0.54). While no differences were observed among intervention groups, all outperformed the control group significantly (P<0.01). Intervention groups also excelled in adjusted scores, confidence, and proficiency for specific ECG findings. CONCLUSION: Web-based, self-directed interventions markedly enhanced ECG interpretation skills across a diverse range of healthcare professionals, providing an accessible and evidence-based solution.

Predictors of ECG Interpretation Proficiency in Healthcare Professionals.

Accurate ECG interpretation is vital, but variations in skills exist among healthcare professionals. This study aims to identify factors contributing to ECG interpretation proficiency. Survey data and ECG interpretation test scores from participants in the EDUCATE Trial were analyzed to identify predictors of performance for 30 sequential 12-lead ECGs. Nonmodifiable factors (being a physician, clinical experience, patient care impact) and modifiable factors (weekly interpretation volume, training hours, expert supervision frequency) were analyzed. Bivariate and multivariate analyses were used to generate a Comprehensive Model (incorporating all factors) and Actionable Model (incorporating modifiable factors only). Among 1206 participants analyzed, there were 72 (6.0%) primary care physicians, 146 (12.1%) cardiology fellows-in-training, 353 (29.3%) resident physicians, 182 (15.1%) medical students, 84 (7.0%) advanced practice providers, 120 (9.9%) nurses, and 249 (20.7%) allied health professionals. Among them, 571 (47.3%) were physicians and 453 (37.6%) were nonphysicians. The average test score was 56.4% ± 17.2%. Bivariate analysis demonstrated significant associations between test scores and >10 weekly ECG interpretations, being a physician, >5 training hours, patient care impact, and expert supervision but not clinical experience. In the Comprehensive Model, independent associations were found with weekly interpretation volume (9.9 score increase; 95% CI, 7.9-11.8; P < 0.001), being a physician (9.0 score increase; 95% CI, 7.2-10.8; P < 0.001), and training hours (5.7 score increase; 95% CI, 3.7-7.6; P < 0.001). In the Actionable Model, scores were independently associated with weekly interpretation volume (12.0 score increase; 95% CI, 10.0-14.0; P < 0.001) and training hours (4.7 score increase; 95% CI, 2.6-6.7; P < 0.001). The Comprehensive and Actionable Models explained 18.7% and 12.3% of the variance in test scores, respectively. Predictors of ECG interpretation proficiency include nonmodifiable factors like physician status and modifiable factors such as training hours and weekly ECG interpretation volume.

ECG Interpretation Proficiency of Healthcare Professionals.

ECG interpretation is essential in modern medicine, yet achieving and maintaining competency can be challenging for healthcare professionals. Quantifying proficiency gaps can inform educational interventions for addressing these challenges. Medical professionals from diverse disciplines and training levels interpreted 30 12-lead ECGs with common urgent and nonurgent findings. Average accuracy (percentage of correctly identified findings), interpretation time per ECG, and self-reported confidence (rated on a scale of 0 [not confident], 1 [somewhat confident], or 2 [confident]) were evaluated. Among the 1206 participants, there were 72 (6%) primary care physicians (PCPs), 146 (12%) cardiology fellows-in-training (FITs), 353 (29%) resident physicians, 182 (15%) medical students, 84 (7%) advanced practice providers (APPs), 120 (10%) nurses, and 249 (21%) allied health professionals (AHPs). Overall, participants achieved an average overall accuracy of 56.4% ± 17.2%, interpretation time of 142 ± 67 seconds, and confidence of 0.83 ± 0.53. Cardiology FITs demonstrated superior performance across all metrics. PCPs had a higher accuracy compared to nurses and APPs (58.1% vs 46.8% and 50.6%; P < 0.01), but a lower accuracy than resident physicians (58.1% vs 59.7%; P < 0.01). AHPs outperformed nurses and APPs in every metric and showed comparable performance to resident physicians and PCPs. Our findings highlight significant gaps in the ECG interpretation proficiency among healthcare professionals.

Education curriculum assessment for teaching electrocardiography: Rationale and design for the prospective, international, randomized controlled EDUCATE trial.

