Shapiro, Brian P.

Background: Gaps in ECG interpretation competency among medical professionals exist, with a need for practical, evidence-based, and accessible learning solutions. We conducted an international, prospective, randomized controlled trial to assess the effectiveness of web-based, self-directed ECG learning. Methods: A total of 1206 diverse medical learners and professionals underwent an initial test, followed by random assignment to one of four groups: (i) online question-bank (questions), (ii) online lectures (lectures), (iii) online, question-bank and lectures (hybrid), or (iv) no resources (control). After 4 months, a post-test was administered to evaluate the overall change in performance. Results: Of all participants, 863 (72%) completed the trial. After the 4-month follow-up, all three online, self-directed intervention groups (questions, lectures, and hybrid) showed significant improvement in overall performance (P<0.001), while the control group did not (P=0.544). The questions, lectures, and hybrid interventions demonstrated score improvements of +11.4% (95% CI, 9.1-13.7; P<0.001), +9.8% (95% CI, 7.8-11.9; P<0.001), and +11.0% (95% CI, 9.2-12.9; P<0.001) respectively, compared to +0.8% (95% CI, -1.2-2.8; P=0.544) for the control group. These improvements were consistent across medical professional groups (Figure 1) . Conclusions: Web-based, self-directed learning resources effectively improved ECG interpretation proficiency for diverse medical learners and professionals.

Background: ECG interpretation is crucial in medical practice, but professionals struggle with achieving and maintaining competency. Identifying proficiency gaps aids in designing educational interventions. Methods: Medical professionals from various disciplines interpreted 30 12-lead ECGs containing commonly taught urgent and non-urgent findings. Performance metrics evaluated were overall adjusted score (% of correctly identified findings using a point-value score based on clinical relevance), unadjusted score (% of correctly identified findings), interpretation time per ECG, and self-reported confidence (rated on an ordinal scale of 0 [not confident], 1 [somewhat confident], or 2 [confident]). Results: Among 1206 participants, there were 72 (6%) primary care physicians (PCPs), 146 (12%) cardiology fellows-in-training (FIT), 353 (29%) resident physicians, 182 (15%) medical students, 84 (7%) advanced practice providers (APPs), 120 (10%) nurses, 249 (21%) allied health professionals, 571 (47%) physicians, and 453 (38%) non-physicians. Participants had a mean adjusted score of 46.9% (± 15.9%), unadjusted score of 56.4% (± 17.2%), interpretation time of 142 seconds (± 67 seconds), and confidence of 0.83 (± 0.53) (Table 1) . Performance varied across groups; cardiology FIT had superior performance in all metrics. Physicians generally outperformed non-physicians, with higher overall adjusted score (52% vs. 43%; p<0.01), unadjusted score (62% vs. 52%; p<0.01), and confidence (0.91 vs. 0.80; p<0.01). Unadjusted score for PCPs was higher than nurses and APPs (58% vs. 47% and 51%; p<0.01) but lower than resident physicians (58% vs. 60%; p<0.01). Allied health professionals outperformed nurses and APPs and closely matched resident physicians and PCPs. Conclusions: Significant gaps in ECG interpretation proficiency exist, emphasizing the need for comprehensive, scalable, and accessible educational tools.

Introduction: Tricuspid regurgitation is a common echocardiographic finding leading to excess morbidity and mortality in adult population. Hypothesis: Racial and ethnic disparities have been observed in various cardiovascular disorders’ prevalence and natural course, including valvular lesions. However, little is known about the epidemiology and clinical correlations of TR among non-Hispanic Black adults. Methods: To examine risk factors and clinical outcomes in non-Hispanic Black adults with moderate or more severe TR, 685 patients (7%) self-identified as non-Hispanic Black and 9127 (93%) self-identified as non-Hispanic White with a first echocardiographic report of moderate or more severe TR between 2005-2016 were studied. Results: Non-Hispanic Black patients had more severe TR when compared to white patients (25% vs. 20%, p<0.001). After adjusting for age and sex, non-Hispanic Black patients had significantly higher 10-year all-cause mortality (HR=1.34 (1.18, 1.52), p<0.001). Black race remained a risk factor for all-cause mortality even after adjustment for comorbidities like CHF, COPD, DM, CKD, hypertension, and ischemic heart disease (HR=1.23 (1.08, 1.40), p=0.002). Conclusions: Significant racial disparities exist in demographic, clinical and echocardiographic characteristics between non-Hispanic Black and White patients with moderate or more severe TR. Black race is a potential disease modifier leading to excess mortality.

