Search Results (2,010)

Metabolic dysfunction-associated steatotic liver disease (MASLD) and heart failure (HF) frequently coexist within a shared cardiometabolic environment, yet their mitochondrial abnormalities are stage- and phenotype-dependent rather than uniform. In MASLD, mitochondrial adaptation evolves from increased oxidative metabolism in early steatosis toward impaired respiratory flexibility, oxidative stress, and defective quality control with disease progression, whereas the failing myocardium develops reduced energetic reserve and altered substrate utilization. These organ-specific disturbances can modify mitochondria-linked metabolites, mitochondrial damage-associated molecular patterns, stress-responsive endocrine mediators, and extracellular vesicle-associated mitochondrial cargo. However, similar mitochondrial abnormalities or circulating signals in the liver and heart do not by themselves establish direct inter-organ communication. This review distinguishes shared systemic drivers and organ-intrinsic mitochondrial stress from source-resolved cardio-hepatic signaling, highlighting hepatic ketogenesis, fibroblast growth factor 21 (FGF21), mitochondrial DNA (mtDNA)-dependent inflammatory pathways, and extracellular vesicle-mediated cargo transfer as mechanistically distinct examples with different levels of evidence. We further discuss biomarker limitations, HF-related hemodynamic liver injury, and therapeutic strategies ranging from established cardiometabolic unloading to emerging mitochondria-centered interventions. A stage-, phenotype-, and source-resolved framework may improve interpretation of mitochondrial signals and guide future mechanistic and translational studies in the MASLD–HF overlap. Full article

Cardiometabolic multimorbidity is highly prevalent among postmenopausal women and is associated with adverse metabolic outcomes and a greater burden of climacteric symptoms. This secondary analysis of a quasi-experimental controlled clinical trial investigated the effects of a 12-week aerobic training program on climacteric symptoms, menopause-related quality of life, body composition, and cardiometabolic biomarkers in postmenopausal women with and without cardiometabolic multimorbidity. Forty-one postmenopausal women (50–70 years) were allocated to a single-cardiometabolic-condition group (SINGLE, n = 18) or a multimorbidity group (MULTI, n = 23) and completed supervised walking/jogging aerobic exercise three times per week at 65–75% of heart rate reserve. Climacteric symptoms, quality of life, anthropometric measures, body composition, and biochemical markers were assessed before and after the intervention. Generalized Estimating Equations (GEEs) with Bonferroni post hoc adjustment were used to compare group, time and group*time interactions with alpha of 5%. Significant group-by-time interactions were observed for the Menopause Rating Scale total score and psychological symptoms, as well as for the Cervantes Scale total score, indicating greater improvements among women with multimorbidity. The MULTI group demonstrated significant reductions in overall menopausal symptoms, psychological symptoms, and menopause-related quality of life scores following training. Body weight, triglycerides, and very-low-density lipoprotein cholesterol also decreased significantly only in the MULTI group, whereas several body composition parameters improved over time regardless of cardiometabolic burden. These findings indicate that aerobic training may be associated with improvements in menopausal symptoms, quality of life, body composition, and selected cardiometabolic markers in postmenopausal women, with some outcomes showing greater changes among women with cardiometabolic multimorbidity. Full article