BACKGROUND: Electrocardiogram (ECG) interpretation training is a fundamental component of medical education across disciplines. However, the skill of interpreting ECGs is not universal among medical graduates, and numerous barriers and challenges exist in medical training and clinical practice. An evidence-based and widely accessible learning solution is needed. DESIGN: The EDUcation Curriculum Assessment for Teaching Electrocardiography (EDUCATE) Trial is a prospective, international, investigator-initiated, open-label, randomized controlled trial designed to determine the efficacy of self-directed and active-learning approaches of a web-based educational platform for improving ECG interpretation proficiency. Target enrollment is 1000 medical professionals from a variety of medical disciplines and training levels. Participants will complete a pre-intervention baseline survey and an ECG interpretation proficiency test. After completion, participants will be randomized into one of four groups in a 1:1:1:1 fashion: (i) an online, question-based learning resource, (ii) an online, lecture-based learning resource, (iii) an online, hybrid question- and lecture-based learning resource, or (iv) a control group with no ECG learning resources. The primary endpoint will be the change in overall ECG interpretation performance according to pre- and post-intervention tests, and it will be measured within and compared between medical professional groups. Secondary endpoints will include changes in ECG interpretation time, self-reported confidence, and interpretation accuracy for specific ECG findings. CONCLUSIONS: The EDUCATE Trial is a pioneering initiative aiming to establish a practical, widely available, evidence-based solution to enhance ECG interpretation proficiency among medical professionals. Through its innovative study design, it tackles the currently unaddressed challenges of ECG interpretation education in the modern era. The trial seeks to pinpoint performance gaps across medical professions, compare the effectiveness of different web-based ECG content delivery methods, and create initial evidence for competency-based standards. If successful, the EDUCATE Trial will represent a significant stride towards data-driven solutions for improving ECG interpretation skills in the medical community.

Impact of Computer-Interpreted ECGs on the Accuracy of Healthcare Professionals.

The interpretation of electrocardiograms (ECGs) involves a dynamic interplay between computerized ECG interpretation (CEI) software and human overread. However, the impact of computer ECG interpretation on the performance of healthcare professionals remains largely unexplored. The aim of this study was to evaluate the interpretation proficiency of various medical professional groups, with and without access to the CEI report. Healthcare professionals from diverse disciplines, training levels, and countries sequentially interpreted 60 standard 12-lead ECGs, demonstrating both urgent and nonurgent findings. The interpretation process consisted of 2 phases. In the first phase, participants interpreted 30 ECGs with clinical statements. In the second phase, the same 30 ECGs and clinical statements were randomized and accompanied by a CEI report. Diagnostic performance was evaluated based on interpretation accuracy, time per ECG (in seconds [s]), and self-reported confidence (rated 0 [not confident], 1 [somewhat confident], or 2 [confident]). A total of 892 participants from various medical professional groups participated in the study. This cohort included 44 (4.9%) primary care physicians, 123 (13.8%) cardiology fellows-in-training, 259 (29.0%) resident physicians, 137 (15.4%) medical students, 56 (6.3%) advanced practice providers, 82 (9.2%) nurses, and 191 (21.4%) allied health professionals. The inclusion of the CEI was associated with a significant improvement in interpretation accuracy by 15.1% (95% confidence interval, 14.3-16.0; P < 0.001), decrease in interpretation time by 52 s (-56 to -48; P < 0.001), and increase in confidence by 0.06 (0.03-0.09; P = 0.003). Improvement in interpretation accuracy was seen across all professional subgroups, including primary care physicians by 12.9% (9.4-16.3; P = 0.003), cardiology fellows-in-training by 10.9% (9.1-12.7; P < 0.001), resident physicians by 14.4% (13.0-15.8; P < 0.001), medical students by 19.9% (16.8-23.0; P < 0.001), advanced practice providers by 17.1% (13.3-21.0; P < 0.001), nurses by 16.2% (13.4-18.9; P < 0.001), allied health professionals by 15% (13.4-16.6; P < 0.001), physicians by 13.2% (12.2-14.3; P < 0.001), and nonphysicians by 15.6% (14.3-17.0; P < 0.001).CEI integration improves ECG interpretation accuracy, efficiency, and confidence among healthcare professionals.

Exploring Factors Influencing ECG Interpretation Proficiency of Medical Professionals.

The electrocardiogram (ECG) is a crucial diagnostic tool in medicine with concerns about its interpretation proficiency across various medical disciplines. Our study aimed to explore potential causes of these issues and identify areas requiring improvement. A survey was conducted among medical professionals to understand their experiences with ECG interpretation and education. A total of 2515 participants from diverse medical backgrounds were surveyed. A total of 1989 (79%) participants reported ECG interpretation as part of their practice. However, 45% expressed discomfort with independent interpretation. A significant 73% received less than 5 hours of ECG-specific education, with 45% reporting no education at all. Also, 87% reported limited or no expert supervision. Nearly all medical professionals (2461, 98%) expressed a desire for more ECG education. These findings were consistent across all groups and did not vary between primary care physicians, cardiology FIT, resident physicians, medical students, APPs, nurses, physicians, and nonphysicians. This study reveals substantial deficiencies in ECG interpretation training, supervision, and confidence among medical professionals, despite a strong interest in increased ECG education.

