Background: Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), affects millions globally, with persistent symptoms impacting quality of life. This meta-analysis synthesizes prospective cohort studies to estimate the prevalence of Long COVID symptoms and identify risk factors. Methods: We systematically searched PubMed for prospective cohort studies (2020–2025) on Long COVID, focusing on prevalence and risk factors. Studies with ≥100 participants and follow-up ≥3 months were included. Data were extracted on symptom prevalence (e.g., fatigue, dyspnoea) and risk factors (e.g., sex, hospitalization). Random-effects models were used to pool prevalence and odds ratios (OR). Risk of bias was assessed using the Newcastle–Ottawa Scale (NOS). Results: Fourteen prospective studies (n = 168,679) were included. Pooled prevalence of Long COVID was 18.0% (95% CI: 12.5–23.5%, I² = 9.8%) among survivors followed for ≥6 months. Fatigue (41.0%, 95% CI: 33.2–49.4%) and dyspnoea (22.5%, 95% CI: 15.6–29.8%) were the most common symptoms. Female sex (OR = 1.52, 95% CI: 1.25–1.92) and prior hospitalization (OR = 2.35, 95% CI: 1.98–2.90) were significant risk factors. High heterogeneity (I² > 90%) was noted. Conclusions: Long COVID affects over one-fifth of SARS-CoV-2 survivors, with fatigue and dyspnoea persisting in many. Female sex and severe acute infection increase risk. Standardized definitions and longer follow-up are needed.

Background: Endothelial and microvascular dysfunction play a central role in the pathogenesis of both cardiovascular and neurodegenerative disorders. However, whether impaired peripheral endothelial function independently predicts cognitive decline, cerebral small-vessel disease (SVD) progression, or stroke remains uncertain. Methods: We conducted a systematic review and meta-analysis of prospective cohort studies assessing the prognostic value of non-invasive peripheral endothelial tests—flow-mediated dilation (FMD), peripheral arterial tonometry (PAT/EndoPAT), and sublingual microcirculatory imaging—for cognitive or cerebrovascular outcomes. Databases (PubMed, Embase, Scopus, Web of Science) were searched from inception through 30 September 2025. Study quality was appraised using the Newcastle–Ottawa Scale (NOS), and evidence certainty was graded via GRADE. Random-effects models (DerSimonian–Laird or REML) pooled hazard ratios (HRs) using inverse-variance weighting. PROSPERO-registered (CRD42025211876). Results: Fifteen prospective cohorts (n = 13,972 participants; median follow-up 4.3 years) met inclusion criteria. Across all modalities, impaired endothelial or microvascular function predicted cognitive decline, SVD progression, or cerebrovascular events (pooled HR = 1.72, 95% CI 1.38–2.14, p < 0.001; I² = 57%). Subgroup analyses confirmed consistent associations for FMD (HR = 1.59, 95% CI 1.27–1.98) and PAT/EndoPAT (HR = 1.84, 95% CI 1.40–2.41). Evidence certainty was rated moderate-to-high according to GRADE. Conclusions: Peripheral endothelial dysfunction, measured by validated non-invasive techniques, independently predicts future cognitive and cerebrovascular events. These findings support the concept of a vascular–neural continuum, suggesting that endothelial health represents a modifiable biomarker for early neurovascular risk stratification. Routine assessment of endothelial function may help identify high-risk individuals and guide preventive interventions aimed at preserving brain and vascular health.

Background/Objectives: Acute pulmonary edema (APE) has emerged as an overlooked but life-threatening manifestation of COVID-19, reflecting the intersection of inflammatory, endothelial, and cardiac injury pathways. This study aimed to determine the incidence, independent predictors, and long-term pulmonary sequelae of APE in hospitalized COVID-19 patients. Materials and Methods: We conducted a retrospective cohort study including 127 consecutively admitted adults with confirmed SARS-CoV-2 infection at a tertiary-care center in Romania. Demographic, clinical, biochemical, and imaging data were analyzed. Multivariate logistic regression identified independent predictors of APE and in-hospital mortality, while three-month follow-up assessed pulmonary recovery and biomarker dynamics. Results: APE occurred in 36.2% of patients and was associated with a four-fold increase in in-hospital mortality (43.5% vs. 12.3%, p < 0.001). Elevated NT-proBNP, troponin I, and IL-6 levels independently predicted both APE occurrence and mortality. APE patients required more frequent ICU admission (52.2% vs. 18.5%, p < 0.001) and had longer hospital stays. At three months, 39% of APE survivors exhibited fibrotic CT changes, and 37% had restrictive ventilatory defects, correlating with persistently increased NT-proBNP and IL-6 concentrations. Conclusions: Acute pulmonary edema delineates a distinct cardio-inflammatory phenotype of COVID-19, driven by endothelial dysfunction and biomarker-elevated cardiac stress. Early biomarker-guided fluid management and structured multidisciplinary follow-up may mitigate both acute mortality and chronic pulmonary sequelae in post-COVID populations.

