Background and Objectives: Obstructive sleep apnea (OSA) is a prevalent disorder associated with increased cardiovascular (CV) risk. Materials and Methods: We conducted a PRISMA-compliant systematic review and meta-analysis of prospective cohort studies assessing OSA and incident CV outcomes. Results: From 2463 records, 18 studies (>25,000 participants; median follow-up 9 years) were included. OSA was associated with increased CV risk (pooled HR 1.82, 95% CI 1.45–2.28). Dose–response analysis showed a progressive risk increase: mild OSA (HR 1.21, 95% CI 0.98–1.50), moderate (HR 1.56, 95% CI 1.20–2.03), and severe (HR 2.45, 95% CI 1.85–3.25). Continuous positive airway pressure (CPAP) adherence (≥4 h/night) reduced risk (HR 0.76, 95% CI 0.60–0.96). Conclusions: OSA confers a severity-dependent CV risk, which is mitigated by adequate CPAP adherence. Systematic screening and adherence support may reduce CV morbidity and mortality. PROSPERO: CRD420251168363.

Background: Systemic inflammation plays a pivotal role in heart failure (HF) progression, yet no meta-analysis has synthesized prospective cohort data on interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), and neutrophil-to-lymphocyte ratio (NLR) as prognostic biomarkers. Objectives: To quantify the independent prognostic value of IL-6, hs-CRP, and NLR for mortality and HF-related outcomes across HF phenotypes. Methods: Following PRISMA and MOOSE guidelines, we searched PubMed, Embase, Scopus, Web of Science, and CENTRAL from January 2014 to October 2025 for prospective cohorts reporting adjusted hazard ratios (HRs). Random-effects meta-analysis pooled HRs; heterogeneity was assessed via I² statistic, with subgroup and sensitivity analyses for robustness. Quality was evaluated using Newcastle–Ottawa Scale (NOS) and GRADE. Results: Thirteen cohorts (n ≈ 19,000) were included. Elevated IL-6 (five studies) was associated with increased all-cause mortality and composite outcomes (low-moderate heterogeneity, I² < 35%). hs-CRP (five studies) showed similar prognostic strength, with trajectories amplifying risk. NLR (three studies) independently predicted adverse events with negligible heterogeneity. Associations persisted across HFrEF and HFpEF, acute/chronic settings, and geographic regions, independent of natriuretic peptides and comorbidities (NOS median 8/9; GRADE moderate-to-high). Conclusions: IL-6, hs-CRP, and NLR are robust, independent prognostic biomarkers in HF, supporting their integration into clinical risk stratification and inflammation-targeted therapies. PROSPERO: CRD420251207035.

Background and objectives: To minimize stroke-related deaths and maximize the likelihood of cerebral reperfusion, medical professionals developed the “code stroke” emergency protocol, which allows for the prompt evaluation of patients with acute ischemic stroke symptoms in pre-hospital care and the emergency department (ED). This research will outline our experience in implementing the stroke code protocol for acute ischemic stroke patients and its impact on door-to-needle time (DTN) in the ED. Methods: Our study included patients with a “code stroke alert” upon arrival at the emergency department. The final sample of this study consisted of 258 patients eligible for intravenous (IV) thrombolysis with an onset-to-door time < 4.5 h. ED admissions were categorized into two distinct groups: “day shift” (from 8 a.m. to 8 p.m.) (n = 178) and “night shift” (from 8 p.m. to 8 a.m.) (n = 80) groups. Results: An analysis of ED time targets showed an increased median during the day shift for onset-to-ED door time of 310 min (IQR, 190–340 min), for door-to-physician (emergency medicine doctor) time of 5 min (IQR, 3–9 min), for door-to-physician (emergency medicine doctor) time of 5 min (IQR, 3–9 min), and for door-to-physician (neurologist) time of 7 min (IQR, 5–10 min), also during the day shift. During the night shift, an increased median was found for door-to-CT time of 21 min (IQR, 16.75–23 min), for door-to-CT results of 40 min (IQR, 38–43 min), and for door-to-needle time of 57.5 min (IQR, 46.25–60 min). Astonishingly, only 17.83% (n = 46) of these patients received intravenous thrombolysis, and the proportion of patients with thrombolysis was significantly higher during the night shift (p = 0.044). A logistic regression analysis considering the door-to-needle time (minutes) as the dependent variable demonstrated that onset-to-ED time (p < 0.001) and door-to-physician (emergency medicine physicians) time (p = 0.021) are predictors for performing thrombolysis in our study. Conclusions: This study identified higher door-to-CT and door-to-emergency medicine physician times associated with an increased DTN, highlighting further opportunities to improve acute stroke care in the emergency department. Further, door-to-CT and door-to-CT results showed statistically significant increases during the night shift.

