Congestion represents a defining hallmark of heart failure (HF) leading to increased morbidity and mortality in HF patients. While it was traditionally viewed as a simple and uniform state of volume overload, contemporary understanding has emphasized its complexity, distinguishing between intravascular, interstitial, and tissue congestion. Congestion contributes to overt clinical manifestation of HF. However, subclinical congestion often goes undetected, increasing the risk of adverse outcomes. Residual congestion, in particular, remains a frequent and challenging issue, with its persistence at discharge being strongly linked to rehospitalization and poor prognosis. Clinical evaluation often fails to reliably identify the resolution of congestion, highlighting the need for supplementary diagnostic methods. Improvement in imaging modalities, including lung ultrasound, venous Doppler, and echocardiography, have significantly enhanced the detection of congestion. Moreover, biomarkers such as natriuretic peptides, bioactive adrenomedullin, soluble CD146, and carbohydrate antigen 125 offer valuable, complementary insights into fluid distribution and the severity of HF congestion. Therefore, a comprehensive, multimodal strategy that integrates clinical evaluation with imaging and biomarker data is crucial for optimizing the management of congestion in HF. Future approaches should prioritize personalized decongestive therapy, addressing both intravascular and tissue congestion, while aiming to preserve renal function and limit neurohormonal activation. Refinement of these strategies holds promise for improving long-term outcomes, reducing rehospitalizations, and enhancing overall patient prognosis.

Background/Objectives: Diabetes mellitus (DM) represents a major global public health challenge and is consistently associated with an increased risk of atrial fibrillation (AF). Despite extensive epidemiological evidence linking the two conditions, the underlying mechanisms and the influence of glucose-lowering therapies on AF susceptibility remain incompletely defined. This review aims to summarize the current knowledge on the pathophysiological pathways linking DM and AF and to assess the impact of commonly used antidiabetic therapies on arrhythmic risk. We conducted a narrative review of epidemiological studies, mechanistic research, and cardiovascular outcome trials that evaluate the association between DM and AF. We included data addressing structural, electrical, autonomic, metabolic, and inflammatory mechanisms of AF in diabetes, as well as clinical evidence regarding the impact of metformin, insulin, dipeptidyl peptidase-4 (DPP-4) inhibitors, sodium–glucose cotransporter-2 (SGLT-2) inhibitors, and glucagon-like peptide-1 (GLP-1) receptor agonists on AF incidence or recurrence. Results: DM promotes AF development through multiple complementary mechanisms, including atrial fibrosis, electrical conduction abnormalities, autonomic dysfunction, inflammation, glycemic fluctuations, oxidative stress, and expansion of epicardial adipose tissue. These changes create a vulnerable atrial substrate that facilitates both initiation and maintenance of AF. Evidence from recent trials indicates that the arrhythmic effects of glucose-lowering therapies are heterogeneous. Metformin and SGLT-2 inhibitors appear to offer favorable or neutral effects on AF risk. GLP-1 receptor agonists provide substantial cardiovascular benefits, although their specific impact on AF remains under investigation. Insulin therapy has been linked to a higher AF risk, whereas DPP-4 inhibitors show an overall neutral effect with inconsistent findings across studies. Conclusions: AF in patients with DM results from complex interactions between metabolic disturbances, structural remodeling, and inflammatory activation. Although several antidiabetic drugs appear to have potential antiarrhythmic effects, further dedicated research is needed to clarify their role in AF prevention and management.

Introduction and Aim: Assessing decongestion in patients with acute decompensated heart failure (ADHF) is challenging, requiring multiple parameters and often remaining imprecise. The study aimed to investigate the utility of indirectly estimating plasma variation (∆ePVS) for evaluating decongestion in ADHF patients in relation to natriuretic peptides. Materials and Methods: This prospective, observational, single-center study included 111 patients (mean age 74 years, 40% female) hospitalized with ADHF and treated with intravenous diuretics along with optimized medical therapy. Patients were clinically and echocardiographically evaluated at admission, with blood tests performed at both admission and discharge. A decrease of ≥30% in NT-proBNP at discharge was considered a marker of decongestion. ∆ePVS was calculated using the Strauss formula: ∆ePVS (%) = 100 × [(Hb admission/Hb discharge) × (1 − Hct discharge)/(1 − Hct admission)] − 100. A negative ∆ePVS (<0%) at discharge was considered a marker of hemoconcentration. Patients were divided into two groups: G1 (∆ePVS < 0%, 81 patients) and G2 (∆ePVS ≥ 0%, 30 patients). Results: Both groups had similar left ventricular ejection fraction (LVEF) values of 46%, mean hemoglobin (Hb) (12 g/dL), and creatinine (1.16 ± 0.65 mg/dL). NT-proBNP decreased in 88% patients in G1 and in 26% patients in G2 (p < 0.001). During hospitalization, five patients from G2 died. At 6 months, rehospitalization occurred in 35% of G2 and 21% of G1 (p = 0.04), with mortality rates of 37% in G2 and 11% in G1 (p = 0.012). Multivariate regression identified ∆ePVS as the only significant predictor of NT-proBNP decrease (OR 0.11, 95% CI 0.04–0.33, p < 0.001). Conclusions: Indirect estimation of plasma volume and its variation are valuable, accessible, and cost-effective parameters for assessing decongestive treatment in ADHF patients, complementing natriuretic peptides.

