Background/Objectives: Hypertension damages the microcirculation, endothelium, and large arteries, yet these domains are rarely assessed together. We examined whether nailfold microvascular abnormalities track the standardized in-hospital blood-pressure phenotype and carotid wall thickness. Methods: Cross-sectional secondary analysis of 217 treated hypertensive adults hospitalized July 2025–June 2026. Phenotyping included nailfold capillaroscopy, flow-mediated dilation, reactive hyperemia index, pulse wave velocity, and carotid ultrasonography. A prespecified exploratory 0–10 microvascular score summarized rarefaction, impaired flow, and morphological abnormalities. Outcomes were the uncontrolled standardized in-hospital BP phenotype (SBP ≥ 140 and/or DBP ≥ 90 mmHg) and mean carotid intima–media thickness (cIMT). Results: Of 217 patients (mean age 61.3 ± 9.9 years; 50.7% men), 145 (66.8%) met the uncontrolled standardized in-hospital BP phenotype. The score was higher in that group (median 3 [IQR 2–4] vs. 2 [1–3], p < 0.001) and correlated with cIMT (Spearman ρ = 0.536; FDR-adjusted p < 0.001). Each point was associated with higher adjusted odds of the uncontrolled standardized in-hospital BP phenotype (OR 1.70, 95% CI 1.31–2.20; p < 0.001) and 0.0076 mm higher cIMT (95% CI 0.0004–0.0147; p = 0.040), attenuated in the expanded sensitivity model (p = 0.138). Conclusions: Greater nailfold microvascular abnormality burden was associated with the uncontrolled standardized in-hospital BP phenotype and an adverse multidomain vascular phenotype. The cIMT association was modest and adjustment-sensitive. These cross-sectional findings concern a protocolized in-hospital BP measurement session and do not establish 24 h, home, or long-term BP control or distinguish sustained uncontrolled hypertension from white-coat or masked uncontrolled BP patterns. Prospective external validation is required.

Background and Objectives: Type 2 diabetes mellitus (T2DM), visceral adiposity, and hypertension frequently coexist, but their independent associations with carotid intima–media thickness (cIMT) remain uncertain. We compared cardiometabolic profiles by diabetes status and evaluated adjusted associations with cIMT. Materials and Methods: This retrospective cross-sectional study included 147 adults admitted to Clinical CF Hospital Timișoara between 1 July 2025 and 30 June 2026. Bilateral cIMT was available in 141 patients. Group comparisons, Spearman correlation, and heteroscedasticity-robust multivariable linear regression were performed. Results: T2DM was present in 39 patients (26.5%), hypertension in 125 (85.0%), and obesity in 120 (81.6%). Compared with participants without diabetes, those with T2DM had higher homeostasis model assessment of insulin resistance (HOMA-IR; 4.11 vs. 3.08; p = 0.005) and fasting glucose (6.60 vs. 5.06 mmol/L; p < 0.001), but lower total cholesterol (205.2 vs. 225.9 mg/dL; p = 0.009) and non-high-density lipoprotein cholesterol (156.5 vs. 176.6 mg/dL; p = 0.006). These lower lipid values may reflect treatment or other residual confounding and should not be interpreted as an intrinsic T2DM phenotype. Mean cIMT was numerically higher in T2DM (0.619 vs. 0.592 mm; p = 0.284). Visceral fat area correlated with cIMT before adjustment (ρ = 0.237; p = 0.005), but not after adjustment. Age (β = 0.057 mm/decade; p < 0.001) and hypertension (β = 0.046 mm; p = 0.042) retained adjusted associations with cIMT. Conclusions: T2DM identified metabolic dysregulation, whereas age and hypertension showed the strongest adjusted associations with cIMT. Visceral adiposity showed an unadjusted but not independent association, supporting comprehensive cardiovascular risk assessment and rigorous blood pressure management.

Background and Objectives: Anthropometric measures incompletely capture the inflammatory and adipokine heterogeneity underlying insulin resistance. We examined associations of tumor necrosis factor-alpha (TNF-α), serum uric acid, and the leptin/adiponectin ratio with HOMA-IR after adjustment. Materials and Methods: This single-center cross-sectional secondary analysis included 147 of 239 hospitalized adults with HOMA-IR and predefined core data; fasting glucose, insulin, and biomarker testing was elective and patient-funded. Continuous ln(HOMA-IR) was the primary outcome. A secondary upper-quartile phenotype (HOMA-IR ≥ 4.78; n = 37) was cohort-specific and non-diagnostic. Robust linear regression used HC3 standard errors. Sensitivity analyses excluded T2DM and replaced BMI with waist circumference or visceral fat area. Binary and AUC analyses were exploratory (expanded complete-case model, n = 112). Results: Each doubling of (TNF-α + 1) was associated with a 10.2% higher HOMA-IR in the expanded model (p = 0.021). The association persisted after excluding T2DM (12.1% higher HOMA-IR per doubling; n = 81; p = 0.012) and when BMI was replaced by waist circumference (p = 0.022) or visceral fat area (p = 0.018). Uric acid and the leptin/adiponectin ratio did not reach statistical significance in the adjusted continuous-outcome model. The 112 complete cases and 35 incomplete cases were broadly similar in measured baseline characteristics, although uric acid was higher among complete cases (p = 0.020). Conclusions: In this selected hospitalized cohort, TNF-α showed the most consistent adjusted association with the observed fasting glucose-insulin phenotype. The binary and discrimination analyses remain preliminary and do not establish diagnostic or clinical prediction utility. Prospective external validation is required.

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.