The healing of skin wounds remains an important concern in medicine, especially in chronic wounds caused by various diseases such as diabetes. Using herbs or herbal products to heal skin wounds is a therapeutic challenge for traditional medicine. In this context, the main aim of our work was to highlight the in vitro healing potential of Stellaria media (L.) Vill. (SM) extract using the scratch assay on normal human dermal fibroblasts (NHDF). The ability to stimulate cell migration and proliferation under the influence of different concentrations of SM extract (range between 12.5 and 200 µg/mL) was determined compared to the control (untreated in vitro-simulated wound) and positive control (allantoin 50 µg/mL). Our results showed that the concentration of 100 µg/mL SM extract applied on the simulated wound recorded the strongest and fastest (24 h) migration (with wound closure) and proliferation of NHDF compared with the control. In addition, the SM extract was characterized in terms of bioactive compounds (total phenols and flavonoids content), antioxidant capacity (FRAP (The Ferric-Reducing Antioxidant Power) assay and electrochemical method), and antimicrobial activity. The results show that the SM extract contains a considerable amount of polyphenols (17.19 ± 1.32 mg GAE/g dw and 7.28 ± 1.18 mg QE/g dw for total phenol and flavonoid content, respectively) with antioxidant capacity. Antimicrobial activity against Gram-positive bacteria (S. aureus) is higher than E. coli at a dose of 15 µg/mL. This study showed that Stellaria media is a source of polyphenols compounds with antioxidant capacity, and for the first time, its wound healing potential was emphasized.

The impact of metabolic syndrome (MS) on stent performance and outcomes of patients underwent percutaneous coronary intervention (PCI), including stent implantation, had not yet been fully established. The aim of the present study was to investigate long-term safety and efficacy of 2nd generation DES vs. other stent types in MS patients underwent successful PCI for an acute coronary event. Descriptive epidemiology, angiographic characteristics and one-year clinical outcomes, including major adverse cardiovascular events (MACE) and target lesion revascularization (TLR) procedures were evaluated according to the stent type inserted for 204 patients. The occurrence of TLR (6.62% vs. 9.43%, p = 0.50) and the composite outcomes (20.52% vs. 24.52%, p = 0.54) did not differ significantly between patients having 2nd generation drug eluting stents (DES) or other stent types implanted at the index procedure. It seems that the PCI in acute coronary syndrome (ACS) is similarly efficient regardless of the stent type, suggesting that for the treatment of ACS in MS patients, all stent types show similar results, in terms of TLR or MACE.

Background and Objectives: Diastolic dysfunction (DD) is a frequent complication following percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS), potentially contributing to adverse outcomes. This study aimed to investigate the association between post-procedural inflammatory markers and the severity of DD and to propose a preliminary risk score for early prediction. Materials and Methods: We retrospectively analyzed 181 ACS patients undergoing PCI, assessing C-reactive protein (CRP), leukocyte, neutrophil counts, and N-terminal pro-B-type natriuretic peptide (NT-proBNP) measured 24–48 h post-PCI. Echocardiographic DD grading was performed according to ASE/EACVI guidelines. Spearman correlation, ordinal regression, and decision-curve analysis were used to evaluate predictive performance. Results: CRP correlated with DD severity (ρ = 0.232, p = 0.002) and showed a borderline independent association (OR 1.004, 95% CI 0.999–1.009, p = 0.081). NT-proBNP correlated positively with both CRP and DD severity, while leukocyte and neutrophil counts were not significant. A three-parameter risk score (CRP > 10 mg/L, NT-proBNP > 125 pg/mL, age ≥ 65 years) identified patients at higher risk of moderate-to-severe DD (score ≥ 2: sensitivity 62%, specificity 71%). Decision-curve analysis demonstrated clinical utility in guiding post-PCI monitoring. Conclusions: A simple 0–3 point score combining age, CRP, and NT-proBNP showed potential for early identification of patients at risk of moderate-to-severe diastolic dysfunction after PCI. While the model demonstrated acceptable discrimination and calibration, its single-center design, limited sample size, and timing of biomarker assessment warrant cautious interpretation. External validation in larger, multicenter cohorts is required before clinical application.

