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/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.