Background: Acute kidney injury (AKI) is associated with poor outcomes in patients with cirrhosis. However, most studies evaluate AKI as a single clinical entity, whereas predictors of mortality and renal recovery, specifically in non-hepatorenal syndrome AKI (non-HRS-AKI), remain poorly defined. Methods: We performed a retrospective cohort study including consecutive patients with liver cirrhosis admitted with non-HRS-AKI to a multidisciplinary emergency hospital between 1 January 2024 and 31 December 2025. Only variables available at hospital admission were included in the multivariable analyses. Independent predictors of in-hospital mortality and factors associated with incomplete renal recovery in survivors at hospital discharge were identified using multivariable logistic regression. Results: A total of 139 patients were included. Overall, 57 patients (41.0%) died during hospitalization. Among the 82 survivors, complete renal recovery occurred in 35 cases (42.7%), whereas 47 patients (57.3%) had incomplete renal recovery at discharge. Independent predictors of in-hospital mortality were a higher MELD-Na score (adjusted OR 1.16 per 1-point increase, 95% CI 1.07–1.26; p < 0.001), an advanced AKI stage (KDIGO stage 3 vs. stage 1, adjusted OR 6.71, 95% CI 1.73–26.04; p = 0.006), the absence of pre-existing chronic kidney disease (adjusted OR 0.233, 95% CI 0.085–0.644; p = 0.005), and higher admission C-reactive protein (adjusted OR 1.12 per 10 mg/L increase, 95% CI 1.01–1.23; p = 0.029). Factors independently associated with incomplete renal recovery among hospital survivors at hospital discharge were pre-existing heart failure (adjusted OR 3.07, 95% CI 1.10–8.62; p = 0.033) and higher admission C-reactive protein (adjusted OR 1.17 per 10 mg/L increase, 95% CI 1.00–1.34; p = 0.047). Conclusions: In patients with cirrhosis-associated non-HRS-AKI, in-hospital mortality was primarily associated with the severity of liver disease and AKI, whereas incomplete renal recovery at hospital discharge was independently associated with pre-existing heart failure. Admission C-reactive protein was independently associated with both outcomes, supporting the role of systemic inflammation in determining short-term prognosis and suggesting that C-reactive protein may serve as a simple, readily available biomarker for early risk stratification. Full article

The heart–kidney axis has emerged as a central framework for understanding the bidirectional interactions that drive cardiorenal syndrome and broader cardiovascular–kidney–metabolic (CKM) disease. However, existing interpretations have often emphasized hemodynamic and neurohormonal mechanisms without fully integrating the growing evidence for endocrine, inflammatory, and metabolic mediators that coordinate injury across organs. This Review was therefore undertaken to provide an updated and clinically relevant synthesis of the physiological basis of heart–kidney communication, the mechanisms underlying its disruption, and the therapeutic implications of these insights. To achieve this aim, we performed a systematic narrative review of the literature using PubMed, Embase, Web of Science, and Scopus for studies, supplemented by manual screening of reference lists. Priority was given to original studies, large cohort analyses, randomized controlled trials, meta-analyses, and authoritative reviews. We integrated evidence spanning physiological regulation, maladaptive signaling pathways, emerging mediators, experimental models, and evolving treatment strategies. The reviewed evidence indicates that heart–kidney crosstalk is driven not only by altered perfusion and venous congestion, but also by sustained activation of the renin–angiotensin–aldosterone system (RAAS) and sympathetic nervous system (SNS), inflammation, oxidative stress, mitochondrial dysfunction, anemia, uremic toxins, and disordered mineral metabolism. Among novel mediators, fibroblast growth factor 23 (FGF23) emerges as a major bone-derived, chronic kidney disease (CKD)-associated endocrine mediator linking renal injury to cardiac hypertrophy, fibrosis, calcium mishandling, and diastolic dysfunction, whereas Klotho appears to exert counter-regulatory protective effects. Heart-derived natriuretic peptides, including atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), remain important modulators of renal blood flow, natriuresis, and volume homeostasis. We further highlight the translational relevance of newer biomarkers and therapies, including sodium–glucose cotransporter 2 inhibitors (SGLT2is), glucagon-like peptide-1 receptor agonists (GLP-1 receptor agonists), and mineralocorticoid receptor antagonists (MRAs), which may help address cardiac and renal dysfunction in parallel. Overall, this Review supports a revised conceptual model in which the heart–kidney axis is governed by multidirectional hemodynamic, neurohormonal, immune, and endocrine signaling networks. A more integrated understanding of these mechanisms may improve biomarker discovery, refine risk stratification, and promote therapies that target both organs simultaneously. Full article

