Citations

Abstract Purpose Clinician educators are essential to the academic medicine workforce, yet understanding how they assess their own teaching competencies is limited. The Clinical Educator Milestones (CEMs) guide growth across key educator domains, but their use and perceived relevance remain underexplored. This study aims to (1) evaluate clinician educators’ self-reported performance on the CEMs; (2) examine differences by career level, specialty, and experience; and (3) inform faculty development efforts through a clearer understanding of educators’ perceived strengths and gaps. Method Clinician educators from 9 US academic institutions completed a self-assessment rating their performance across 4 universal pillars and 11 educational theory and practice competencies on a 1- (novice) to 5- (expert) point scale in 0.5-point increments from August to November 2024. Descriptive statistics and mean difference tests were used to analyze variation across demographic and professional characteristics. Results A total of 484 responses to at least 1 CEM were received. Respondents rated themselves highest in commitment to professional responsibilities (mean [SD], 4.30 [0.68]), teaching and facilitating learning (mean [SD], 3.96 [0.74]), and professionalism (mean [SD], 3.93 [0.73]) and lowest in medical education scholarship (mean [SD], 3.11 [1.15]), program evaluation (mean [SD], 3.33 [1.03]), and the science of learning (mean [SD], 3.43 [1.10]). Statistically significant group differences were found by years of posttraining clinical experience (F2,413 = 16.87, P < .001, η2 = .076), years of teaching experience (F2,433 = 20.87, P < .001, η2 = .088), and academic rank (F2,403 = 13.96, P < .001, η2 = .065). Conclusions This study identifies key trends in self-perceived strengths and needs among clinician educators and highlights the limited awareness of the CEM framework. As institutions aim to build effective educator development systems, the CEMs can serve as a useful structure for tailoring support to individuals and identifying institutional needs.

Abstract Background Left atrial appendage (LAA) closure or amputation is commonly performed in atrial fibrillation (AF) patients undergoing cardiac surgery to reduce stroke risk. It has been shown that LAA closure or amputation results in persistent blood pressure (BP) decrease, which may be due to a surge in atrial natriuretic peptide (ANP) and by suppression of sympathetic activity due to activation of mechanoreceptors by atrial distention. We hypothesize that size of the LAA, a compliant structure, affects atrial distension. Consequently, patients with smaller LAA remnants (i.e. more complete amputation) have more distension of the atrium and a more pronounced BP response upon LAA amputation. Methods We analyzed 33 patients with persistent AF from the MARK AF registry who underwent LAA amputation concomitant to thoracoscopic AF ablation. Systolic BP was measured at baseline, 12 hours (h), 24h, and 48h, 1 month, 1 year, and 2 years postoperatively. Complete amputation was defined as LAA remnant depth <10mm and a remnant LAA was defined as depth ≥ 10 mm on contrast enhanced CT 6 months post surgery. The postoperative LAA remnant/LA volume ratio was calculated by segmenting the atria and quantifying the volume of the contrast pools. T-tests and linear regression analyzed BP changes by remnant size and LAA remnant/LA volume ratio. Results were visualized using a boxplot and scatter plots with regression lines. Results 25/33 Patients had a LAA remnant. Baseline systolic BP was similar with 147 ± 31 mmHg in the complete amputation group vs. 137 ± 23 mmHg in the remnant group, p=0.389. Complete amputation correlated with greater systolic BP reductions in relation to baseline at 12h (-18%, p=0.018), 24h (-14%, p=0.025), 48h (-15%, p=0.028), 1 month (-20%, p=0.024), and 1 year (-16%, p=0.001), Figure 1. BP returned to baseline by 2 years in both groups. Lower LAA remnant/LA volume ratios were significantly associated with greater systolic BP reductions at 12h (β=7.4, p=0.005), 24h (β=9.9, p<0.001), 48h (β=10.1, p=0.002), and 1 month (β=11.1, p=0.01), Figure 2. However, this association was not observed at 1 and 2 years. Conclusion Patients with smaller LAA remnants after LAA amputation experienced a more pronounced transient reduction in blood pressure. Our findings suggest that increased atrial distension—due to the loss of compliant LAA tissue—could play a key role in modulating hemodynamics via sympathoinhibition and suppression of the Renin-Angiotensin-Aldosterone System (RAAS). Further investigation is needed to confirm these results and explore the neurohumoral effects of LAA amputation.Figure 1 Figure 2

Abstract Background The clinical efficacy of tafamidis in patients with transthyretin amyloid cardiomyopathy (ATTR-CM) was demonstrated during the phase 3, multinational, randomised, placebo-controlled Tafamidis in Transthyretin Cardiomyopathy Clinical Trial (ATTR-ACT).(1) In ATTR-ACT, the risk of any cardiovascular (CV)-related hospitalisation was significantly reduced among patients who received tafamidis meglumine 80 mg (the approved dose) vs placebo (relative risk ratio 0.70 [95% CI 0.57, 0.85]; P=0.0005).(2) The benefit of tafamidis treatment was largest among patients with New York Heart Association (NYHA) class I/II vs III symptoms at baseline.(1,3,4) Purpose ATTR-CM is a progressive disease with a natural history that typically includes an increasing frequency of CV-related hospitalisation as the condition worsens. This post hoc analysis adds to current knowledge by evaluating the risk of recurrent (≥1) CV-related hospitalisation by baseline NYHA class in ATTR-ACT patients taking the approved dose of tafamidis or placebo. Methods Patients aged 18 to 90 years with biopsy-confirmed wild-type or variant ATTR-CM and NYHA class I-III symptoms took part in ATTR-ACT between 2013 and 2018. During the trial, the cause of hospitalisation was adjudicated by an independent committee. The hazard ratio (HR) for first CV-related hospitalisation was calculated using a Cox proportional hazards model. The HR for recurrent CV-related hospitalisation was calculated using the Liu-Wei-Yang-Ying (LWYY; also known as the modified Anderson-Gill) model. Models compared tafamidis meglumine 80 mg vs placebo and adjusted for transthyretin genotype (wild-type or variant). In the overall population, the LWYY model was also adjusted for baseline NYHA class. Results The frequency of adjudicated CV-related hospitalisations during ATTR-ACT by NYHA class are shown in the Figure. Across patients who were NYHA class I-III at baseline, the risk of recurrent CV-related hospitalisation was 37% lower in those who received tafamidis vs placebo treatment (HR 0.627 [95% CI 0.463, 0.848]; P=0.0025; Table). Among those who were NYHA class I/II at baseline, a lower proportion of tafamidis- vs placebo-treated patients (44% vs 61%) had ≥1 CV-related hospitalisation. The risks of first and recurrent CV-related hospitalisation were 40% (HR 0.601 [95% CI 0.420, 0.861]; P=0.0055) and 55% (HR 0.449 [95% CI 0.305, 0.661]; P<0.0001) lower with tafamidis vs placebo treatment. Consistent with the survivor bias previously observed in ATTR-ACT,(1-4) the risk of recurrent CV-related hospitalisation was statistically similar in tafamidis- and placebo-treated patients who were NYHA class III at baseline (HR 1.113 [95% CI 0.688, 1.799]; P=0.6624). Conclusions Building on previous findings, this analysis found the risk of recurrent CV-related hospitalisation to be reduced by tafamidis meglumine 80 mg treatment in patients with early stage ATTR-CM.