Background: Post-procedural infection worsens outcomes in acute coronary syndrome (ACS). High-sensitivity cardiac troponin (hs-cTn) reflects myocardial injury, but its utility for infection risk prediction after percutaneous coronary intervention (PCI) is uncertain. Objective: This study aimed to evaluate whether high-sensitivity troponin (hs-cTn) levels are associated with the risk of infection and systemic inflammation. Methods: We performed an exploratory pilot study of consecutive ACS patients undergoing PCI (n = 181) at a tertiary interventional cardiology unit in Romania. Herein, hs-cTn was measured at 24- and 48-h post-PCI. The primary outcome was in-hospital infection (clinical and/or microbiological documentation), with the acknowledgment that nearly half were clinically diagnosed without microbiological confirmation. We assessed discrimination for hs-cTn48h using ROC analysis and explored associations with systemic markers (CRP, ESR, and leukocytes) and NT-proBNP using Spearman correlations. Results: Infections occurred in 9/181 patients (5.0%; 95% CI, 2.6–9.2). Notably, hs-cTn48h showed AUC = 0.49 (approx. 95% CI, 0.30–0.68) for infection discrimination. Correlations between hs-cTn48h and inflammatory markers were weak and non-significant (CRP ρ = 0.126, p = 0.091; ESR ρ = 0.119, p = 0.111; fibrinogen ρ = 0.134, p = 0.073), whereas hs-cTn48h correlated modestly with NT-proBNP (ρ = 0.232, p = 0.002). Conclusions: In this cohort, hs-cTn48h did not predict in-hospital infection after PCI in ACS. These negative findings highlight that troponin should be interpreted primarily as a marker of myocardial necrosis, not infectious risk. Larger multicenter studies with microbiological adjudication and broader biomarker panels are warranted.

Background: Post-infarction heart failure (HF) remains a major contributor to morbidity and mortality despite advances in reperfusion and pharmacological management. However, the combined influence of clinical background, myocardial injury, neuro-hormonal activation, and angiographic disease on HF severity is not fully defined. Methods: We retrospectively analyzed 181 patients with confirmed myocardial infarction treated in a tertiary cardiology center. Demographics, cardiovascular risk factors, prior chronic HF, inflammatory markers (CRP, fibrinogen, ESR, leukocyte indices), and high-sensitivity troponin (hs-Tn) were measured at admission (pre-intervention), immediately after percutaneous coronary intervention (PCI), and at 48 h, angiographic lesion distributions were collected. HF severity was graded on a five-level scale and further dichotomized as no/mild HF (grade 0–1) versus moderate–severe HF (grade ≥ 2). Group comparisons and multivariable logistic regression were used to identify independent determinants of severe HF. Results: Moderate–severe HF occurred in 42.5% of patients (77/181). Compared to HF 0–1, the HF ≥ 2 group was older (64.0 vs. 60.5 years, p = 0.042) and exhibited substantially higher systemic inflammation (CRP 41.5 vs. 9.75 mg/L, p < 0.001; fibrinogen 435 vs. 346 mg/dL, p = 0.0002; ESR 28 vs. 18 mm/h, p = 0.0004). hs-Tn levels and NT-proBNP were significantly elevated in HF ≥ 2 (NT-proBNP 3449 vs. 1243 pg/mL, p = 0.0003), while left ventricular ejection fraction was reduced. Prior HF increased the likelihood of HF ≥ 2 (54.5% vs. 33.7%, p = 0.0078), and conservative therapy was associated with adverse outcomes (87.5% vs. 40.5%, p = 0.0235). In multivariable analysis, NT-proBNP remained the only independent predictor of moderate–severe HF, while CRP showed a positive but non-significant trend after adjustment. Conclusions: Post-MI HF severity reflects the combined influence of myocardial injury, neurohormonal stress, and systemic inflammatory activation. However, in multivariable analysis, NT-proBNP emerged as the dominant independent predictor of moderate–severe HF, while CRP reflected an associated but non-independent inflammatory signal.