The interferon regulatory factor (IRF) family exerts dual regulatory roles in vascular inflammation. Pro-inflammatory IRF1/3/5/7 drive endothelial dysfunction, macrophage M1 polarization, vascular smooth muscle cell (VSMC) transdifferentiation, and adaptive immune amplification via nuclear factor-κB (NF-κB), NOD-like receptor pyrin domain-containing 3 (NLRP3), cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), and Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathways. Conversely, IRF4/8 mediate anti-inflammatory effects by promoting M2 polarization, reverse cholesterol transport, and dendritic cell regulation. In atherosclerosis, IRFs display spatiotemporal specificity: endothelial IRF3 in early stages, macrophage IRF1/5 in mid-stages, and smooth muscle IRF7/IRF8 in late stages, supporting phase-specific precision interventions—early IRF3 blockade, mid-stage modulation of IRF5/IRF4 balance, and late combined inhibition of IRF7/8 to stabilize plaques. IRFs also critically participate in hypertensive remodeling, acute coronary syndrome, heart failure, and aortic aneurysm through conserved innate and adaptive immune axes, highlighting their potential as cross-disease biomarkers and therapeutic targets. Major challenges include network redundancy and functional compensation, necessitating single-cell multi-omics and targeted delivery systems for spatiotemporally precise, individualized modulation. Full article

Background and Objectives: Although modern oncologic therapies have substantially improved cancer survival and overall prognosis, they have also led to an increasing burden of cardiovascular toxicity. Preventing severe complications such as heart failure and death remains a major priority, while maintaining the need for effective and potentially curative cancer therapy. Careful patient monitoring and early detection of cardiovascular complications may allow the timely implementation of cardioprotective strategies and treatments that could delay or prevent myocardial toxicity. Materials and Methods: A total of 92 women with breast cancer were enrolled in a prospective observational cohort study. All patients received an anthracycline-based chemotherapy regimen, cyclophosphamide, docetaxel and trastuzumab. Biomarker assessment, including NT-proBNP, high-sensitivity cardiac troponin I (hs-cTnI), Gal-3, and GDF-15, was performed at baseline and at the initiation of trastuzumab-based therapy. A comprehensive diastolic function assessment was performed, including transmitral Doppler flow parameters and tissue velocities. Patients were followed for 12 months, and all cardiovascular events occurring during the follow-up period were recorded. Results: Biological and ecocardiographic parameters were analyzed and multiple models of prediction were made. To identify predictors of estimated left ventricular filling pressure (eLVFP), stepwise multiple linear regression analyses were performed, and four significant predictors of left ventricular end-diastolic filling pressure were identified: one echocardiographic parameter (baseline LV filling pressure) and three biological variables (changes in Gal-3, GDF-15, and hs-cTnI levels after treatment). The overall regression model was highly significant (p < 0.001) and explained 77.07% of the variance in the dependent variable. Gal-3 was the strongest predictor of left ventricular filling pressure (p < 0.001). Conclusions: The regression analyses suggest that this phenotype is multifactorial, with echocardiographic indices capturing the functional component and circulating biomarkers reflecting complementary aspects of the underlying biological response. This multimodal approach may therefore help identify patients with early treatment-related cardiac changes and potentially those at increased risk of subsequent CTRCD, particularly during a period when conventional LVEF-based surveillance may still appear reassuring. Full article

