Cardiovascular involvement in patients with human immune deficiency (HIV) has gained significant attention as the improved life expectancy of individuals with HIV has changed the paradigm regarding the long-term impact of the virus on cardiovascular health. We reviewed current literature on the prevalence, diagnosis, and unique characteristics of cardiovascular disease (CVD) in HIV patients, including those treated with protease inhibitors (PIs) and complementary therapies. The incidence of infectious, immunosuppressive, and nutritionally related pathologies in HIV patients has declined, largely due to advancements in highly active antiretroviral therapies (HAART) and supportive care. However, issues related to autoimmunity and chronic inflammation persist. Elevated levels of high-sensitivity C-reactive protein, along with activated cytokines and other pro-inflammatory molecules, are common in HIV patients and contribute significantly to the increased risk for endothelial dysfunction, coagulation disorders, and accelerated atherogenesis. The advent of HAART has significantly improved the prognosis for HIV patients, leading to prolonged life expectancy and a reduction in AIDS-related complications. However, this success has also resulted in a shift in the clinical presentation, with HIV patients showing more chronic and insidious cardiovascular manifestations.

Background and Objectives: Inflammatory activation and left atrial remodelling may capture complementary dimensions of residual risk in heart failure with reduced ejection fraction (HFrEF). This study evaluated the prognostic value of routinely available inflammatory biomarkers and the left atrial volume index (LAVI) for early identification of patients at risk of heart-failure-related readmission. Materials and Methods: In this single-centre observational cohort study, 150 clinically stable patients with HFrEF were enrolled, including 75 with ischaemic cardiomyopathy and 75 with idiopathic dilated cardiomyopathy. Baseline C-reactive protein (CRP), fibrinogen, neutrophil-to-lymphocyte ratio (NLR), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and LAVI were assessed. The primary outcome was documented readmission for heart-failure decompensation within 6 months. Group comparisons, Spearman correlations, logistic regression, receiver-operating-characteristic analysis, and bootstrap internal validation were performed. Results: All participants completed 6-month follow-up, no deaths occurred, and 45 patients (30.0%) were readmitted. Compared with non-readmitted patients, those readmitted had higher NT-proBNP (3058 (2019–4567) vs. 648 (229–1267) pg/mL), fibrinogen (407.8 ± 59.0 vs. 331.3 ± 52.3 mg/dL), CRP (5.60 (3.86–7.82) vs. 2.12 (1.00–2.84) mg/L), and LAVI (33.90 (32.70–34.50) vs. 30.90 (30.20–31.90) mL/m²; all q < 0.001). In the primary model, each CRP doubling (adjusted odds ratio (OR) 16.16, 95% confidence interval (CI) 4.62–56.51) and each 1 mL/m² increase in LAVI (OR 2.50, 95% CI 1.23–5.10) independently predicted readmission. The augmented model achieved an apparent AUC of 0.962 and a bootstrap-corrected AUC of 0.944, compared to 0.856 and 0.828, respectively, for the clinical model. Conclusions: Adding CRP and LAVI to a conventional clinical model provided substantial incremental prognostic information for 6-month readmission in HFrEF. The findings support the integration of inflammatory and left-atrial remodelling measures with, rather than in place of, established clinical risk factors, although external validation is required before clinical implementation.