Ischemic stroke is now widely recognized as a disease with a strong inflammatory profile. Cerebral vascular damage is both preceded and followed by a chain of molecular events involving immune cells and inflammatory markers, irrespective of the etiology of the ischemic injury. Over time, an increasingly comprehensive understanding of these markers has led to a better insight into the mechanisms behind the vascular event and recovery following ischemic stroke. However, to date, there are still no available circulating or tissue biomarkers for early diagnosis or prognostic stratification, making ischemic stroke diagnosis contingent on clinical and instrumental investigations. However, neurological and internal medicine research is progressing in identifying markers that could potentially take on this role. This manuscript, therefore, aims to review the most recent and innovative results of medical advances, summarising the current state of the art and future perspectives. If ischaemic stroke is an inflammatory disease, it is also true that it is not just a singular condition, but a group of entities with their own neuroinflammatory features. Thus, given that, in ischemic cerebral vascular damage, “time is brain,” tracking increasingly accurate markers in the diagnosis of ischemic stroke is a valuable tool that will potentially enable earlier recognition of this disease and, hopefully, make it less disabling and more widely treated.

Heart failure (HF) is a complex and heterogeneous clinical syndrome defined by progressive structural, functional, and molecular alterations in the myocardium, representing a significant global health challenge. Beyond haemodynamic compromise, HF arises from intricate interactions among neurohormonal activation, chronic inflammation, oxidative stress, mitochondrial dysfunction, impaired calcium handling, and extracellular matrix remodelling. These processes drive maladaptive cardiac remodelling and progressive functional decline across multiple HF phenotypes, including HF with reduced (HFrEF), mildly reduced (HFmrEF), and preserved ejection fraction (HFpEF). Recent advances in molecular biology have highlighted the critical roles of genomic, epigenetic, and transcriptomic mechanisms in the progression of HF. DNA methylation, histone modifications, chromatin remodelling, and non-coding RNAs regulate gene expression in response to environmental and metabolic stimuli, thereby connecting systemic risk factors to cardiac dysfunction. Proteomic and post-translational modifications, such as phosphorylation, acetylation, and redox signalling, modulate protein function and contribute to contractile impairment and metabolic dysregulation. Metabolomic studies have revealed significant changes in myocardial energy metabolism, including reduced oxidative capacity, decreased metabolic flexibility, and limited bioenergetic reserves. The integration of multi-omics approaches—including genomics, transcriptomics, proteomics, metabolomics, and epigenomics—has provided unprecedented insight into the biological heterogeneity of HF, facilitating the identification of distinct molecular subtypes and novel therapeutic targets. Systems biology and network-based analyses, supported by artificial intelligence and machine learning, enable the synthesis of complex datasets and enhance risk classification, prognosis, and personalised treatment approaches. This narrative review synthesises the current understanding of the molecular mechanisms underlying HF, with particular emphasis on the interplay between metabolic and epigenetic regulation in disease progression. It also highlights emerging translational opportunities, including omics-based biomarkers, targeted therapies, and precision medicine approaches. Despite significant advances, challenges remain in translating these findings into clinical practice, underscoring the need for standardised methodologies, extensive validation, and integrative frameworks. Ultimately, a systems-level, multi-omics perspective is crucial for redefining HF as a biologically stratified condition in the landscape of advancing tailored cardiovascular medicine.

Background: The rapid and accurate identification of the pathogens responsible for sepsis is essential for prompt and effective antimicrobial therapy. The T2Bacteria^® Panel (T2B) and T2Candida^® Panel (T2C) are rapid molecular tests performed on whole blood that exploit T2 Magnetic Resonance (T2MRsup^®) technology. Objectives: This study evaluates the impact of the T2MR system as a point-of-care device for managing sepsis and septic shock patients. Methods: This single-center retrospective study was conducted at the Sant’ Elia Hospital of Caltanissetta from 1 January 2023 to 31 July 2023. The study population was composed of patients with suspected sepsis and septic shock according to the Sepsis-3 criteria and for whom concurrent T2MR and BC samples were requested for diagnosis. Results: A total of 81 consecutive patients were enrolled in this study. Concordant T2/BC results were obtained in 69/81 (85.2%) patients; 58/81 (71.6%) were concordant-negative and 11/81 (13.6%) were concordant-positive. Discordant T2MR+/BC− results were observed in 9/81 patients (11.1%), while T2MR−/BC+ results were detected in 3/81 patients (3.7%). Furthermore, the median time for reporting positive T2MR test results (5.2 h) was significantly shorter than that for BC (122 h). Conclusions: Due to its high reliability, faster detection time, and simple workflow, T2MR in combination with BC improved the etiological diagnosis of sepsis in the enrolled patients.