Background: Hypertensive emergencies are severe clinical conditions characterized by sudden elevation of blood pressure accompanied by acute target organ damage, including cardiovascular, cerebrovascular, renal, and retinal complications. Although blood pressure elevation is the defining feature, accumulating evidence indicates that activation of the renin–angiotensin–aldosterone system (RAAS) may play a central role in the molecular and cellular mechanisms underlying vascular injury. This review critically examines the current evidence regarding the involvement of the RAAS in the pathophysiology of hypertensive emergencies, highlighting its contribution to endothelial dysfunction, oxidative stress, inflammation, microvascular damage, and target organ injury, as well as its therapeutic implications and future research perspectives. Methods: A comprehensive narrative review of the literature was conducted using narrative reviews, systematic reviews, meta-analyses, experimental, translational, and clinical studies published in major biomedical databases, with particular emphasis on recent evidence addressing RAAS signaling, hypertensive emergencies, target organ damage, and emerging therapeutic approaches. Current international guidelines and landmark studies were also considered to provide an updated overview of the diseases. Results: Available evidence indicates that excessive activation of the classical ACE/angiotensin II/AT1 receptor axis contributes to acute vasoconstriction, endothelial dysfunction, reactive oxygen species generation, inflammatory activation, impaired vascular autoregulation, and microvascular injury, thereby promoting acute damage to the brain, heart, kidneys, retina, and large arteries. Conversely, the counter-regulatory ACE2/angiotensin-(1–7)/Mas receptor axis exerts protective vascular effects, although its role in hypertensive emergencies is unclear. Current therapies primarily focus on controlled blood pressure reduction, whereas the potential benefits of targeted RAAS modulation during the acute phase remain uncertain. Conclusions: The RAAS may play an important role in the pathophysiological processes underlying hypertensive emergencies, extending beyond its classical function of blood pressure regulation. However, direct human evidence remains limited and heterogeneous, warranting caution in interpreting these findings. A deeper understanding of the interactions between RAAS activation, vascular dysfunction, and target organ injury could help identify potential biomarkers and therapeutic targets, ultimately contributing to improved management and prognosis in patients with hypertensive emergencies. Full article

The integration of digital therapeutics (DTx), wearable electronic devices, and artificial intelligence (AI) represents a significant advancement in personalized healthcare. The primary purpose of this structured narrative review is to evaluate the convergence of these technologies, providing a consolidated framework that bridges the gap between raw biometric data acquisition and actionable, AI-driven clinical insights. This paper synthesizes the latest literature on the intersection of mobile health (mHealth), machine learning (ML), and physiological tracking, with a primary focus on heart rate variability (HRV) and associated biochemical markers, such as cortisol, salivary alpha-amylase, and interleukins. Instead of viewing wearable outputs simply as raw data, we critically evaluate the technical verification and clinical validation required to define them as true “digital biomarkers.” By evaluating multimodal sensor technologies and advanced predictive algorithms, this paper outlines the clinical utility of digital biomarkers in diagnosing and proactively managing cardiovascular, neurological, metabolic, and psychiatric conditions, noting classification accuracies frequently exceeding 85% in controlled settings. However, we strongly caution that internally validated performance in controlled settings does not inherently demonstrate external clinical utility. The clinical relevance of this study lies in its holistic approach to identifying how continuous monitoring can broaden healthcare accessibility while improving precision medicine. Furthermore, it deeply addresses the technical challenges of highly variable ambulatory data quality, the necessity for robust artifact reduction (e.g., via LSTM and GAN architectures), and the limitations of small, homogeneous training datasets. We highlight the essential need for demographic-aware algorithmic models, external validation, and decentralized privacy-preserving models (e.g., federated learning) in diverse populations to ensure the safe, equitable clinical translation of DTx, mHealth, ML, and AI technologies. Full article