Abstract Background Approximately one-third of patients with heart failure and preserved ejection fraction (EF) (HFpEF) have exercise-induced left atrial hypertension (EILAH), characterized by normal pulmonary capillary wedge pressure (PCWP) at rest, but with pathologic PCWP elevation during exercise. It has been proposed that EILAH may represent an early stage of HFpEF that progresses to resting LA hypertension (RELAH) over time, but this has never been shown. Purpose This observational study aimed to investigate the natural history of patients with EILAH, evaluating patients who underwent multiple invasive hemodynamic evaluations over time. Methods Consecutively-evaluated patients with HFpEF and EILAH (PCWP<15 mmHg at rest and ≥25 mmHg during exercise) who underwent subsequent invasive hemodynamic testing were identified. Prevalence and characteristics of transition to RELAH (PCWP≥15 mmHg at rest) were evaluated. Results Of 659 patients with EILAH, 84 underwent repeat invasive hemodynamic evaluations over a median follow-up of 1.81 (IQR 0.48-3.40) years (55 female, mean age 66 years). Of this group, 33 (39%) patients changed to RELAH and 51 (61%) remained EILAH. Patients with change to RELAH experienced greater increase in NT-proBNP (+16.6%; 95% CI: 7.1% to 26.0%, P<0.001), decreased left ventricular EF (-6.1%, 95% CI: -9.7 to -2.5, P=0.001), right ventricular (RV) global longitudinal strain (-4.5%, 95% CI: -8.8 to -0.3, P=0.037), RV free wall longitudinal strain (-7.3%, 95% CI: -13.1 to -1.6, P=0.013) and worsening tricuspid regurgitation (15% vs 2%, P=0.025) compared to those with no change (Figure 1). Upon invasive hemodynamic at rest, patients with change to RELAH experienced an increase in right atrial pressure (RAP) (+4.4 mmHg, 95% CI: 2.6 to 6.1, P<0.001) and mean pulmonary artery (PA) pressure (+6.6 mmHg, 95% CI: 4.2 to 9.0, P<0.001) (Figure 1). At the baseline, there were no significant differences in the exercise-induced increases in PCWP, mean PAP, and RAP between the two groups from rest to peak exercise (Figure 2). However, at the final evaluation, patients with change to RELAH displayed a greater increase in PCWP, mean PAP, and RAP during exercise as compared to those who remained EILAH (Figure 2). Of characteristics at the index evaluation, history of atrial fibrillation (OR 3.73; 95% CI 1.09-12.8, P=0.036), and lower resting PA compliance (OR 0.49; 95% CI 0.24-0.99, P=0.048) were independently associated with the transition to RELAH after adjusting the duration from baseline to final examination. Conclusions Approximately 40% of patients with HFpEF that first present with EILAH to RELAH, suggesting that EILAH can be considered an earlier form of HFpEF. History of atrial fibrillation and reduced PA compliance are associated with progression to RELAH, suggesting that interventions to address atrial myopathy and pulmonary vascular disease may be effective to attenuate or prevent this transition.

Abstract Introduction/Background Transthyretin amyloidosis (ATTR) is a debilitating disease that leads to progressive cardiac dysfunction. Tafamidis is the gold standard therapy for ATTR cardiomyopathy. In recent observational studies, sodium-glucose cotransporter-2 inhibitors (SGLT2-Is) have demonstrated cardiovascular benefits in ATTR cardiomyopathy, but their role in ATTR cardiomyopathy as combination therapy with tafamidis remains unclear. Purpose To investigate the impact of combination therapy with tafamidis and SGLT2-Is versus just tafamidis in patients with known ATTR cardiomyopathy. Methods This retrospective cohort study utilized data from the TriNetX multinational database. Patients diagnosed with ATTR cardiomyopathy who received tafamidis were identified and stratified into two cohorts based on SGLT2-I use. Outcomes were assessed over three years, including all-cause mortality, all-cause hospitalizations, acute myocardial infarction (AMI), acute heart failure (HF) hospitalizations, ischemic stroke, atrial fibrillation/flutter, end-stage renal disease (ESRD) or requirement for renal replacement therapy, and ventricular tachycardia. Propensity score matching was used to balance both cohorts based on clinical comorbidities, medication use, and laboratory data. Adjusted