Background/Objectives: Telemedicine and remote patient monitoring have emerged as promising strategies to improve outcomes in heart failure (HF), but prior meta-analyses reported conflicting results, partly due to insufficient differentiation between intervention modalities. This systematic review and meta-analysis evaluated the impact of distinct telemedicine strategies on clinically relevant outcomes in HF. Methods: Conducted according to PRISMA 2020 and a prospectively registered PROSPERO protocol (CRD420261355507), this analysis included randomized controlled trials (RCTs) comparing telemedicine-based strategies—non-invasive telemonitoring, structured remote patient management (RPM), or haemodynamic-guided monitoring—against standard care, identified through searches of PubMed/MEDLINE, Embase, and CENTRAL (inception to 15 March 2026). Random-effects meta-analyses (DerSimonian–Laird) were performed, with predefined subgroup, sensitivity, and publication bias analyses. Results: Sixteen RCTs (n = 8618) were included. Telemedicine significantly reduced all-cause mortality (RR 0.82, 95% CI 0.73–0.92; I² = 34%; GRADE: moderate), all-cause hospitalization (RR 0.79, 95% CI 0.71–0.88; GRADE: moderate), HF-related hospitalization (RR 0.68, 95% CI 0.59–0.78; GRADE: high), and composite outcomes (RR 0.75, 95% CI 0.67–0.84; GRADE: moderate). A prespecified subgroup analysis revealed a significant mechanistic gradient (p for interaction = 0.008): haemodynamic-guided monitoring conferred the largest mortality reduction (RR 0.71), followed by structured RPM (RR 0.79), whereas non-invasive telemonitoring alone did not reach statistical significance (RR 0.93; p = 0.14). Conclusions: Telemedicine-based strategies yield clinically meaningful reductions in mortality and hospitalization in HF, but benefit is contingent upon intervention intensity and physiological specificity. Haemodynamic-guided monitoring and structured RPM provide robust outcome reductions, whereas passive telemonitoring alone is insufficient. These findings support consideration of structured remote patient management and haemodynamic-guided monitoring in appropriately selected patients and settings, while implementation and comparative effectiveness research remains necessary.

Background/Objectives: Orthodontic treatment induces controlled mechanical forces that alter the periodontal environment, including changes in oral microbiota composition and activation of local inflammatory pathways. Despite the widespread and growing use of orthodontic appliances across all age groups, the magnitude, timing, and multi-domain biological impact of these changes have not been comprehensively quantified in a single systematic synthesis. This systematic review and meta-analysis aimed to synthesize the available evidence on periodontal clinical parameters, oral microbiota composition, and local inflammatory biomarkers associated with orthodontic treatment using fixed appliances and clear aligners, and to provide a structured, GRADE-rated evidence base for clinical practice. Methods: A systematic review and meta-analysis was conducted in accordance with PRISMA 2020 guidelines. PubMed/MEDLINE, Scopus, and Web of Science were searched from inception to March 2026. Prospective cohort studies, longitudinal clinical studies, and randomized controlled trials evaluating periodontal parameters, oral microbiota, and inflammatory biomarkers during orthodontic treatment were included. Quantitative synthesis was performed using mean differences or standardized mean differences with 95% confidence intervals, primarily assessing within-group (pre–post) changes. Results: Eighteen studies (n = 812 patients; follow-up 3–12 months) met inclusion criteria. Fixed orthodontic appliances were consistently associated with transient increases in plaque index (MD 0.45, 95% CI 0.32–0.58; I² = 62%), gingival index (MD 0.38, 95% CI 0.25–0.51; I² = 55%), and bleeding on probing (MD 15.2%, 95% CI 10.1–20.3%; I² = 48%), particularly during early treatment phases. Microbiological analyses demonstrated within-group shifts toward increased prevalence of periodontopathogenic species (Streptococcus mutans OR 2.45, 95% CI 1.89–3.18; Porphyromonas spp. OR 2.14, 95% CI 1.67–2.75) in patients treated with fixed appliances. Local inflammatory responses were characterized by elevated IL-1β (MD 1.2, 95% CI 0.8–1.6) and IL-6 (MD 0.9, 95% CI 0.6–1.2) in gingival crevicular fluid. Certainty of evidence was rated moderate for plaque and gingival indices and low for microbiological and inflammatory outcomes (GRADE). Conclusions: Orthodontic treatment—particularly with fixed appliances—is associated with transient, reversible deterioration of periodontal indices, shifts toward a more dysbiotic oral microbiome, and elevation of local inflammatory mediators in gingival crevicular fluid during active treatment phases. These changes are manageable through structured preventive protocols and regular periodontal monitoring. Future prospective studies with concurrent control groups and standardized multi-domain outcome measures are needed to better define the magnitude and reversibility of these biological responses. PROSPERO: CRD420261336117.

(1) Background: Antibiotic co-administration during COVID-19 hospitalization is common, but evidence supporting routine use without confirmed bacterial co-infection is limited, and the impact on post-COVID recovery remains largely uninvestigated; (2) Methods: Single-center prospective observational cohort of 127 hospitalized COVID-19 adults (March 2020–December 2024) across four pandemic waves. Antibiotic exposure was the primary variable. Endpoints were 30-day mortality, ICU admission, and persistent dyspnea at three months. Multivariable logistic regression with Firth’s penalized profile likelihood 95% CI was performed; ROC analysis assessed procalcitonin (PCT) discrimination; (3) Results: Of 127 patients (median age 70.3 years; 63.8% male; 61.4% unvaccinated), 68 (53.5%) received antibiotics. Notably, 61.5% of patients with PCT ≤ 0.25 ng/mL (viral etiology likely) received antibiotics. After adjustment, antibiotic use was not independently associated with 30-day mortality (OR 0.98, 95% CI 0.27–4.05), ICU admission (OR 1.12, 95% CI 0.31–4.05), or persistent dyspnea at three months (OR 1.51, 95% CI 0.62–4.16). COVID-19 severity was the sole independent mortality predictor (OR 3.563, p = 0.018). At three months, 35.6% reported persistent dyspnea and 14.4% had CT pulmonary fibrosis; (4) Conclusions: Antibiotic exposure did not independently predict short- or long-term outcomes after adjustment for severity, while prescribing was misaligned with PCT-based bacterial probability—supporting biomarker-guided stewardship in epidemic respiratory disease.