Cardiopulmonary bypass (CPB) alters blood flow patterns and may induce endothelial activation; however, the effects of different CPB configurations on endothelial-associated biomarkers remain unclear. In this exploratory pilot study, we compared circulating biomarkers and tissue immunohistochemical findings between beating-heart partial CPB and cardioplegic total CPB in juvenile pigs. Ten 8-week-old female crossbred piglets underwent partial CPB with continued cardiac beating (n = 5) or total CPB with aortic cross-clamping and cardioplegic arrest (n = 5) for 60 min. Serum vascular cell adhesion molecule-1 (VCAM-1), a disintegrin and metalloproteinase-17 (ADAM-17), and thrombospondin-1 (TSP-1) concentrations were measured using an enzyme-linked immunosorbent assay, and tissue VCAM-1 and platelet endothelial cell adhesion molecule-1 (PECAM-1) were assessed immunohistochemically. At the end of the CPB procedure, serum VCAM-1 was higher in the total CPB group than in the partial CPB group (581 [339–759] ng/mL vs. 239 [224–304] ng/mL; |rank-biserial r| = 0.84 (95%CI, 0.36 to 1.00); Hodges–Lehmann estimate of the location shift = 341.7 ng/mL, 95% CI, 5.1–607.0 ng/mL; p = 0.03), whereas ADAM-17 and TSP-1 and tissue findings showed no consistent intergroup differences. Total CPB was associated with an early increase in circulating VCAM-1. Because the CPB configurations differed in several physiological and procedural factors, this response should be interpreted as configuration-associated rather than as evidence of an isolated effect of reduced pulsatility. Full article

Background/Objectives: Age may influence myocardial recovery after acute myocardial infarction (AMI) beyond changes in left ventricular ejection fraction (LVEF). We investigated age-related patterns in ischemic delay, admission biomarkers, biventricular function, myocardial deformation, and exploratory patterns of prescribed heart failure guideline-directed medical therapy (HF-GDMT) classes after primary percutaneous coronary intervention (PCI). Methods: This prospective frequency-matched cohort study included 90 AMI patients treated with primary PCI, stratified into younger (25–44 years; n = 30) and older (≥45 years; n = 60) groups. Clinical data, ischemic time, cardiac biomarkers, serial echocardiography at baseline, 6, and 12 months, and HF-GDMT intensity were analyzed. Results: Older patients had longer pain-to-balloon time (720 [480–1230] vs. 540 [420–660] min; p = 0.021), higher hs-cTnI (p = 0.045), and higher NT-proBNP (4776 [3013–5952] vs. 833.5 [95.7–1939.5] pg/mL; p < 0.001). Baseline and 12-month LVEF were similar between groups. Younger patients showed greater 12-month global longitudinal strain (GLS) improvement (−3.7 [−5.1 to −1.9] vs. −2.3 [−3.0 to −1.3] percentage points; p = 0.002), despite comparable absolute GLS. In exploratory post hoc analyses, prescribed HF-GDMT drug-class count showed an association with LVEF change primarily in older patients, who also had significantly lower baseline LVEF (ρ = 0.59; p < 0.001). Conclusions: In this prospective exploratory cohort, 12-month conventional systolic recovery assessed by LVEF and absolute GLS was comparable between age groups after primary PCI. However, the older comparator group had longer ischemic delay and higher admission biomarkers reflecting cardiomyocyte injury and myocardial wall stress, while younger patients showed greater longitudinal GLS improvement over time. These findings suggest that age-stratified recovery after AMI is better characterized by ischemic timing, baseline biomarker profile, and deformation trajectory than by LVEF alone. Because infarct size was not directly quantified, admission biomarker differences should not be interpreted as evidence of larger infarcts. Full article

Kawasaki disease (KD) is an acute, self-limiting systemic vasculitis that mainly affects young children. It is the leading cause of acquired heart disease in the developed world and is unique among childhood vasculitides for its predilection toward coronary artery involvement. This review describes the clinical spectrum of KD, highlighting diagnostic difficulties, especially in atypical presentations, and the challenges of managing treatment resistance. While intravenous immunoglobulin and aspirin remain the standard of care, especially in reducing coronary inflammation, early recognition and prompt therapy are crucial to preventing lifelong cardiac complications. To support this, various clinical risk scores have been developed over the decades to predict coronary artery lesions and IVIG resistance, enabling earlier intensification of treatment to prevent cardiac complications. Although the etiopathogenesis of KD remains unknown, extensive and robust research is ongoing to identify biomarkers, including epigenetic markers, innate and adaptive immunity activation markers, cytokine profiles, and to explore the influence of external triggers and the gut microbiome–immunity interplay. This review attempts to provide a concise overview of KD, aiming to assist clinicians in understanding the complexity of the problem rather than addressing all issues in detail. Full article

