Background and Objectives: Heart failure (HF) and chronic kidney disease (CKD) frequently coexist and are closely interrelated, significantly affecting clinical outcomes. Among CKD-related markers, albuminuria and estimated glomerular filtration rate (eGFR) have emerged as key prognostic indicators in HF. However, their specific predictive value across different HF phenotypes—namely HF with preserved ejection fraction (HFpEF) and HF with reduced ejection fraction (HFrEF)—remains incompletely understood. This systematic review aims to evaluate the prognostic significance of albuminuria and eGFR in patients with HF and to compare their predictive roles in HFpEF versus HFrEF populations. Materials and Methods: We conducted a systematic search of major databases to identify clinical studies evaluating the association between albuminuria, eGFR, and adverse outcomes in HF patients. Inclusion criteria encompassed studies reporting on cardiovascular events, all-cause mortality, or HF-related hospitalizations, with subgroup analyses based on ejection fraction. Data extraction and quality assessment were performed independently by two reviewers. Results: Twenty-one studies met the inclusion criteria, including diverse HF populations and various biomarker assessment methods. Both albuminuria and reduced eGFR were consistently associated with increased risk of mortality and hospitalization. In HFrEF populations, reduced eGFR demonstrated stronger prognostic associations, whereas albuminuria was predictive across both HF phenotypes. Heterogeneity in study design and outcome definitions limited comparability. Conclusions: Albuminuria and eGFR are valuable prognostic biomarkers in HF and may enhance risk stratification and clinical decision-making, particularly when integrated into clinical assessment models. Differential prognostic implications in HFpEF versus HFrEF highlight the need for phenotype-specific approaches. Further research is warranted to validate these findings and clarify their role in guiding personalized therapeutic strategies in HF populations. Limitations: The current evidence base consists primarily of observational studies with variable methodological quality and inconsistent reporting of effect estimates.

Background and Objectives: The perioperative use of beta-blockers remains controversial due to conflicting evidence of their risks and benefits. The aim of this study was to evaluate the association between chronic beta-blocker (bb) therapy and perioperative cardiac events in non-cardiac surgeries using 24 h continuous Holter monitoring. Materials and Methods: A prospective observational study was conducted on patients undergoing elective or emergency non-cardiac surgery at a Romanian tertiary care hospital. The patients were divided into two groups: G1 (not receiving Bb) and G2 (on chronic Bb). The incidences of perioperative cardiac events, such as severe bradycardia (<40 b/min), new-onset atrial fibrillation (AF), extrasystolic arrhythmia (Ex), and sustained ventricular tachycardia (sVT) and arterial hypotension, were compared between the two groups using clinical, electrocardiography (ECG), and Holter ECG data. Beta-blocker indications, complications, and outcomes were analyzed using chi-squared tests and logistic regression. Results: A total of 100 consecutive patients (63% men, mean age of 53.7 years) were enrolled in the study. G2 included 30% (n = 30) of patients on chronic beta-blocker therapy. The indications included atrial fibrillation (46.7%, n = 14), arterial hypertension (36.7%, n = 11), extrasystolic arrhythmias (10%, n = 3), and chronic coronary syndrome (6.6%, n = 2). Beta-blocker use was significantly associated with severe bradycardia (n = 6; p < 0.001) in G2, whereas one patient in G1 had bradycardia, and 15 and 1 patients had hypotension (p < 0.001) in G1 and G2, respectively. The bradycardia and arterial hypotension cases were promptly treated and did not influence the patients’ prognoses. The 14 patients with AF in G2 had a 15-fold higher odds of requiring beta-blockers (p < 0.001, odds ratio (OR) = 15.145). No significant associations were found between beta-blocker use and the surgery duration (p = 0.155) or sustained ventricular tachycardia (p = 0.857). Ten patients developed paroxysmal postoperative atrial fibrillation (AF), which was related to longer surgery durations (165 (150–180) vs. 120 (90–150) minutes; p = 0.002) and postoperative anemia [hemoglobin (Hg): 10.4 (9.37–12.6) vs. 12.1 (11–13.2) g/dL; p = 0.041]. Conclusions: Patients under chronic beta-blocker therapy undergoing non-cardiac surgery have a higher risk of perioperative bradycardia and hypotension. Continuous Holter monitoring proved effective in detecting transient arrhythmic events, emphasizing the need for careful perioperative surveillance of these patients, especially the elderly, in order to prevent cardiovascular complications These findings emphasize the necessity of tailored perioperative beta-blocker strategies and support further large-scale investigations to optimize risk stratification and management protocols.

