Background/Objectives: Periodontal disease is a chronic inflammatory condition associated with systemic vascular dysfunction and elevated cardiovascular risk. This systematic review and meta-analysis aimed to quantitatively evaluate the association between periodontitis and endothelial dysfunction and to assess the effects of periodontal therapy on endothelial function and inflammatory biomarkers. Methods: Conducted per PRISMA 2020 and registered in PROSPERO (CRD420261309247). Electronic databases (PubMed, Scopus, Cochrane Library) were searched for observational and interventional studies assessing endothelial function in patients with periodontitis. Risk of bias was evaluated using RoB 2, ROBINS-I, and the Newcastle–Ottawa Scale; certainty of evidence was assessed with GRADE. Pooled effects on flow-mediated dilation (FMD) and inflammatory markers were estimated using random-effects meta-analysis (DerSimonian–Laird). Results: Fourteen studies were included in qualitative synthesis; six contributed quantitative FMD data. Observational studies consistently demonstrated impaired endothelial function and elevated inflammatory markers in patients with periodontitis versus controls. Meta-analysis showed that periodontal therapy significantly improved endothelial function (pooled FMD: +3.3 percentage points; 95% CI 1.7–4.9; I² = 77%; p < 0.001), though results should be interpreted cautiously given substantial heterogeneity and the limited number of studies (n = 6). Periodontal treatment reduced CRP levels (mean difference −0.38 mg/L; I² = 41%); IL-6 showed a favorable direction but with very low certainty of evidence. Publication bias could not be reliably assessed given the small number of included studies. Conclusions: Periodontitis is associated with impaired endothelial function and systemic inflammation. Periodontal therapy leads to measurable improvements in both, supporting its role as a potentially modifiable contributor to cardiovascular risk. Larger randomized trials with long-term cardiovascular endpoints are warranted.

Background/Objectives: Native valvular heart disease (VHD) lacks established lesion-modifying pharmacotherapy. Sodium–glucose cotransporter 2 inhibitors (SGLT2is) improve heart-failure and cardiorenal outcomes, but their relevance to VHD differs by phenotype and treatment setting. Methods: MEDLINE/PubMed, Scopus, Web of Science Core Collection and Cochrane CENTRAL were searched from inception to 27 July 2026, together with trial registries, conference proceedings and reference lists. Evidence was synthesized by clinical setting, study design and mechanistic proximity to valve tissue. Results: Functional/secondary mitral regurgitation (MR) currently provides the most convincing valve-related signal: EFFORT and DEFORM showed concordant reductions in MR severity with favorable remodeling surrogates, consistent with HF-directed unloading rather than a primary leaflet effect. DapaTAVI provides the strongest hard-outcome evidence after the mechanical correction of aortic stenosis, reducing the 1-year death/worsening-HF composite in selected high-risk patients. In 28,940 HF patients from the SHEBAHEART registry, SGLT2i use was associated with reduced death/HF hospitalization and a 28% lower adjusted risk of tricuspid-regurgitation progression, but these data remain observational. Native aortic-stenosis progression is supported only by target-trial emulation, and no dedicated clinical evidence exists for native aortic regurgitation. Conclusions: SGLT2is should be integrated into guideline-directed HF therapy when indicated. In secondary MR, reassessment after optimized therapy should precede mitral intervention when clinically appropriate. A post-TAVI benefit should be interpreted as cardiorenal/HF protection, not valve modification. The current evidence does not justify SGLT2is solely to modify an untreated native valve lesion.

Background/Objectives: European guidelines recommend increasingly stringent, risk-stratified low-density lipoprotein cholesterol (LDL-C) targets, but real-world attainment remains suboptimal. We evaluated 12-month lipid-target attainment and changes in model-derived cardiovascular risk estimates in an ambulatory dyslipidaemia cohort. Methods: In this prospective, single-centre observational study, 101 consecutive adults were assessed at baseline and after at least 12 months of routine-care lipid-lowering therapy. Patients were classified as moderate/low, high, or very high cardiovascular risk. The primary endpoint was attainment of the risk-specific LDL-C target at 12 months versus baseline. Paired changes were tested using the McNemar exact and Wilcoxon signed-rank tests. Multivariable logistic regression assessed correlates of target attainment, with Firth penalisation used because of sparse outcomes in the higher risk strata. Results: LDL-C target attainment increased from 6.0% to 43.0%, and non-HDL-C attainment from 7.0% to 51.5% (both p < 0.001). At 12 months, 89% of moderate/low-risk patients reached the LDL-C target, compared with 9% of high-risk and 23% of very-high-risk patients (p < 0.001). Higher risk category was strongly associated with non-attainment, although the odds ratios were imprecise because of sparse events. Only one patient received a high-intensity statin and three received a PCSK9 inhibitor, despite 63% of the cohort being at high or very high risk. Model-derived risk scores decreased, partly as a mathematical consequence of updated lipid inputs. Therapy was well tolerated. Conclusions: Lipid control improved substantially, but target attainment remained poorest in patients at greatest cardiovascular risk. Earlier treatment intensification, structured adherence assessment, and more consistent use of combination therapy may reduce this implementation gap.