odds ratios (OR) were calculated by logistic regression models. Results After propensity score matching, 409 patients were included in each cohort with a follow-up duration of 722 days (SD 320.87) for the SGLT2-I cohort and and 755.90 days (SD 363.26) for the non-SGLT2-I cohort. SGLT2-Is were associated with significantly lower rates of all-cause hospitalizations (41.1% vs. 50.9%; OR 0.67 [p = 0.005]) and AMI (6.6% vs. 13.9%, OR 0.44 [p = 0.001]), which persisted by three years (all-cause hospitalizations: 52.1% vs. 61.4%, OR 0.67 [p = 0.006] and myocardial infarction: 11.2% vs. 18.3%, OR 0.56 [p = 0.004]). No significant differences among the two cohorts were observed for all-cause mortality, acute HF hospitalizations, ischemic stroke, atrial fibrillation/flutter, ventricular tachycardia, or ESRD/need for renal replacement therapy. Conclusions SGLT2-Is, in combination with tafamidis, are associated with decreased all-cause hospitalizations and AMI in ATTR cardiomyopathy. While a mortality benefit was not demonstrated, these results depict the magnitude of clinical benefit derived from combination therapy with tafamidis and SGLT2-Is as opposed to prior observational studies which investigated SGLT2-I single therapy

Abstract Background Coronary flow augmentation occurs through the simultaneous interaction and regulation of both endothelium-dependent and endothelium-independent mechanisms. A decrease in coronary flow reserve (CFR) secondary to either mechanism is associated with poor prognosis. However, at the individual level, the integrated impact of these two mechanisms has not been thoroughly investigated. Purpose This study investigated the prognostic implications of an integrated metric, CFRsum, combining endothelium-dependent and -independent CFR. Methods A total of 1441 patients with angina with non-obstructive coronary artery (ANOCA) undergoing coronary reactivity testing were studied. Endothelium-independent CFR was measured during adenosine-induced hyperemia, and endothelium-dependent CFR during intracoronary acetylcholine infusion. CFRsum was calculated by summing these components. Cardiovascular event was defined as composite of cardiovascular death, myocardial infarction, heart failure, and cerebral infarction. Results Our patients had a median age of 51.7 years, 69.0% of whom were female, and their CFRsum was 4.57 [3.88, 5.37]. Patients were divided into three tertile-based groups, and Cox proportional hazards analysis demonstrated that all CFR classes were independent predictors of prognosis, with CFRsum providing the best model fit (Likelihood ratio: 54.62, degrees of freedom: 7, P < 0.001). The Kaplan-Meier curve (Figure) demonstrated a stepwise deterioration in prognosis across CFRsum tertile groups, with lower CFRsum being associated with progressively worse outcomes (p < 0.001). Stratification by follow-up duration (3 years) revealed that patients with middle-range CFRsum exhibited comparable outcomes to those with the highest CFRsum during the early phase (<3y) but significantly worse outcomes in the late phase (≥3y) (P = 0.459 and P < 0.001, respectively). Conclusion CFRsum showed superior prognostic value over traditional CFR metrics in patients with ANOCA, identifying a compensated group with time-varying outcomes. This novel metric improves the assessment of microvascular function and supports better clinical management.

Abstract Introduction Arteriovenous fistulas (AVF) are the preferred method for establishing long-term, reliable vascular access in patients undergoing haemodialysis for end-stage renal disease. However, previous research has shown that high-flow AVFs may increase cardiovascular strain after kidney transplantation, often necessitating fistula closure in these patients. Currently, there is no established guideline for managing high-flow fistulas in post-transplant patients with stable kidney function, and the haemodynamic effects of AVF closure are unknown. Objective This study aims to perform a systematic review and meta-analysis of haemodynamic and echocardiographic changes following AVF closure compared to AVF persistence. Methods We systematically searched PubMed, Cochrane, and Web of Science up to December 2024 for observational studies or