Burden and Depression in Caregivers of Blind Patients in New York State.

PURPOSE: To describe the degree of burden of care and the proportion at risk of depression among individuals caring for legally blind patients. METHODS: We performed a cross-sectional study of 486 individuals providing care to their family members who were legally blind. Best-corrected visual acuity of the better-seeing eye in patients determined group placement: Group 1, 20/200-10/200; group 2, 10/200 to light perception (LP); group 3, no light perception (NLP); group VF, visual field loss to <20 central degrees. Burden was evaluated using the Burden Index of Caregivers (BIC-11) and the prevalence at risk of depression was determined by the Center for Epidemiologic Studies Depression (CES-D) scale. RESULTS: Total mean BIC-11 scores ranged from 8.78 ± 4.82 (group 1) to 12.03 ± 5.22 (group 3; p = 0.04). Daily hours spent on close supervision, intensity of caregiving and presence of multiple chronic illnesses in caregivers were the significant covariates affecting BIC-11 scores (p < 0.05). The prevalence of caregivers at risk of depression increased with vision loss from 6.9% (group 1) to 17.9% (group 3; p < 0.05). Female caregivers had an odds ratio (OR) of 2.89 for depression (95% confidence interval, CI, 1.07-3.97; p = 0.04). Caregivers with ≥2 comorbidities had OR 4.24 (95% CI 2.41-6.11) for risk of depression (p < 0.01). CONCLUSION: Burden of care was highest among caregivers who provided greater hours of supervision. Patients with more limitations in their activities of daily living had caregivers who reported higher burden. Female caregivers and caregivers with multiple chronic illnesses were at higher risk of depression.

Comparing Hospitalist-Resident to Hospitalist-Midlevel Practitioner Team Performance on Length of Stay and Direct Patient Care Cost.

BACKGROUND: A perception exists that residents are more costly than midlevel providers (MLPs). Since graduate medical education (GME) funding is a key issue for teaching programs, hospitals should conduct cost-benefit analyses when considering staffing models. OBJECTIVE: Our aim was to compare direct patient care costs and length of stay (LOS) between resident and MLP inpatient teams. METHODS: We queried the University HealthSystems Consortium clinical database (UHC CDB) for 13 553 "inpatient" discharges at our institution from July 2010 to June 2013. Patient assignment was based on bed availability rather than "educational value." Using the UHC CDB data, discharges for resident and MLP inpatient teams were compared for observed and expected LOS, direct cost derived from hospital charges, relative expected mortality (REM), and readmissions. We also compared patient satisfaction for physician domain questions using Press Ganey data. Bivariate analysis was performed for factors associated with differences between the 2 services using χ(2) analysis and Student t test for categorical and continuous variables, respectively. RESULTS: During the 3-year period, while REM was higher on the hospitalist-resident services (P < .001), LOS was shorter by 1.26 days, and per-patient direct costs derived from hospital charges were lower by $617. Patient satisfaction scores for the physician-selected questions were higher for resident teams. There were no differences in patient demographics, daily discharge rates, readmissions, or deaths. CONCLUSIONS: Resident teams are economically more efficient than MLP teams and have higher patient satisfaction. The findings offer guidance when considering GME costs and inpatient staffing models.

The Institute of Medicine, the Food and Drug Administration, and the calcium conundrum.

In the present article we aim to bring forward the apparent disconnect between two US government-sponsored entities - the Institute of Medicine (IOM) and the Food and Drug Administration (FDA) - regarding the safe upper limit of Ca intake. In light of the 2011 US Congress-appointed IOM report indicating an upper limit of elemental Ca intake of 2000-2500 mg/d in adults (based on age group), it is perplexing that the FDA has not yet required a change on the labelling of over-the-counter Ca-containing antacids, some of which indicate an upper limit of elemental Ca intake of 2800-3000 mg/d. Even more concerning is that Ca intake is rarely from supplementation in isolation. National Health and Nutrition Examination Survey (NHANES) data from 2003-2006 indicate that mean dietary Ca intakes for males ranged from 871 to 1266 mg/d and for females from 748 to 968 mg/d depending on the age group. The estimated total Ca (diet + supplements) intake exceeded the upper limit in 5 % of the population older than 50 years. Furthermore, NHANES data from 1999-2000 indicate that when Ca is taken as part of an antacid preparation, patients often fail to report this as Ca intake. Thus, individuals taking the maximum allowable dose of supplemental Ca as antacids are at high risk for complications associated with excess Ca intake. Our hope is that by describing Ca homeostasis and highlighting the risks and dangers of Ca overload, the FDA will align its recommendation with the IOM and solve the current Ca conundrum in the USA for the sake of patient safety.