Acute coronary syndromes (ACS) are a major cause of mortality worldwide, and although interventional treatment has significantly improved mortality and morbidity related to ischemic heart disease, there is constant concern about optimizing drug treatment. In this regard, multiple studies have been conducted on inflammation in myocardial infarction (MI), starting from its implications in the atherosclerosis process. The aim of this review is to analyse the current evidence related to the subject and the correlation between the inflammatory state at presentation and the prognosis of patients with MI, identifying key points, possible therapeutic limitations, and future research directions. Both innate and acquired immune components are involved in the inflammatory cascade, with an increase in inflammatory cell and cytokine levels. To analyse the degree of inflammation and determine when it is excessive, numerous inflammatory markers have been studied, from acute phase proteins such as high-sensitivity C-reactive protein (hsCRP) and fibrinogen, to the ratios between inflammatory cells and interleukins involved in the main inflammatory pathways. Their association with post-infarction mortality and morbidity has been observed, but they must be integrated into the clinical context for the selection of patients who would benefit most from their reduction. New anti-inflammatory therapies are being studied in light of these findings, and progress is expected. Early trials with non-selective anti-inflammatory drugs have highlighted the importance of selective inhibition so as not to disrupt healing, and drugs are now being studied that target specific pathways that are exacerbated in infarction and lead to excessive remodelling. Several inflammatory pathways have been investigated but the results are inconclusive in terms of improving prognosis, requiring further studies to formulate future therapeutic indications.

Background and Objectives: Post-stroke spasticity is a frequent complication that contributes to impaired mobility, reduced functional independence, and decreased exercise tolerance. While botulinum toxin A (BoNT-A) is widely used to improve muscle tone, its effects on cardiopulmonary exercise capacity remain insufficiently characterized. This study aimed to evaluate the impact of BoNT-A treatment on cardiopulmonary performance and functional outcomes in patients with post-stroke spasticity. Materials and Methods: A prospective before–after study was conducted including 50 patients with post-stroke spasticity. Cardiopulmonary exercise testing was performed before and after BoNT-A administration. The primary outcome was peak oxygen consumption (VO₂ peak), while secondary outcomes included anaerobic threshold (AT), exercise duration, maximal workload, 10 m walk test time, Barthel Index, and modified Rankin Scale (mRS). Paired comparisons and multivariable linear regression analyses were performed to assess changes and associated factors. Results: VO₂ peak increased significantly following treatment (12.96 ± 2.70 vs. 13.55 ± 2.85 mL/kg/min; mean change 0.59 mL/kg/min, 95% CI 0.36–0.82; p < 0.001). Similar improvements were observed for AT (10.47 ± 2.77 vs. 10.97 ± 2.97 mL/kg/min; p < 0.001), exercise duration (6.70 ± 1.48 vs. 7.11 ± 1.55 min; p < 0.001), and maximal workload (44.70 ± 10.97 vs. 48.06 ± 12.60 W; p < 0.001). Functional performance improved, as indicated by reduced 10 m walk time (18.33 ± 4.67 vs. 17.36 ± 4.82 s; p < 0.001) and increased Barthel Index (57.62 ± 19.18 vs. 61.92 ± 21.10; p < 0.001). A modest but significant reduction in disability was observed on the mRS (p = 0.003). Baseline values were the strongest predictors of post-treatment outcomes, while smoking status was associated with worse walking performance. Conclusions: BoNT-A treatment was associated with modest but consistent improvements in cardiopulmonary exercise capacity and functional performance in patients with post-stroke spasticity. These findings suggest that spasticity management may be associated with functional and exercise-related benefits extending beyond local neuromuscular effects, although causal relationships cannot be established based on the present study design. Further controlled studies are needed to confirm these findings and evaluate their long-term clinical significance.

Background: Albuminuria reflects systemic endothelial dysfunction and cardiorenal interaction in heart failure (HF), yet its short-term prognostic value in acute decompensated HF (ADHF) remains incompletely characterized. Methods: We conducted a prospective observational cohort study including 144 patients with complete follow-up hospitalized for ADHF. Urinary albumin-to-creatinine ratio (ACR), NT-proBNP, and estimated glomerular filtration rate (eGFR) were measured within 24 h of admission. Prior HF hospitalization within 12 months was recorded. The primary endpoint was a 90-day post-discharge composite of all-cause mortality or HF rehospitalization. Associations were examined using logistic regression, and discrimination was assessed using ROC curves with AUC comparisons. Results: Twenty-six patients (18.1%) experienced the 90-day composite endpoint. In univariable analysis, log₁₀-transformed ACR was strongly associated with events (OR 3.90, 95% CI 1.92–7.91; p < 0.001). In multivariable analysis, ACR remained independently associated with the endpoint in Model 1 (ACR + prior HF hospitalization: OR 4.21, 95% CI 1.93–9.17; p < 0.001) and Model 2 (additional adjustment for log₁₀ NT-proBNP: OR 3.49, 95% CI 1.54–7.91; p = 0.003). NT-proBNP was not independently associated with outcome in the fully adjusted model (p = 0.080). Discrimination improved from AUC 0.724 for ACR alone to 0.821 for Model 1 and 0.836 for Model 2; the AUC difference between Model 1 and Model 2 was not statistically significant (p = 0.404). Conclusions: Urinary ACR independently predicts 90-day adverse outcomes after ADHF hospitalization and improves discrimination when combined with recent HF hospitalization history; NT-proBNP did not provide significant incremental discrimination beyond this model.