randomised controlled trials (RCTs), including patients with chronic kidney disease (CKD) undergoing AVF ligation versus maintenance. Key parameters indicative of cardiac and renal function were assessed. The statistical analysis was performed on Cochrane’s RevMan tool, using random effects model. Heterogeneity was assessed through I² statistics. Results We included 841 patients from 12 studies, 10 observational and 2 RCTs. 406 (48.2%) patients underwent AVF ligation, and follow-up ranged from 3 to 62.5 months. Arteriovenous fistula ligation was associated with a decrease in left ventricular mass index (MD -10.88 g/m²; 95% CI -17.84, -3.93; p=0.007; I²=8%; Figure 1A), left ventricular end diastolic volume (MD -19.55 ml; 95% CI -20.52, -18.58; p=<0.00001; I²=0%; Figure 1B), and cardiac index (MD -0.56 1/min/m²; 95% CI -1.05, -0.07; p=0.03; I²=70%; Figure 1C). There was no significant difference in posterior wall thickness (MD -0.46 mm; 95% CI -1.32, 0.4; p=0.23; I2=57%), left ventricular ejection fraction (MD -0.12%; 95% CI -3.01, 2.77; p=0.92; I2=50%), and left ventricular end systolic volume (MD -6.28 ml; 95% CI -12.64, 0.07; p=0.05; I²=52%). Systolic blood pressure (MD -2.47 mmHg; 95% CI -9.57, 4.63; p=0.41 I²=62%; Figure 2A) and diastolic blood pressure (MD 1.54 mmHg; 95% CI -3.12, 6.19; p=0.44 I²=69%) were not significantly different between groups. Patients undergoing AVF ligation had a significant decrease in serum creatinine (MD -0.12 mg/dl; 95% CI -0.22, -0.03; p=0.02; I²=0%; Figure 2B), however, no difference was seen for eGFR (MD 2.78 ml/min/1.73 m²; 95% CI -3.25, 8.81; p=0.24; I²=2%; Figure 2C) between groups. Conclusion In chronic kidney disease patients, AVF ligation was associated with improved the patient’s overall echocardiographic parameters and reduced the risk of remodelling, with no significant blood pressure changes. Although creatinine seems to improve in this patient population, no differences were seen on eGFR. Further randomised studies are needed to better characterise the haemodynamic changes associated with AVF ligation.

Abstract Background Management of acute cardiogenic shock for post-cardiotomy and post-transplant patients remains challenging. The use of veno-arterial extracorporeal membrane oxygenation (VA-ECMO) for circulatory support is a key intervention, yet the optimal cannulation strategy—central vs. peripheral—remains debated. This study evaluates outcomes associated with each approach to inform clinical decision-making. Methods A retrospective analysis was conducted on 319 patients who received VA-ECMO for CS intraoperatively or within 24 hours postoperatively at Mayo Clinic (2010–2023). Patients were categorized into central (n=241) and peripheral (n=78) ECMO groups. Propensity score (PS) weighting using stabilized inverse probability of treatment weighting was applied to minimize baseline imbalances. Outcomes included in-hospital mortality, bleeding requiring reoperation, limb ischemia, prolonged ventilation (>7 days), and sepsis. Results The median age at ECMO initiation was 68.5 years, with 37.3% female patients. Right ventricular (RV) dysfunction was the predominant indication for ECMO initiation (p<0.001). After PS weighting, no significant difference was observed in in-hospital mortality (49.8% vs. 44.5%, p=0.416) or other major complications between central and peripheral ECMO (see Table 1). Stroke was more frequent in central ECMO (P = 0.159), though not statistically significant. Reoperation for bleeding occurred significantly more often in central ECMO in the unweighted analysis (P = 0.047), but the difference lost statistical significance after weighting (P = 0.071). Renal failure was comparable between groups (P = 0.888). Notably, sternal infection rates were comparable between groups (P=0.921). Acute limb ischemia was more common in the peripheral group (P = 0.209). Limb ischemia associated with central ECMO was not caused by the ECMO cannulas but was instead related to concomitant use of femoral intra-aortic balloon pump. Conclusions After propensity score weighting, analysis showed no significant differences in mortality or complications between central ECMO and peripheral ECMO for post-cardiotomy and post-transplant cardiogenic shock.