Background/Objectives: This study aimed to evaluate adipose tissue dysfunction, assessed through adipocytokines and proinflammatory cytokines, in relation to hepatic steatosis (HS) in patients with newly diagnosed type 2 diabetes (T2D). Methods: An observational study evaluated 155 consecutive patients with new-onset T2D; 118 (76.1%) were found to have HS, while the remaining 37 served as the control group without steatosis. Anthropometric status and body mass index (BMI) were evaluated. The biochemical assessment encompassed the measurements of fasting serum lipids, fasting plasma glucose (FPG), liver function tests, adiponectin, leptin, resistin, tumor necrosis factor (TNF-α), and interleukin 6 (IL-6). Insulin resistance (IR) was determined using the homeostasis model assessment (HOMA). HS was evaluated using ultrasonographic criteria. Quantitative evaluation of HS was performed by calculating the hepatic steatosis index (HSI). Results: There were statistically significant differences between the groups for age, BMI, weight, waist circumference (WC) and hip circumference, HSI, glucose profile (fasting plasma glucose (FPG), HOMA-IR), liver function tests, adiponectin, leptin, resistin, TNF-α, and IL-6. In multivariate logistic regression analysis, age, smoking, BMI, WC, HOMA-IR, and hypoadiponectinemia were the only independent factors associated with HS. Conclusions: The adipose tissue dysfunction assessed through adipocytokines and proinflammatory cytokines is part of the associated disorders in HS and new-onset T2D. In patients with newly diagnosed T2D, age, smoking, and hypoadiponectinemia consistently emerged as independent predictors of hepatic steatosis. More prospective trials are needed to clarify the “the temporal onset” of adipose tissue dysfunction.

Background and Objectives: Lower extremity amputations (LEAs) represent a significant health problem. The aim of our study was to analyse the type and trends of diabetes-related LEAs in patients hospitalized in one surgical centre in Bucharest between 2018 and 2021. The second aim was to assess the impact of the COVID-19 pandemic on the trends of LEAs. Materials and Methods: We performed a retrospective analysis of all lower limb amputations performed between 01 January 2018 and 31 December 2021 in the Department of Surgery, Dr. I. Cantacuzino Clinical Hospital, Bucharest, Romania. We evaluated demographic parameters, type of LEA, the level, the laterality and trends of the amputations, the main aetiologies leading to amputation, and the length of hospitalization. Results: During the study period, 1711 patients underwent an LEA. The mean age was 64.53 ± 9.93 years, 71.6% (n = 1481) being over 60. Men outnumbered women by a ratio of 3.62:1. The most frequent interventions were ray amputations in 41.2% (n = 705) of patients; then, there were amputations of the toe (20.4%, n = 349), transtibial amputations (18.9%, n = 323), transfemoral amputations (10.6%, n = 181), and midfoot amputations (9%, n = 154). Wet gangrene was the most frequent aetiology (40.9%, n = 699). The total number of LEAs decreased constantly throughout the analysed period, such that 616 LEAs were performed in 2018 and 323 LEAs in 2021 (p < 0.001). There was a statistically significant increase in the rate of major LEAs in the pandemic vs. pre-pandemic period (37% vs. 24.4%, p < 0.001). Conclusions: In our study, the total number of LEAs decreased throughout the analysed period, but there was an increase in the rate of major LEAs in the pandemic vs. pre-pandemic period. Being over 65 years of age, leucocytosis, sepsis at presentation, and diabetic polyneuropathy were important risk factors for the necessity of LEA in complicated diabetes-related foot disease.

Background: Residual systemic congestion is common after treatment for acute decompensated heart failure (ADHF) and remains difficult to assess non-invasively. We investigated internal jugular vein distensibility (DIJV) as a dynamic marker of residual congestion and its association with established congestion parameters and clinical outcomes. Methods: In this prospective single-center study, 112 patients hospitalized with ADHF underwent clinical, laboratory, echocardiographic, and venous ultrasound assessment at admission and after decongestive treatment. DIJV was calculated as the ratio of maximal internal jugular vein diameter during Valsalva to resting diameter, with DIJV ≥ 4 indicating preserved distensibility. Results: At the final in-hospital assessment, 59 patients (52.7%) had persistent DIJV < 4. These patients had higher NT-proBNP, larger inferior vena cava diameter, greater portal vein pulsatility, higher pulmonary artery systolic pressure, and lower TAPSE/PASP compared with patients with preserved DIJV. They also had longer hospital stays and higher rates of ADHF rehospitalization and six-month mortality. Higher admission DIJV remained associated with lower odds of six-month ADHF rehospitalization after multivariable adjustment (OR 0.31 per 1-unit increase, 95% CI 0.15–0.59; p < 0.001). Conclusions: DIJV improves with decongestive treatment, but frequently remains impaired. Persistent impairment is associated with a broader residual-congestion profile and adverse clinical outcomes, supporting DIJV as a simple, dynamic adjunct to multiparametric congestion assessment.