The infection with the SARS-CoV-2 virus is associated with numerous systemic involvements. Besides the severe respiratory injuries and cardiovascular complications, it became obvious early on that this disease carries an increased risk of thromboembolic events, but a higher propensity for bleedings as well. We researched the medical literature over significant PubMed published articles debating on the prevalence, category of patients, the moment of occurrence, and evolution of venous thromboembolism (VTE), but also of venous and arterial “in situ” thrombosis (AT), and hemorrhagic events as well. Most researchers agree on an increased prevalence of thromboembolic events, ranging between 25 and 31% for VTE, depending on the analyzed population. For AT and hemorrhagic complications lower rates were reported, namely, about 2–3%, respectively, between 4.8 and 8%, occurring mostly in older patients, suffering from moderate/severe forms of COVID-19, with associated comorbidities. It is important to mention that patients suffering from hemorrhages frequently received thromboprophylaxis with anticoagulant drugs. As a consequence of thromboembolic and hemorrhagic complications which are both important negative prognostic factors, the evolution of patients infected with the SARS-CoV-2 virus is aggravated, determining an augmented morbidity and mortality of this population.

Background: Chronic kidney disease (CKD) progression is shaped not only by biological risk factors but also by social determinants of health. Educational attainment is a key socioeconomic indicator, yet data from Eastern Europe remain limited. Methods: We conducted a retrospective cohort study including 428 adults with cardio-renal-metabolic (CRM) syndrome having CKD stages G3a–G4 enrolled between 2022 and 2024 and followed until December 2024. Patients were stratified by educational attainment using the International Standard Classification of Education (ISCED 2011): low (ISCED 0–2) vs. high (ISCED 3–8). The primary outcome was a composite of a ≥40% decline in estimated glomerular filtration rate (eGFR) or initiation of kidney replacement therapy (KRT). Secondary outcomes were eGFR slope, doubling of urine albumin-to-creatinine ratio (uACR), and KRT initiation. Results: Of 428 patients, 245 (57.2%) had low education. These patients had lower use of renoprotective therapies. During a median follow-up of 32 months, 88 primary outcome events occurred: 66 (27%) in the low education group vs. 22 (12%) in the high education group. In adjusted analyses, low education remained independently associated with the primary outcome (HR 1.47, 95% CI 1.04–2.36, p = 0.04). The annual eGFR decline was steeper in patients with low education (−3.0 vs. −2.1 mL/min/1.73 m²/year, p < 0.001), and doubling of uACR was more frequent (24% vs. 15%, HR 1.47, 95% CI 1.02–2.19, p = 0.02). Conclusions: In a Romanian CRM-CKD cohort, lower educational attainment was an independent predictor of faster kidney function decline and adverse renal outcomes. Beyond reflecting individual disadvantage, educational status in Eastern Europe highlights systemic inequities in access to nephrology care and therapies. Incorporating education into risk stratification and implementing equity-focused interventions may improve CKD outcomes in disadvantaged populations.

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: 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: Cardiovascular involvement is among the most consequential sequelae of SARS-CoV-2 infection. Myocardial injury, arrhythmia, and thromboembolic disease have been characterized in depth, yet the relationship between COVID-19 and valvular heart disease (VHD), and its interplay with heart failure (HF), has received comparatively limited synthesis. This narrative review consolidates current evidence on the mechanisms, diagnosis, differential assessment, and clinical outcomes linking acute and post-acute COVID-19 to valvular dysfunction and to incident or worsening heart failure, with emphasis on practical implications for cardiologists and internists. Methods: We searched PubMed, Scopus, and Web of Science (January 2020–January 2026) for studies on valvular dysfunction, heart failure, myocardial injury, and endothelial pathology in SARS-CoV-2 infection, and synthesized findings narratively. Results: Convergent pathways—endothelial injury, systemic hyperinflammation, micro- and macrovascular thrombosis, and pressure–volume overload—contribute to functional and, less frequently, structural valvular changes. Available evidence suggests that clinically relevant post-COVID valvular abnormalities are more often secondary/functional (mitral and tricuspid regurgitation) than primary structural lesions, although dedicated prospective valvular studies remain scarce. Pre-existing severe VHD markedly worsens acute COVID-19 prognosis. Elevated NT-proBNP, troponin, and interleukin-6 consistently predict decompensation and mortality, and a substantial minority of survivors show persistent fibrotic pulmonary changes and restrictive ventilatory defects on follow-up (pulmonary rather than cardiac findings). Conclusions: Post-COVID valvular dysfunction appears, on currently available but largely indirect evidence, predominantly functional and inflammation-related, and may overlap with HFpEF phenotypes in selected patients when objective diagnostic criteria are fulfilled. Biomarker-guided, multimodality follow-up is reasonable in high-risk survivors, and prospective longitudinal studies with standardized valvular endpoints remain a priority. Dedicated longitudinal evidence on valvular outcomes specifically remains very limited.

Background and Objectives: Routine records may conflate valvular heart disease (VHD), functional classification, and shared diagnostic assessment. We quantified the cross-sectional association between a registry VHD label and explicitly documented heart failure (HF), while recognizing that every observed valve lesion was regurgitant. Materials and Methods: The analytic sample comprised all 224 eligible adults admitted to the Internal Medicine II Department of a railway-affiliated hospital between 1 August 2025 and 31 July 2026: 38 with documented VHD and 186 without documented VHD. The primary outcome was an explicit HF diagnosis; a combined HF/NYHA-positive field was examined as an over-inclusive sensitivity outcome. Logistic regression was adjusted for age, sex, body mass index, smoking history, and total cholesterol. Results: Explicit HF was documented in 24/38 patients with VHD (63.2%) and 72/186 without VHD (38.7%; adjusted OR 2.87, 95% CI 1.38–5.99). The combined outcome was present in 28/38 (73.7%) and 101/186 (54.3%), respectively (adjusted OR 2.38, 95% CI 1.09–5.21). All 38 exposed patients had documented mitral, aortic, and/or tricuspid regurgitation; no stenosis, prolapse, or prior valve intervention was recorded. Conclusions: Documented valvular regurgitation was associated with explicit HF documentation. Because regurgitation may be secondary to ventricular or atrial disease, reverse causation, shared ascertainment, non-adjudicated diagnoses, and residual confounding preclude causal, temporal, prognostic, or lesion-specific inference.