Variable clinical presentation of an MUC1 mutation causing medullary cystic kidney disease type 1.

BACKGROUND AND OBJECTIVES: The genetic cause of medullary cystic kidney disease type 1 was recently identified as a cytosine insertion in the variable number of tandem repeat region of MUC1 encoding mucoprotein-1 (MUC1), a protein that is present in skin, breast, and lung tissue, the gastrointestinal tract, and the distal tubules of the kidney. The purpose of this investigation was to analyze the clinical characteristics of families and individuals with this mutation. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: Families with autosomal dominant interstitial kidney disease were referred for genetic analysis over a 14-year period. Families without UMOD or REN mutations prospectively underwent genotyping for the presence of the MUC1 mutation. Clinical characteristics were retrospectively evaluated in individuals with the MUC1 mutation and historically affected individuals (persons who were both related to genetically affected individuals in such a way that ensured that they could be genetically affected and had a history of CKD stage IV or kidney failure resulting in death, dialysis, or transplantation). RESULTS: Twenty-four families were identified with the MUC1 mutation. Of 186 family members undergoing MUC1 mutational analysis, the mutation was identified in 95 individuals, 91 individuals did not have the mutation, and111 individuals were identified as historically affected. Individuals with the MUC1 mutation suffered from chronic kidney failure with a widely variable age of onset of end stage kidney disease ranging from 16 to >80 years. Urinalyses revealed minimal protein and no blood. Ultrasounds of 35 individuals showed no medullary cysts. There were no clinical manifestations of the MUC1 mutation detected in the breasts, skin, respiratory system, or gastrointestinal tract. CONCLUSION: MUC1 mutation results in progressive chronic kidney failure with a bland urinary sediment. The age of onset of end stage kidney disease is highly variable, suggesting that gene-gene or gene-environment interactions contribute to phenotypic variability.

OCRL1 mutations in Dent 2 patients suggest a mechanism for phenotypic variability.

BACKGROUND/AIMS: Dent disease is an X-linked renal proximal tubulopathy associated with mutations in CLCN5 (Dent 1) or OCRL1 (Dent 2). OCRL1 mutations also cause the oculocerebrorenal syndrome of Lowe. METHODS: Dent patients with normal sequence for CLCN5 were sequenced for mutations in OCRL1. By analyzing these and all other OCRL1 mutations reported, a model relating OCRL1 mutations to the resulting disease (Dent 2 or Lowe's) was developed. RESULTS: Six boys with Dent disease had novel OCRL1 mutations: two missense (R301H, G304E) and four mutations predicted to produce premature termination codons (L56DfsX1, S149X, P161PfsX3, and M170IfsX1). These include one of the original patients reported by Dent and Friedman. Slit lamp examinations revealed early cataracts in only one boy with normal vision. None of these Dent 2 patients had metabolic acidosis; 3 had mild mental retardation. Analysis of all known OCRL1 mutations show that Dent 2 mutations fall into two classes that do not overlap with Lowe mutations. Bioinformatics analyses identified expressed OCRL1 splice variants that help explain the variability of those clinical features that distinguish Dent disease from Lowe syndrome. CONCLUSIONS: OCRL1 mutations can cause the renal phenotype of Dent disease, without acidosis or the dramatic eye abnormalities typical of Lowe syndrome. We propose a model to explain the phenotypic variability between Dent 2 and Lowe's based on distinctly different classes of mutations in OCRL1 producing splice variants.

Dent Disease with mutations in OCRL1.

