Congestion not only represents a cardinal sign of heart failure (HF) but is also now recognized as the primary cause of hospital admissions, rehospitalization, and mortality among patients with acute heart failure (AHF). Congestion can manifest through various HF phenotypes in acute settings: volume overload, volume redistribution, or both. Recognizing the congestion phenotype is paramount, as it implies different therapeutic strategies for decongestion. Among patients with AHF, achieving complete decongestion is challenging, as more than half still experience residual congestion at discharge. Residual congestion is one of the strongest predictors of future cardiovascular events and poor outcomes. Through this review, we try to provide a better understanding of the congestion phenomenon among patients with AHF by highlighting insights into the pathophysiological mechanisms behind congestion and new diagnostic and management tools to achieve and maintain efficient decongestion.

Congestion not only represents a cardinal sign of heart failure but is also now recognized as the primary cause for hospital admissions, rehospitalizations, and mortality among patients with acute heart failure. Congestion can manifest through various heart failure phenotypes in acute settings: volume overload, volume redistribution, or both. Recognizing the congestion phenotype is paramount, as it implies different therapeutic strategies for decongestion. Complete decongestion is hardly achieved among patients with acute heart failure, as more than half still have residual congestion at discharge. Residual congestion is one of the strongest predictors of future cardiovascular events and poor outcomes. Through this review, we try to provide a better understanding of the congestion phenomenon among patients with acute heart failure by highlighting insights into the pathophysiology mechanisms behind congestion and new diagnostic and management tools to achieve and maintain efficient decongestion.

Essential hypertension (HTN) has a complex spectrum of pathophysiological determinants and current guidelines provide limited information on high-risk groups that should be targeted for its primary prevention. The objective of our research was to identify clusters of social and metabolic factors associated with prevalent HTN in men and women from a population-based survey in Romania. Of the 1477 participants in the main study, 798 with complete data were analyzed here. Using two-step cluster analysis, one high-risk cluster in women and two high and intermediate risk for prevalent HTN in men were identified. Older age, rural area, lower education, and higher burden of metabolic factors characterized clusters with higher risk, while intermediate risk in men was characterized by a more metabolically healthy phenotype in younger individuals. In logistic regression, men in Cluster 1 vs. those in Cluster 3 had an odds ratio (OR) of 9.6 (95%CI: 4.6; 20.0), p < 0.001 for prevalent HTN, while OR for Cluster 2 vs. Cluster 3 was 3.2 (95%CI: 1.4; 7.4), p = 0.005. In women, the OR for HTN was 10.2 (95%CI: 5.7; 18.5) if assigned to Cluster 2 vs. Cluster 1, p < 0.001. These results pointed out the subgroups and communities that the primary prevention of HTN should be prioritized in.

Background: NT-proBNP levels with a wide range at admission play both a diagnostic and a prognostic role in patients with HF. The differences regarding the clinical profiles and demography in decompensated HF patients according to NT-proBNP levels at admission are not clear. Methods: This study aimed to analyze and compare clinical profiles and demographics in patients hospitalized for decompensated heart failure according to levels of NT-proBNP at admission. The study included 302 patients hospitalized for decompensated HF who were divided into three groups based on admission NT-proBNP levels: group A (n = 46, with NT-proBNP level < 3000 pg/mL), group B (n = 130, NT-proBNP level between 3000–10,000 pg/mL), and group C (n = 126, NT-proBNP level > 10,000 pg/mL). Results: Patients hospitalized with decompensated HF and very high levels of NTproBNP, above 10,000 pg/mL at admission, are older, have a lower LVEF, higher NYHA class, more renal dysfunction, and longer hospital stay, resulting in a more severe clinical profile. Conclusions: The presence of very high levels of NT-proBNP may identify a category of patients with a more severe prognosis that requires more aggressive management and closer follow-up.

Background and Methods: This prospective observational study investigated the prognostic value of the hemoglobin-to-red cell distribution width ratio (HRR) in 278 patients hospitalized with decompensated heart failure (HF). The primary endpoint was a composite of all-cause mortality or HF rehospitalization at 12 months. Multivariable Cox regression was employed to adjust for risk factors including age, sex, NT-proBNP, LVEF, and eGFR. Results: The median HRR was 0.89. During follow-up, the primary endpoint occurred in 167 (60.1%) patients. Unadjusted analysis showed a lower HRR was significantly associated with reduced event-free survival (log-rank p = 0.027). However, after multivariable adjustment, this association was no longer statistically significant (p = 0.240). Older age and male sex remained independent predictors. Conclusions: In patients with decompensated HF, a lower baseline HRR correlates with increased risk but does not maintain independent prognostic value after adjusting for powerful confounders. HRR may serve as a simple, initial marker of risk rather than an independent predictor.

Background: Current guidelines emphasize the importance of initiating or optimizing the four pillars of heart failure with reduced ejection fraction (HFrEF) therapy—beta-blockers (BB), mineralocorticoid receptor antagonists (MRA), angiotensin receptor–neprilysin inhibitors (ARNI), and sodium–glucose cotransporter-2 inhibitors (SGLT2i)—during hospitalization for acute decompensation. This study compares clinical characteristics and outcomes in HFrEF patients hospitalized for decompensated heart failure based on whether they were newly initiated on or were already receiving at least one of these four pillars. Methods: This prospective observational study included 203 HFrEF patients hospitalized for acute decompensation. Patients were divided into two groups: Group A (n = 126), not receiving any of the four pillars prior to admission, and Group B (n = 77), receiving at least one. Clinical and biological parameters were evaluated during hospitalization, with outcomes including changes in weight, blood pressure, heart rate, renal function (serum creatinine), electrolyte levels (sodium, potassium), and 30-day mortality. Statistical analyses included the non-parametric Mann–Whitney test and Chi-squared test. Results: Baseline characteristics (age, gender, LVEF, NT-proBNP) were similar between the two groups. No significant difference was observed in 30-day mortality (Group A: 7.14%, Group B: 5.55%, p = 0.74). Both groups experienced significant improvements in systolic and diastolic blood pressure and heart rate during hospitalization (p < 0.05). While serum creatinine levels remained stable in both groups, creatinine dynamics (Δcreatinine) were significantly different (p = 0.02), with Group B exhibiting a higher increase. The improvement in ejection fraction was more pronounced in Group A (p = 0.057) compared to Group B. Both groups demonstrated significant improvements in NYHA functional class (p < 0.001). In Group B, the use of MRAs and SGLT2 inhibitors significantly increased during hospitalization (p = 0.01 and p < 0.001, respectively). Conclusions: The initiation or optimization of the four pillars of HFrEF therapy during hospitalization for acute decompensation is feasible and well-tolerated. Early intervention leads to improvements in clinical parameters and functional status, supporting guideline recommendations for in-hospital initiation or optimization of HFrEF therapy. Special consideration should be given to renal function when optimizing therapy.