Heart failure (HF) is a systemic syndrome in which prognosis depends on cardiac dysfunction, congestion, cardiorenal and cardiohepatic interactions, inflammation, and metabolic dysregulation. The liver is exposed to elevated systemic venous pressure and reduced forward flow, and contributes to albumin and coagulation factor synthesis, bile acid metabolism, iron homeostasis, and the acute-phase response. Cardiohepatic injury involves hemodynamic stress, sinusoidal endothelial dysfunction, oxidative stress, inflammatory signaling, fibrogenesis, and altered metabolic regulation. Congestive hepatopathy is associated with right-sided HF, tricuspid regurgitation (TR), pulmonary hypertension, and elevated central venous pressure, whereas hypoxic hepatitis develops during low-output states, shock, or acute circulatory deterioration. These mechanisms may coexist, producing congestive/cholestatic, hypoperfusive/ischemic and mixed/systemic reserve profiles. Composite liver-related scores, including Model for End-Stage Liver Disease (MELD), MELD excluding International Normalized Ratio (MELD-XI), MELD with sodium (MELD-Na), MELD-Albumin and albumin–bilirubin (ALBI) score, may reflect congestion, hepatorenal dysfunction, nutritional status and reduced systemic reserve. This review summarizes hemodynamic and molecular mechanisms of cardiohepatic injury, liver-related biomarkers and composite scores, with emphases on advanced HF, left ventricular assist device (LVAD) therapy and heart transplantation. Liver-related abnormalities remain underrecognized in HF. Their serial interpretation may support risk stratification, but composite scores should complement rather than replace comprehensive clinical assessment. Full article

(1) Introduction: Early identification of patients at high risk of recurrent events after hospitalization for acute decompensated heart failure (ADHF) remains challenging. The Larissa Heart Failure Risk Score (LHFRS) is a simple prognostic tool based on hypertension, coronary artery disease, and red blood cell distribution width. Urinary sodium has recently emerged as an objective marker of natriuretic response and decongestion. We prospectively evaluated whether incorporation of urinary sodium improves the prognostic performance of the LHFRS. (2) Methods: This prospective single-center observational study enrolled 130 consecutive adults hospitalized with ADHF. Clinical, laboratory, electrocardiographic, and echocardiographic data were collected at admission. Spot urinary sodium and chloride were measured at admission and 2 h after intravenous loop diuretic administration according to a standardized decongestion protocol. The primary endpoint was heart failure rehospitalization within 3 months. Secondary endpoints included all-cause mortality and the composite of death or heart failure rehospitalization. Multivariable logistic regression with bootstrap internal validation (1000 resamples) was used to identify independent predictors of outcomes. (3) Results: The study population included patients across the spectrum of heart failure phenotypes (HFrEF 58%, HFmrEF 7%, HFpEF 35%). During follow-up, 48 patients (36.9%) experienced heart failure rehospitalization and 23 (17.7%) died. The LHFRS independently predicted 3-month rehospitalization (B = 0.490, p = 0.041). Admission urinary sodium and 2-h urinary sodium provided incremental prognostic information beyond the LHFRS and remained independently associated with rehospitalization after multivariable adjustment (p = 0.008 and p = 0.001, respectively). Urinary chloride demonstrated similar prognostic associations, whereas conventional renal biomarkers, including serum creatinine, urea, estimated glomerular filtration rate, serum sodium, and NT-proBNP, did not consistently retain independent prognostic significance. The LHFRS was also significantly associated with the composite endpoint of death or rehospitalization (B = 1.173, p = 0.002), while its association with mortality alone was not statistically significant (B = −5.551, p = 0.256). (4) Conclusions: Lower admission and 2-h urinary sodium concentrations were associated with 3-month HF rehospitalization after adjustment for the LHFRS. These findings are hypothesis-generating and require confirmation in larger, externally validated multicenter cohorts. Full article