Dent disease is an X-linked renal proximal tubulopathy associated with mutations in the chloride channel gene CLCN5. Lowe syndrome, a multisystem disease characterized by renal tubulopathy, congenital cataracts, and mental retardation, is associated with mutations in the gene OCRL1, which encodes a phosphatidylinositol 4,5-bisphosphate (PIP(2)) 5-phosphatase. Genetic heterogeneity has been suspected in Dent disease, but no other gene for Dent disease has been reported. We studied male probands in 13 families, all of whom met strict criteria for Dent disease but lacked mutations in CLCN5. Linkage analysis in the one large family localized the gene to a candidate region at Xq25-Xq27.1. Sequencing of candidate genes revealed a mutation in the OCRL1 gene. Of the 13 families studied, OCRL1 mutations were found in 5. PIP(2) 5-phosphatase activity was markedly reduced in skin fibroblasts cultured from the probands of these five families, and protein expression, measured by western blotting, was reduced or absent. Slit-lamp examinations performed in childhood or adulthood for all five probands showed normal results. Unlike patients with typical Lowe syndrome, none of these patients had metabolic acidosis. Three of the five probands had mild mental retardation, whereas two had no developmental delay or behavioral disturbance. These findings demonstrate that mutations in OCRL1 can occur with the isolated renal phenotype of Dent disease in patients lacking the cataracts, renal tubular acidosis, and neurological abnormalities that are characteristic of Lowe syndrome. This observation confirms genetic heterogeneity in Dent disease and demonstrates more-extensive phenotypic heterogeneity in Lowe syndrome than was previously appreciated. It establishes that the diagnostic criteria for disorders resulting from mutations in the Lowe syndrome gene OCRL1 need to be revised.

Evidence for genetic heterogeneity in Dent's disease.

BACKGROUND: Dent's disease (X-linked nephrolithiasis) is a proximal tubulopathy that has been consistently associated with inactivating mutations in the CLCN5 gene encoding the ClC-5 chloride channel expressed in tubular epithelial cells. METHODS: We performed mutation analysis of the coding region of CLCN5 by DNA sequencing in 32 unrelated males, all of whom met the following three clinical criteria for the diagnosis of Dent's disease: (1) low-molecular-weight (LMW) proteinuria; (2) hypercalciuria; and (3) at least one of the following: nephrocalcinosis, kidney stones, renal insufficiency, hypophosphatemia, or hematuria. RESULTS: Sixteen mutations (ten missense, four nonsense, two frameshift) were found in 19 patients. Mutations were confirmed by restriction analysis or allele-specific polymerase chain reaction (PCR), segregated with disease in the families, and were not polymorphisms. In the other 13 patients with Dent's disease, the coding sequence of CLCN5 was normal. In these 13 patients, we also sequenced two regions of the CLCN5 promoter (626 and 586 bp, respectively, 2.1 and 1 kb upstream of exon 2) containing regulatory sites [activating protein-1 (AP-1)-like, AP-4, and cyclic adenosine monophosphate (cAMP)-receptor element binding protein (CREB)] and primary and secondary transcription start sites. We found no mutations in these promoter sequences in any of the 13 patients. In one three-generation family, the absence of mutation was confirmed by sequencing in two additional affected family members, and in this family haplotype analysis excluded linkage to the region of the CLCN5 gene. There were no differences between the 19 patients with CLCN5 mutations and the 13 without mutations with regard to any clinical features of Dent's disease. CONCLUSION: These findings suggest that mutation in other gene(s) may be responsible for the phenotype of Dent's disease in some patients.

Inherited hypercalciuric syndromes: Dent's disease (CLC-5) and familial hypomagnesemia with hypercalciuria (paracellin-1).

Dent's disease and familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) are inherited diseases in which hypercalciuria, nephrocalcinosis, and renal failure are prominent features. Dent's disease resembles a Fanconi syndrome, with impaired reabsorption in the proximal tubule; FHHNC, with urinary loss of magnesium and calcium, is associated with impaired cation transport in the thick ascending limb of Henle's loop. Gene mapping in families and positional cloning led in both cases to identification of the responsible gene. Dent's disease is associated with mutations that disrupt function of a voltage-gated chloride channel, CLC-5, expressed in subapical endosomes of the proximal tubule and in other nephron segments. Impaired function of this channel disturbs reabsorption of filtered proteins, as well as other transport functions of the proximal tubule, and leads, apparently indirectly, to hypercalciuria and renal failure. FHHNC results from mutations in paracellin-1, a tight-junction protein that appears to be important in conducting or regulating paracellular cation transport. Impaired function of paracellin-1 leads specifically to urinary losses of magnesium and calcium, but because transcellular transport is intact these patients do not have hypokalemia or salt wasting. Identification of both genes represent triumphs of a genetic approach to solving problems of pathophysiology.