Background/Objectives: The “weekend effect,” characterized by increased mortality and complication rates for weekend hospital admissions, is well documented in myocardial infarction and stroke but has been less thoroughly investigated in acute decompensated heart failure (ADHF). This study evaluates the weekend effect in ADHF using a national cohort. Methods: A retrospective cohort study was conducted using the 2016–2020 Nationwide Inpatient Sample (NIS). Adult ADHF admissions were identified by ICD-10 codes and classified as weekend or weekday admissions. Over 30 variables, including age, sex, and comorbidities, were analyzed. Propensity score matching (1:1) yielded 489,204 patients per group. Univariate and multivariate logistic regression models were used to assess outcomes, adjusting for key covariates. Results: Of 2,131,915 ADHF hospitalizations, 501,076 (23.5%) occurred on weekends. The cohort was 48% female, with a mean age of 72 years (SD ± 12.3). After 1:1 matching, weekend admissions had higher odds of cardiac arrest (aOR: 1.10; 95% CI: 1.06–1.13, p < 0.001), inpatient mortality (aOR: 1.07; 95% CI: 1.05–1.09, p < 0.001), acute kidney injury (AKI; aOR: 1.07; 95% CI: 1.06–1.08, p < 0.001), and acute respiratory failure (ARF; aOR: 1.28; 95% CI: 1.27–1.30, p < 0.001). No significant differences were observed in mechanical circulatory support (MCS) use or length of stay. Conclusions: Weekend ADHF admissions were associated with a higher risk of mortality and complications, which may be attributable to reduced specialist availability or delayed diagnostics. These findings underscore the need for standardized ADHF protocols to ensure equitable care throughout the week.

Aims: Current cardiogenic shock (CS) management primarily targets mean arterial pressure (MAP), often overlooking the impact of venous congestion on the effective perfusion gradient. Organ perfusion pressure (OPP = MAP – CVP) integrates both. We investigated OPP’s prognostic value for mortality, renal function, and resource utilization. Methods: This retrospective cohort study utilized Medical Information Mart for Intensive Care (MIMIC-IV) database, a single-center, critical care database, to identify adult CS patients. Patients with other forms of shock were excluded. Primary outcomes were in-hospital and intensive care unit (ICU) mortality. Secondary outcomes included ICU length of stay (LOS), vasopressors/inotropes duration (VID), urine output (UO) over the initial 36 hours, renal replacement therapy (RRT) and invasive mechanical ventilation. Multivariable models adjusted for demographics (age, sex), comorbidities (hypertension, diabetes, heart failure, atrial fibrillation, chronic kidney disease), and shock severity (cardiac arrest, vasoactive-inotropic score, maximum lactate) across standardized 12-hour landmarks. Results: Among 189 patients (mean age 65.3 ± 14.2 years, 65.6% male), prevalent comorbidities included coronary artery disease (52.4%) and heart failure with reduced ejection fraction (50.8%). Acute myocardial infarction was present in 26.5% of cases. Every 5 mmHg increase in 24-hour mean OPP was independently associated with reduced in hospital mortality (adjusted odds ratios [aOR] 0.79, 95% CI 0.65–0.96, P = .020). Higher OPP was associated with renal protection, with increased UO (+0.21 mL/kg/hr, P < 0.001) and reduced odds of RRT (aOR 0.65, P < .001). Conclusions: In CS, a higher OPP is independently associated with improved survival, renal preservation, and resource efficiency. OPP provided incremental value especially for renal outcomes. Prospective interventional trials are mandatory for validation.

Pathogenic transthyretin (TTR) variants, such as V142I, demonstrate incomplete, age-dependent penetrance and may be present in patients without clinical transthyretin cardiac amyloidosis cardiomyopathy (ATTR-CM). Distinguishing true ATTR-CM from phenocopies like apical HCM (ApHCM) is critical to guide management. A 61-year-old African-American male with longstanding ApHCM was found to carry the pathogenic TTR V142I variant. Despite genotype positivity, technetium-99m pyrophosphate scintigraphy (H/CL 1.01, visual grade 0) excluded ATTR-CM, and cardiac magnetic resonance imaging confirmed apical-predominant hypertrophy with patchy late gadolinium enhancement consistent with ApHCM. The patient remained stable on medical therapy with ongoing surveillance. This case illustrates genotype-phenotype discordance in TTR carriers and highlights the importance of integrating genetic data with multimodality imaging. Recognition of phenocopies in patients with the TTR gene prevents misdiagnosis and unnecessary therapy and emphasizes the need for longitudinal surveillance in at-risk patients. TTR genotypes can be associated with an HCM phenotype. Clinical and imaging correlation is essential to interpret genetic findings and avoid misdiagnosis.

