Multiple sclerosis (MS) is a chronic progressive neurodegenerative disease that leads to disabilities such as difficulty moving and slowed cognitive processing. It is the leading non-traumatic cause of disability worldwide. MS also has a high potential to become a model for neurodegenerative diseases with a progression like Alzheimer’s or Parkinson’s. Cardiovascular diseases (CVDs) remain the leading cause of global deaths and have a considerable economic impact. The higher incidence of cardiovascular comorbidities in patients with MS compared to healthy individuals of the same age worsens the prognosis of neurological pathology, leading to a higher level of disability, poorer physical outcomes, higher depression scores, cognitive aging, and diminished quality of life. Classical observational studies often have questionable elements that can represent a source of error, making it difficult to establish a causal relationship between MS and CVD. Genetic studies, including genome-wide evaluation, may resolve this issue and may represent a topic for future research. We report the case of a 31-year-old male patient with a history of multiple sclerosis (MS) diagnosed seven years prior, who presented with acute chest pain upon returning from vacation. Despite the previous recommendation for disease-modifying therapy, the patient had discontinued treatment by personal choice. Electrocardiography (ECG) revealed ST-segment elevation in inferior leads, and emergent coronary angiography identified severe multi-vessel coronary artery disease (CAD), requiring immediate revascularization. This case highlights the potential cardiovascular risks in young patients with MS and the importance of continuous medical supervision.

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.