Background: Cardiovascular disorders, especially atherosclerosis, have been associated with allergic inflammation. In addition to traditional inflammatory responses, there is evidence that the development and instability of coronary artery plaque may be influenced by effector cells of allergic inflammation. This review examines the phases of allergic pathology, the immunological mechanisms of atherosclerosis, and the clinical link between allergic diseases (asthma, atopic dermatitis, allergic rhinitis, and food allergy) and cardiovascular disease (CVD), along with future therapeutic perspectives. Material and Method: A literature search was conducted in PubMed, Google scholar; ScienceDirect, Scopus, and studies published between 2014–2024 were taken into consideration. Keywords included allergic inflammation, eosinophils, mast cells, reactive oxygen species, atherosclerosis, Th2 cells, and cytokines. Epidemiological studies and review articles were included. Results: Emerging evidence suggests that allergic inflammation contributes to atherosclerosis through interconnected mechanisms such as eosinophil activation, reactive oxygen species production, mast cell degranulation, and endothelial dysfunction. Th2-driven immune responses, which are mediated by cytokines such as IL-4, IL-5, and IL-13, as well as eosinophil activity and mast cell degranulation, play a crucial role in vascular inflammation and plaque progression. Additionally, changes in lipid metabolism contribute to this process. Epidemiological studies support this connection, indicating that patients with chronic allergic conditions such as asthma, allergic rhinitis, food allergy, and atopic dermatitis experience increased cardiovascular morbidity. However, most current data are observational, and our understanding of the underlying mechanisms in humans remains limited, often relying on insights gained from preclinical models. Conclusions: A potential mechanism for cardiovascular risk is suggested by the interaction between atherosclerosis and allergic inflammation. Promising alternatives for treating allergic inflammation and cardiovascular issues include novel treatments like cytokine inhibitors, mast cell stabilizers, and biologics that target certain pathways. Further research is necessary to see whether concentrating on allergy pathways could lead to innovative treatments for cardiovascular disorders or vice versa.

Despite major advances in guideline-directed cardiovascular therapy, residual cardiovascular risk persists, partly driven by oxidative stress, chronic inflammation, endothelial dysfunction, and mitochondrial injury not fully addressed by current drugs. Translation of plant-based cardioprotectants is constrained by preparation-dependent variability in extract chemistry (plant part/cultivar/processing and extraction method), low and variable systemic exposure for key actives (notably curcuminoids and many polyphenols), and clinically relevant safety/interaction considerations (e.g., hepatotoxicity reports with concentrated green tea extracts and antiplatelet-related bleeding-risk considerations for some botanicals). We therefore provide a mechanism- and translation-oriented synthesis of evidence for cardioprotective botanicals, chosen for long-standing traditional use and scientific validation with reproducible experimental data and, where available, human studies, including Crataegus monogyna, Allium sativum, Olea europaea, Ginkgo biloba, Leonurus cardiaca, and Melissa officinalis. Across studies, polyphenols (especially flavonoids and phenolic acids) and organosulfur compounds are most consistently associated with cardioprotection, while terpene-derived constituents and secoiridoids contribute mechanistically in plant-specific settings (e.g., Ginkgo and Olea). Predominantly in experimental models, these agents engage redox-adaptive (Nrf2), mitochondrial (mPTP), endothelial, and inflammatory (NF-κB) pathways, with reported reductions in ischemia–reperfusion injury, oxidative damage, and apoptosis. Clinical evidence remains heterogeneous and is largely confined to short-term studies and surrogate outcomes (blood pressure, lipids, oxidative biomarkers, endothelial function), with scarce data on hard cardiovascular endpoints or event reduction. Priorities include standardized, chemotype-controlled formulations with PK/PD-guided dosing and adequately powered randomized trials that assess safety and herb–drug interactions.

Background: Bloodstream infections (BSIs) complicate COVID-19 inpatients, increasing morbidity, mortality, and healthcare burden. This systematic review and meta-analysis evaluated prevalence, antimicrobial resistance (AMR), risk factors, and outcomes of BSIs in RT-PCR-confirmed COVID-19 cases. Methods: We searched PubMed, Google Scholar, ScienceDirect, and MDPI journals (January 2020–August 2025) following PRISMA 2020 guidelines. Twenty-two observational studies (~123,500 patients, ~602,000 blood cultures) were included: 10 prospective and 12 retrospective. Random-effects models estimated pooled prevalence, odds ratios (ORs), and mean differences, with subgroup analyses (ICU, non-ICU, pediatric) and meta-regression.Results: Pooled BSI prevalence was 8.2% (95% CI: 5.7–11.0; I² = 50%). Subgroup prevalence was higher in ICU (12.5%) than non-ICU (5.2%) populations. Pediatric cohorts (n = 3) showed a prevalence of 10.8%. Gram-negative pathogens predominated (61%), particularly Klebsiella pneumoniae (26%) and Acinetobacter baumannii (21%). AMR rates were 36% for MRSA and 31% for ESBL-producing Enterobacterales. Risk factors included mechanical ventilation (OR: 2.6), immunosuppression (OR: 2.3), and corticosteroid use (OR: 2.4). BSIs were associated with increased mortality (OR: 2.6), prolonged hospitalization (+6.8 days), and higher ICU admission (OR: 3.1).Conclusions: BSIs, largely driven by multidrug-resistant pathogens, substantially worsen COVID-19 outcomes. Variability in diagnostic criteria (CDC vs. ECDC) and reliance on retrospective designs are limitations, though moderate heterogeneity (I² = 50%) enhances generalizability across diverse populations. Strengthened infection prevention and antimicrobial stewardship are urgently required.