Introduction: Pulmonary arterial hypertension (PAH) is a fatal disease and vasodilators are the mainstay for its therapy. However, they offer restricted advancement opportunities for the control and treatment of PAH. Thus, the PAH field needs a paradigm-shifting strategy for its successful management and control. Objective: To test the hypothesis that gut microbial dysbiosis and its increased permeability are associated with PAH. Methods: Healthy control subjects and patients with PAH were recruited from two hospitals in the Americas to ascertain the wider applicability of our hypothesis. Fecal samples of PAH patients (n=19) and control, reference subjects (n=16) were obtained at the Hospital de Clinicas de Porto Alegre, Brazil, for microbiota analysis. Plasma/serum samples were collected from PAH patients (n=22) and control, reference subjects (n=19) at the Mayo Clinic, Jacksonville, Florida, USA, for analysis of gut leakiness and inflammatory biomarkers. Results: In PAH patients, a significant decrease in abundance, diversity and evenness of gut microbial population was observed as measured by 16S ribosomal DNA analyses of fecal samples. Analysis of fecal bacteria populations also demonstrated significant increases in gram-positive, facultative-anaerobic genera, such as Actinomyces, Bifidobacterium Slackia, and Streptococcus in PAH patients. Further, plasma zonulin and iFABP, the biomarkers for gut leakiness increased by 40.3% (p=0.0018) and 81% (p=0.0012), respectively in PAH patients. High plasma LPS, HMGB1, and TIMP1 levels are involved in increased gut inflammation and gut mucosal injury. We also observed LPS, HMGB1, and TIMP1 levels were increased by 363% (p=0.0096), 20.5% (p=0.0027), and 213% (p<0.0001), respectively in PAH patients. Conclusions: PAH patients demonstrate profound gut microbial dysbiosis and increased permeability and inflammation. Further characterization of PAH specific microbial species holds novel management potential with the use of pre- and probiotics, designer antibiotics, appropriate fecal/bacterial transplantation, on top of background proven therapies.

Introduction: Cross-sectional studies in patient with hypertensive heart disease (HHD) and heart failure with normal ejection fraction (HFnlEF) suggested impairment of longitudinal myocardial mechanics as assessed by tissue Doppler imaging. It has been suggested that enhanced circumferential, and/or radial LV mechanics or LV remodeling compensates for depression in longitudinal function and thus, preserves EF in HHD or HFnlEF. Hypothesis : We hypothesized that if longitudinal performance is depressed, whether due to increased afterload or to intrinsic myocardial dysfunction, circumferential and radial LV mechanics would also be effected. To test this hypothesis, we used an aged canine model of hypertension. Methods: Elderly dogs (n=22) underwent bilateral renal wrapping to induce hypertension. 2D echocardiography (mid-short axis views) was performed before and 8 weeks after renal wrapping; peak radial (PR) and peak circumferential (PC) regional strains were measured by speckle tracking averaging data from 6 segments. Ejection fraction (EF), LV mass index (LVMI), systolic blood pressure (SBP), and circumferential wall stress (CWS) were assessed as well. Results : See table . PR correlated with PC (r=0.65), EF (r=0.67), LWMI (r=0.71) and CWS (r=0.58) (p<0.005 for all). PC correlated also with EF (r=0.60), LWMI (r=0.49) and CWS (r=0.48) (p<0.01 for all). The relationship between EF and CWS (r 2 =0.64, p<0.001) was modified by the addition of either PC (r 2 =0.74, p for PC =0.005) or PR strain(r 2 =0.69, p for PR =0.04). Conclusions : These data show that development of hypertension with LV hypertrophy does not enhance but impairs circumferential and radial LV mechanics as assessed with strain imaging, and that like EF, circumferential and radial strain are related to afterload (wall stress). However, both confer additional information regarding contractility. Conclusions regarding myocardial function based on strain imaging must account for its load dependence.