This study presents a configurable speech signal preprocessing and feature-extraction workflow for identifying candidate acoustic biomarkers in acute heart failure. The workflow was evaluated in 12 patients hospitalized with acute heart failure. Short recordings of repeated vowels /a/, /i/, and /o/ were acquired shortly after admission and again before discharge following treatment and clinical stabilization. The pipeline included active-RMS normalization, automatic segmentation of repeated vowels, optional edge trimming, alternative pitch-estimation variants, and extraction of three feature families: phonatory and temporal measures, spectral-shape descriptors, and MFCC-based cepstral features. Within-patient admission-to-discharge differences were evaluated using two-sided Wilcoxon signed-rank tests, with nominal p-values interpreted as exploratory. Phonatory and temporal measures produced the most consistent exploratory findings. The pause-duration trend for /a/ decreased between admission and discharge and was the most configuration-stable individual candidate. CPP maximum and CPP range for /o/ increased consistently across the evaluated phonatory configurations, indicating systematic changes in cepstral prominence. Shimmer-related measures provided additional exploratory findings. MFCC measures showed complementary changes, particularly in MFCC11 variability for /o/, whereas spectral-shape effects were generally weaker and less consistent. Because the study involved a small, single-center cohort without a control group or external validation, the findings should be regarded as hypothesis-generating candidate acoustic measures rather than clinically validated biomarkers. Full article

Background: Racial and ethnic disparities in heart failure (HF) outcomes are well documented, but little is known about dietary intake and metabolic profiles among individuals with chronic HF and overweight or obesity. This exploratory secondary analysis of baseline data from the Pro-HEART randomized trial compared dietary intake and laboratory biomarkers across racial and ethnic groups. Methods: This secondary analysis used baseline data from the Pro-HEART randomized clinical trial (ClinicalTrials.gov identifier: NCT01423266). Baseline data from 92 adults with chronic HF, type 2 diabetes mellitus (DM), and overweight or obesity were analyzed. Participants self-identified as White (n = 49), Asian/Other (n = 17), Hispanic (n = 14), or Black (n = 12). Dietary intake was assessed using 3-day food records, which were analyzed with the Nutrition Data System for Research. Selected biomarkers included lipid measures, fasting glucose, hemoglobin A1c, albumin, total protein, and creatinine. Group differences were evaluated using one-way analysis of variance and chi-square or Fisher’s exact tests, as appropriate. Because multiple outcomes were examined without a prespecified primary endpoint, p-values were not adjusted for multiplicity and are reported as descriptive. Results: Participants had a mean age of 58.5 ± 9.7 years, were predominantly male (69.6%), married (64.0%), and had New York Heart Association Class II HF (75.0%). Mean age differed across groups (omnibus p = 0.046); no pairwise contrast remained significant after Bonferroni adjustment. No statistically significant between-group differences were identified in the available data for body mass index, waist circumference, left ventricular ejection fraction, dietary intake, or laboratory biomarkers (all p > 0.05); however, the small subgroup sizes and substantial missing dietary data limited the precision of these comparisons. Conclusions: In this exploratory cohort of adults with chronic HF, type 2 DM, and overweight or obesity, no statistically significant racial or ethnic differences were identified in the dietary and laboratory measures examined. However, the small subgroup sizes and substantial missing dietary data limit the precision of these findings, and smaller or clinically meaningful differences cannot be excluded. Larger studies with more complete dietary data are needed to better characterize potential racial and ethnic differences in nutrition and metabolic health in this population. Full article