Heart failure (HF) continues to be a major global health burden, with persistent morbidity and mortality despite guideline-directed and device-based therapies. Evidence suggests the gut–heart axis is a critical and underrecognized contributor to HF progression. Alterations in cardiac output and systemic venous congestion in HF lead to intestinal hypoperfusion, mucosal edema, and loss of barrier integrity, increasing intestinal permeability, gut dysbiosis, and translocation of microbial products. This systemic translocation is associated with chronic low-grade inflammation that activates innate immune pathways that correlate with endothelial dysfunction, oxidative stress, fibroblast activation, and adverse cardiac remodeling. Gut-derived metabolites derived by microbial metabolism modulate cardiovascular health by altering the metabolic profiles. Dysbiosis results in loss of protective short-chain fatty acid (SCFA)-producing bacteria and enriches pro-inflammatory taxa such as trimethylamine N-oxide (TMAO)-producing bacteria. Elevated TMAO is associated with increased mortality and hospitalization in HF, whereas SCFAs enhance barrier integrity and immune tolerance. Secondary bile acids and uremic toxins such as indoxyl sulfate and p-cresyl sulfate further link dysbiosis to fibrosis and vascular stiffness. Circulating markers such as TMAO, lipopolysaccharide-binding protein (LBP), and soluble CD14 carry prognostic value beyond traditional cardiac biomarkers. This review highlights current experimental, translational, and clinical evidence describing gut dysbiosis and its molecular links to HF progression. Targeting the gut–heart axis represents a novel therapeutic approach in HF. Dietary modulation, probiotics/prebiotics, fecal microbiota transplantation, and inhibitors of microbial metabolic pathways show promise. Future research should emphasize microbiota-based interventions in HF management.

Background: Traditional echocardiographic assessment of aortic stenosis (AS) using aortic valve area (AVA) may overestimate severity due to pressure recovery phenomena, while subclinical myocardial dysfunction remains undetected despite preserved ejection fraction. This study evaluated whether energy loss index (ELI)—which accounts for pressure recovery—demonstrates superior correlation with global longitudinal strain (GLS), a marker of subclinical myocardial dysfunction, compared to conventional AVA-based classification in patients with moderate-to-severe AS and preserved left ventricular ejection fraction (LVEF). Methods: This retrospective single-center study analyzed 149 patients with moderate-to-severe AS (AVA < 1.5 cm²) and LVEF > 50% from 2015 to 2019. Among 97 patients with severe AS by AVA (<1.0 cm²), ELI was calculated using the formula ELI = (AVA × Aa)/(Aa − AVA) ÷ BSA, where Aa represents sinotubular junction cross-sectional area. Patients with ELI ≥ 0.6 cm²/m² were reclassified as moderate AS. Spearman correlation assessed relationships between AVA, ELI, and GLS. Multivariable linear regression models determined independent predictors of myocardial dysfunction, adjusting for age, body surface area, hypertension, LVEF, and mean pressure gradient. Results: ELI reclassified 28 of 97 patients (29%) from severe to moderate AS. Reclassified patients had significantly better myocardial function, with less impaired GLS (−15.0 ± 3.9% vs. −12.1 ± 5.0%, p = 0.013) and higher LVEF (60.1 ± 6.2% vs. 56.5 ± 9.1%, p = 0.017) compared to non-reclassified patients. In the overall cohort, ELI demonstrated stronger correlation with GLS than AVA (r = −0.307, p = 0.0003 vs. r = −0.209, p = 0.0115). Critically, among patients with severe AS by AVA criteria, ELI maintained significant correlation with GLS (r = −0.443, p = 0.0003) while AVA showed no correlation (r = −0.144, p = 0.159). In multivariable analysis, ELI independently predicted GLS (β = 5.847, 95% CI: 2.85–8.84, p = 0.0002; adjusted R² = 0.289), whereas AVA did not (β = 2.234, 95% CI: −1.08 to 5.55, p = 0.188; adjusted R² = 0.234). When both parameters were included simultaneously, only ELI remained significant (p = 0.0024). Conclusions: In this retrospective cohort, ELI-based reclassification identified a subgroup of patients with less severe myocardial dysfunction as measured by GLS and LVEF, and ELI demonstrated superior correlation with subclinical myocardial dysfunction compared to AVA. These findings suggest ELI may provide a more physiologically reflective assessment of hemodynamic burden in AS with preserved LVEF. However, the absence of systematic symptom assessment and clinical outcome data represents critical limitations. Prospective studies with standardized symptom evaluation, longitudinal follow-up, and adjudicated clinical endpoints are required to determine whether ELI-based reclassification improves risk stratification and clinical decision-making before this approach can be recommended for routine practice.

Background/Objectives: Atrial fibrillation (AF) is a significant and prevalent cardiovascular complication in end-stage renal disease (ESRD) patients, yet its specific predictors within this population are not well understood. This study aimed to identify the predictors of new-onset AF in ESRD patients undergoing dialysis. Methods: We conducted a retrospective multicenter cohort study within the Northwell Health System, analyzing data from 5326 ESRD patients on dialysis between 2017 and 2019. The mean age was 64.2 ± 13.1 years, with 48.3% females. Multivariable-adjusted logistic regression was used to identify predictors of new-onset AF, the primary outcome. Adjusted odds ratios (ORs) were calculated for potential risk factors. Results: Of the 5326 patients, 1564 (29.4%) developed new-onset AF. Significant predictors included increasing age (OR 1.038 per year, 95% CI 1.032–1.044, p < 0.0001), obesity (BMI > 30 vs. BMI 20–25: OR 1.208, 95% CI 1.026–1.422, p = 0.023), and coronary artery disease (OR 1.678, 95% CI 1.466–1.920, p < 0.0001). African American patients had lower odds of developing AF compared to White patients (OR 0.578, 95% CI 0.494–0.676, p < 0.0001). Hypertension, sex, diabetes, and tobacco use were not significantly associated with AF risk. Conclusions: Age, obesity, and coronary artery disease are significant predictors of new-onset AF in ESRD patients on dialysis. Notable racial disparities exist, with African American patients having a lower risk. These findings may inform targeted prevention strategies and guide future research into the mechanisms underlying AF in ESRD patients.