Abstract Background Renal denervation (RDN) has emerged as a promising therapeutic adjunct for the management of hypertension, yet its efficacy in the long term, particularly in patients with hypertension and concurrent renal insufficiency, remains to be fully elucidated. This study was designed to evaluate the sustained impact of RDN on blood pressure control, renal function, and cardiovascular outcomes in hypertensive patients with pre-existing renal impairment over an extended follow-up period. Methods We conducted a single-center, single-arm, real-world retrospective study involving patients with hypertension and chronic kidney disease (CKD) stages 3-4 who underwent RDN at a hospital between 2011 and 2016. Comprehensive baseline data, including demographic information, comorbidities, and medication history, were meticulously recorded. Long-term follow-up assessments were performed at 1, 5, and 11.5 years post-RDN to monitor changes in office and home blood pressure, 24-hour ambulatory blood pressure results, renal function, and the incidence of cardiovascular events and mortality. Results A total of 20 participants completed the long-term follow-up, with a mean age of 51.7 ± 14.5 years (35% female), and a median follow-up duration of 11.5 years. At baseline, the cohort presented with an average office systolic blood pressure of 183.8 ± 18.6 mmHg and a diastolic blood pressure of 104.7 ± 17.0 mmHg. Following RDN, participants experienced a significant reduction in blood pressure, with an average decrease of -37.94/-20.38 mmHg (P < 0.001) compared to baseline. Additionally, ambulatory systolic and diastolic blood pressures were reduced by 16.87 ± 9 mmHg (P < 0.001) and 9.88 ± 4.05 mmHg (P < 0.001) 11.5 years after the procedure, respectively. The study also revealed a substantial reduction in the need for antihypertensive medications (P < 0.001) and a decrease in average heart rate (P = 0.046) following renal denervation. Assessments of renal function, as measured by estimated glomerular filtration rate and creatinine levels, were consistent with expected age-related decline. Importantly, no significant adverse events associated with RDN were observed in the long-term follow-up. Over the 11.5-year period, the cardiovascular mortality rate and overall mortality were 10% and 20%, respectively. Conclusion This long-term follow-up study demonstrates that RDN is a safe and effective intervention for managing hypertension in patients with renal impairment.

Abstract Background Contemporary prevalence and penetrance of familial hypercholesterolemia (FH) and the associated coronary heart disease (CHD) risk across diverse genetic ancestries in the United States are unclear. Purpose To estimate prevalence of individuals harboring pathogenic/likely pathogenic (P/LP) variants in LDLR, APOB, and PCSK9, distribution of low-density-lipoprotein cholesterol (LDL-C) levels, and associated CHD risk for carriers in an ancestrally diverse cohort. Methods In 242,167 All of Us (AoU) participants with available whole-genome sequencing data, we obtained LDL-C measurements, statin prescriptions, and ascertained P/LP variants in FH-related genes and presence of CHD based on electronic-health record data. P/LP variants in LDLR, APOB, and PCSK9 were identified in AoU data by filtering for high-impact (frameshift, canonical splice site, indels, and stop gain) and predicted-deleterious missense variants, then selecting those classified as P/LP in ClinVar. Untreated LDL-C levels were estimated assuming a 30% reduction if there was a record of a statin prescription in the preceding 12 months and the highest value among multiple measurements for each individual were selected. Penetrance was defined as LDL-C>155 mg/dl. CHD was determined using a validated phenotyping algorithm based on diagnostic and procedural billing codes. Logistic regression models were used to obtain prevalence and penetrance estimates and odds ratios for CHD, along with associated 95% confidence intervals (95% CI). Results We identified 221 FH-related P/LP variants (LDLR=169, APOB=50, PCSK9=2) in the study cohort. Of 125,841 European (EUR), 53,367 African (AFR), 40,189 admixed American (AMR), and 22,770 other ancestry individuals, 1:218 (0.46%, 95% CI 0.42%-0.50%), 1:307 (0.33%,0.28%-0.38%), 1:350 (0.29%, 0.24%-0.34%), and 1:201 (0.50%, 0.41%-0.59%) were carriers of a P/LP variant. In 92,616 individuals with at least one LDL-C measurement, carriers of a P/LP variant had a higher distribution of LDL-C across all ancestries with similarly high penetrance (Figure 1). Harboring a P/LP variant in LDLR, APOB, and PCSK9 was associated with similarly increased odds of CHD across all the different ancestry groups (Figure 2). Conclusions Monogenic FH was prevalent, penetrant, and significantly associated with CHD similarly across diverse ancestry groups in the AoU cohort. These findings support a ‘genotype first’ approach to detection of FH to enable early intervention across diverse ancestry groups.Figure 1 Figure 2