New Findings What is the topic of this review?This review concerns the negative impact of pulmonary hypertension (PH) on the pulmonary haemodynamic and gas exchange responses to exercise, considering the mechanisms by which PH plays a role in exercise intolerance in heart failure (HF) patients. What advances does it highlight?The hallmark limited pulmonary vascular ‘reserve’ and impaired pulmonary gas exchange responses to exercise in HF are worsened by the development of PH; these are key determinants of exercise intolerance. Even HF patients who present with ‘normal’ pulmonary vascular function experience exercise‐induced PH, which plays a role in exercise intolerance. AbstractPatients with heart failure universally complain of exertional intolerance, but the underlying cause(s) of this intolerance may differ between patients with different disease phenotypes. Exercise introduces an impressive stress to the lungs, where elevations in venous return and cardiac output engender substantial increases in pulmonary blood volume and flow. Relative to healthy individuals, the pulmonary vascular reserve to accept this increase in pulmonary perfusion is compromised in heart failure, with a growing body of evidence suggesting that the development of pulmonary hypertension (PH), and in particular a precapillary component of PH, worsens the pulmonary haemodynamic response to exercise in these patients. Characterized by an exaggerated increase in pulmonary arterial pressure and an elevation in pulmonary vascular resistance, this dysfunctional pulmonary haemodynamic response plays a role in exercise intolerance, probably through an impairment of right ventricular function, underperfusion of the pulmonary circulation and a subsequent reduction in systemic blood flow and oxygen delivery. The hallmark abnormalities in ventilatory and pulmonary gas exchange that accompany heart failure, including a greater ventilatory equivalent for carbon dioxide, are also worsened by the development of PH. This raises the possibility that measures of exercise pulmonary gas exchange might help to ‘describe’ underlying PH in heart failure; however, several fundamental issues and questions need to be addressed before such gas exchange measures could truly be considered efficacious measures used to differentiate the type of PH and track the severity of PH in heart failure.exercise intolerance, heart failure, pulmonary gas exchange, pulmonary haemodynamics, pulmonary hypertension

We sought to describe incidental imaging features of increased intrapericardial pressure due to pericardial effusion on chest computed tomography (CT) and correlate them with cardiac CT, cardiac magnetic resonance imaging, and echocardiography. It is important for the radiologist to become familiar with imaging findings of increased intrapericardial pressure in the setting of pericardial effusion when identified on chest CT. Recognizing the imaging findings of increased intrapericardial pressure can better guide the care of these patients.

Objectives: Pulmonary arterial hypertension (PAH) is a deadly disease without any effective cure. Identification of the PAH-associated gut microbiome may shift conceptual paradigms of the disease that could lead to new therapeutic advancement. We tested the hypothesis that PAH patients have distinct gut microbiome composition contributing to PAH that predicts the disease. Methods: A total of 71 participants were recruited. Fecal microbiomes of 18 type 1 PAH patients (mean pulmonary arterial pressure [mPAP] 57.4±16.7 mmHg) and 13 reference subjects were compared by shotgun metagenomics methods. Plasma from 22 PAH patients (mPAP 48.3± 18.4 mmHg) and 18 reference subjects was used in untargeted metabolomic analysis. Results: Significant taxonomic and functional changes in the microbiome of the PAH cohort were observed. PAH patients had increased gut barrier dysfunction and inflammation as evidenced by plasma markers and metagenomics. A random forest model predicted PAH from gut microbiome composition with 82.6% accuracy. Changes in the gut microbiome were associated with purine metabolism, arginine biosynthesis, trimethylamine production and tryptophan biosynthesis, all previously associated with PAH. Area under the curve of the multi-variate receiver operating characteristics (ROC) plot for metabolites of these pathways had a predictive accuracy of 0.965. Conclusions: The gut microbiome/metabolites of PAH patients predict disease in random forest models and ROC analyses. The unique PAH gut microbiome influences carnitine, arginine and purine metabolisms contributing to pathophysiology. These highlight previously unknown roles of gut bacteria and their metabolites in PAH that could lead to new therapeutic or management paradigms.