Background/Objectives: We compared BMI and LDL-C across database-defined reference controls, hypertension, and preserved-EF ischemic heart disease without assuming HFpEF. Methods: This single-center retrospective cross-sectional study included 128 adults (20 controls, 46 with hypertension, and 62 in the preserved-EF ischemic group). Analyses included nonparametric tests, multinomial regression, clinical-group models with and without statin adjustment, and a post hoc common-age sensitivity analysis. Results: Median BMI was 25.89, 28.25, and 29.00 kg/m², respectively (p < 0.001); median LDL-C was 86.0, 109.5, and 100.0 mg/dL (p = 0.055), alongside statin use of 0%, 50.0%, and 87.1%. Per 5 kg/m² higher BMI, the adjusted RRR for preserved-EF ischemic versus control status was 3.94 (95% CI 1.60–9.71; p = 0.003) and remained 3.48 (95% CI 1.35–8.97; p = 0.010) among participants aged 40–68 years. In clinical-group models, BMI estimates were similar without and with statin adjustment (OR 1.76 and 1.89); LDL-C was not independently associated with preserved-EF ischemic status. Conclusions: BMI differed more consistently across groups than treated, contemporaneous LDL-C. These associations are imprecise and describe group status; they do not establish causation, progression, prospective HF risk, or HFpEF.

Background/Objectives: Atrial fibrillation (AF) and heart failure (HF) frequently coexist, but later-pandemic data from Eastern Europe are limited. We evaluated their documented coexistence in patients hospitalized with COVID-19; the study was not designed to determine whether SARS-CoV-2 modifies the established AF–HF relationship. Methods: We retrospectively analysed 395 adults admitted with RT-PCR-confirmed SARS-CoV-2 infection between 1 September 2022 and 31 December 2024. AF was identified from the admission record, while HF was determined by an audited, rule-based review of cardiovascular free-text entries. A modified Poisson model with robust variance was the primary analysis and estimated adjusted prevalence ratios (aPRs) after adjustment for age, sex, body mass index, hypertension, ischaemic heart disease, pre-existing type 2 diabetes, chronic kidney disease, chronic obstructive pulmonary disease, smoking, and prior ischaemic stroke. Logistic regression and a restrictive NYHA-coded HF definition were sensitivity analyses. Results: AF was documented in 68 patients (17.2%), HF in 106 (26.8%), and both conditions in 26 (6.6%). HF prevalence was 38.2% among patients with AF and 24.5% among those without AF. AF was associated with documented HF in the primary model (aPR 1.51, 95% confidence interval 1.06–2.16; p = 0.022); age was also associated with HF (aPR 1.02 per year, 95% confidence interval 1.01–1.04; p = 0.010). Results were similar with the restrictive HF definition (aPR 1.54, 95% confidence interval 1.07–2.23) and logistic regression (adjusted odds ratio 1.89, 95% confidence interval 1.06–3.37). Exploratory mortality estimates were imprecise and were not used for prognostic inference. Conclusions: AF identified a subgroup with a higher prevalence of documented HF within this hospitalized COVID-19 cohort. The findings are best interpreted as evidence of cardiovascular and multimorbidity complexity, not as proof of a COVID-specific, temporal, or causal AF–HF effect.

Background/Objectives: Post-COVID follow-up may provide an opportunity to reassess persistent and modifiable cardiometabolic risk. We characterized six-month cardiometabolic and vascular trajectories after COVID-19 hospitalization and explored associations with routinely documented dietary counseling and omega-3 recommendations. Methods: This single-center retrospective longitudinal cohort included 238 adults hospitalized with COVID-19 between March 2020 and December 2024. Patients were classified according to recorded post-discharge management as usual care (n = 64), dietary management (n = 60), omega-3 supplementation (n = 59), or combined management (n = 55). Outcomes were assessed at the index visit and at visits labeled approximately three and six months later. Longitudinal changes were estimated using generalized estimating equations; six-month associations were evaluated using baseline-adjusted ANCOVA with robust standard errors and Benjamini–Hochberg correction. Results: Mean age was 54.0 ± 10.6 years, 54.6% were women, 82.4% had hypertension, 40.8% had diabetes, and mean body mass index was 33.8 ± 4.6 kg/m². At six months, endpoint-specific data were available for 182 participants for blood pressure, total cholesterol, triglycerides, and HDL-C; 180 for waist circumference; 179 for SCORE; 177 for LDL-C and bilateral carotid IMT analyses; 173 for HOMA-IR; and 164 for IL-6. Across the cohort, systolic and diastolic blood pressure decreased by 7.91 and 4.75 mmHg; several lipid, anthropometric, and insulin-resistance markers also improved. No omnibus group-by-time interaction was significant. After false-discovery-rate correction, only higher six-month HDL-C in the dietary and combined-management groups versus usual care remained statistically significant; all other between-group findings were nonsignificant after correction. Conclusions: Several cardiometabolic risk markers improved during follow-up, but no recorded management category showed consistent trajectory-level superiority. Because intervention content and adherence, time-updated medication use, acute COVID-19 severity, and lifestyle changes were not captured, the comparative findings are exploratory and noncausal. The isolated HDL-C associations should not be interpreted as evidence of cardiovascular benefit. No cardiac biomarkers, echocardiographic measures, incident heart failure, or cardiovascular events were assessed.