Hypertensive emergencies (HE) represent high cardiovascular risk situations defined by a severe increase in blood pressure (BP) associated with acute, hypertension mediated organ damage (A-HMOD) to the heart, brain, retina, kidneys, and large arteries. Blood pressure values alone do not accurately predict the presence of HE; therefore, the search for A-HMOD should be the first step in the management of acute severe hypertension. A rapid therapeutic intervention is mandatory in order to limit and promote regression of end-organ damage, minimize the risk of complications, and improve patient outcomes. Drug therapy for HE, target BP, and the speed of BP decrease are all dictated by the type of A-HMOD, specific drug pharmacokinetics, adverse drug effects, and comorbidities. Therefore, a tailored approach is warranted. However, there is currently a lack of solid evidence for the appropriate treatment strategies for most HE. This article reviews current pharmacological strategies while providing a stepwise, evidence based approach for the management of HE.

Worsening chronic heart failure (HF) is responsible for recurrent hospitalization and increased mortality risk after discharge, irrespective to the ejection fraction. Symptoms and signs of pulmonary and systemic congestion are the most common cause for hospitalization of acute decompensated HF, as a consequence of increased cardiac filling pressures. The elevated cardiac filling pressures, also called hemodynamic congestion, may precede the occurrence of clinical congestion by days or weeks. Since HF patients often have comorbidities, dyspnoea, the main symptom of HF, may be also caused by respiratory or other illnesses. Recent studies underline the importance of the diagnosis and treatment of hemodynamic congestion before HF symptoms worsen, reducing hospitalization and improving prognosis. In this paper we review the role of integrated evaluation of biomarkers and imaging technics, i.e., echocardiography and pulmonary ultrasound, for the diagnosis, prognosis and treatment of congestion in HF patients.

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.

Acute decompensated heart failure (ADHF) represents a major healthcare burden, with residual congestion at discharge being a critical determinant of poor outcomes. Despite its prognostic significance, the assessment of decongestion status before discharge remains suboptimal, highlighting the need for a more comprehensive evaluation approach. This descriptive review synthesizes current evidence on congestion assessment methods in ADHF, focusing on their role in discharge decision-making and prognostic value. We describe various evaluation tools, including clinical examination, biomarkers, imaging techniques, and congestion scores, presenting their integration into a practical assessment algorithm. A comprehensive algorithm for congestion assessment before discharge is presented, incorporating multimodal evaluation techniques, with the aim of highlighting the practical utility of various assessment methods in guiding treatment decisions and determining optimal discharge timing. Integration of multiple parameters provides superior accuracy in evaluating decongestion status compared to single-method approaches. A standardized, multimodal approach to congestion assessment before discharge is essential for optimal ADHF management. The proposed assessment algorithm, combining clinical, biochemical, and imaging parameters, offers a practical framework for more reliable discharge decision-making, potentially improving patient outcomes.

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: 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.