Pharmaceutical companies keep producing novel drugs and drug treatments for improving the life of every sick individual, most often following a pattern; a specific drug for a specific condition. Evidence suggests that different medications can have a positive effect on different pathological conditions. The full potential of existing therapies can be revealed through drug repurposing—also referred to as drug repositioning, reprofiling, or re-tasking—which involves identifying new therapeutic uses for approved or investigational drugs beyond their original indications. One significant target in this context is the renin–angiotensin–aldosterone system (RAAS), a crucial regulator of blood pressure and fluid homeostasis, and a central focus in the treatment of chronic cardiovascular conditions such as arterial hypertension (AH) and heart failure (HF). Interestingly, novel investigations show that AT1 antagonists (sartans) are able to broaden their therapeutic scope and potentially combat other diseases such as neurodegenerative diseases, cancer, and osteoarthritis, and even help people with methamphetamine and opioid addiction.

Background and Aim: The association of atrial fibrillation (AF) with the ischemic stroke has emerged as an area of clinical research. The purpose of the present study is to investigate possible correlations between the severity, progress, and outcome of ischemic stroke and the presence of AF. Materials and Methods and Results: The clinical assessment of patients was based on the neurological status at the time of diagnosis utilizing the National Institutes of Health Stroke Scale (NIHSS), the neurological semiology during hospitalization (improvement, deterioration, and without differentiation), and the final outcome at the end of the treatment optimizing the modified Rankin scale (mRS). A total of 344 patients diagnosed with an ischemic stroke were enrolled in the study. The presence of AF was found to be associated with higher severity, poorer progress, and more adverse clinical outcomes of the ischemic stroke. Furthermore, a lower frequency of transient ischemic attacks was observed in patients with AF. Finally, patients with AF presented higher incidence of middle cerebral artery occlusion and were more frequently found with a lesion on the left brain hemisphere. Conclusion: AF was found to be highly associated with higher severity and poorer prognosis of ischemic strokes, independently from the presence of other cardiovascular risk factors.

Background: Systemic inflammation is a key driver of heart failure (HF) progression across all ejection fraction (EF) phenotypes, with diet emerging as a modifiable factor influencing cardiac metabolism and inflammatory signaling. This narrative review integrates current evidence on the inflammatory mechanisms underlying HF, their links with common comorbidities and emerging anti-inflammatory therapeutic strategies, with a particular focus on the role of nutrition in supporting healthy cardiac metabolism. Methods: We searched MEDLINE/PubMed, EMBASE, Web of Science, the Cochrane Library, Scopus and reference lists of relevant publications using terms related to systemic inflammation, dietary patterns and HF prioritizing high-impact studies on nutrition–inflammation–HF interactions published from 2000 onward. Results: Major HF comorbidities sustain chronic, low-grade inflammation through elevated cytokine activity. Dietary patterns—especially those with high Dietary Inflammatory Index (DII)—substantially shape inflammatory milieu. The Mediterranean diet appears to have a favorable inflammatory profile with reduction in circulating pro-inflammatory biomarkers, especially C-reactive protein (CRP) and interleukin-6 (IL-6). Established therapies for HF with reduced ejection fraction and vagus nerve stimulation elicit anti-inflammatory efficacy through cytokine suppression. Sodium glucose cotransporter-2 (SGLT2) inhibitors demonstrate positive metabolic effects and anti-inflammatory actions through decrease in IL-6 and tumor necrosis factor-α (TNF-α). Interleukin-1 blockade has produced heterogeneous clinical outcomes, while definitive findings examining the role of IL-6 inhibitors in inflammation suppression and possible benefit on cardiac outcomes are anticipated. Preliminary data show the potential synergistic effects of dietary patterns/nutrients and pharmacological agents combination on improvement of endothelial function and attenuation of the fibrotic process, although there is a need for further research in large-scale trials. Conclusions: Systemic inflammation demonstrates a key role in HF initiation and progression, and the effect of diet on inflammatory pathways is central. Dietary patterns targeting inflammation-related mechanisms (inflammasome, gut dysbiosis) can lead to attenuation of systemic inflammatory response and restoration of cardiac metabolic flexibility. A deeper mechanistic discernment of cardiac inflammatory cascades, together with identification of HF subpopulations with excessive inflammatory activity, may facilitate the design of targeted randomized controlled trials (RCTs) aiming for novel personalized, inflammation-targeted HF therapies with potential clinical benefit.

Objective: The objective of this study was to provide data on implantable loop recorder (ILR)-based atrial fibrillation (AF) rates, recurrent stroke rates, and predictors of AF in patients with cryptogenic stroke (CS) after 1, 6, 12, 24, and 36 months of follow-up. Methods: We searched MEDLINE/PubMed, Cochrane Central Register of Controlled Trials, EMBASE, Web of Science, and reference lists of retrieved reports, which were published by April 30, 2023, which was the date of our last search. We utilized random-effects meta-analysis for detection rates, and meta-regression analysis, t-test (for normally distributed variables), and Mann-Whitney (for skewed variables) for predictor factors. Results: Thirteen studies were analyzed, which included data from 3,377 patients with CS or embolic stroke of undetermined source. The ILR-based AF rates in patients with CS were 4.73% (95% confidence interval [CI] 3.91–5.71) at 1 month, 13.45% (95% CI 12.19–14.81) at 6 months, 17.5% (95% CI 16.25–18.82) at 12 months, 20.69% (95% CI 19–22.49) at 24 months, and 25.98% (95% CI 23.21–28.58) at 36 months. Age and CHA₂DS₂-VASc score were positively associated with AF detection. Specifically, the mean difference of age and CHA₂DS₂-VASc score in the group with AF versus the group without AF was 7.47 (95% CI 4.58–10.36, P < 0.001) and 0.75 (95% CI 0.22–1.28, P = 0.01), respectively. Finally, AF detection was positively associated with recurrent strokes with an estimated risk ratio of 1.27 (95% CI 0.69–2.31). Conclusions: There is a correlation between AF detection rate and ILR monitoring duration. One out of eight patients was diagnosed with AF after 6 months of follow-up and about one quarter after 3 years. Our results demonstrate the critical use of ILRs, especially in older patients, and in patients with high CHA₂DS₂-VASc scores.

Hypoglycaemia in patients with type 1 diabetes mellitus (T1DM) remains a major clinical burden and, beyond its metabolic complications, can cause serious cardiac arrhythmias. Multiple mechanisms lead to different types of arrhythmias during hypoglycaemia. However, existing studies often involve mixed diabetes populations, small cohorts, or limited monitoring during nocturnal periods, leaving a critical gap in understanding the links between glucose fluctuations and arrhythmic events. This review provides an updated combination of experimental and clinical evidence describing how autonomic dysfunction and ionic imbalances lead to electrophysiological instability and structural remodelling of the myocardium during hypoglycaemia. Continuous glucose monitoring (CGM) combined with electrocardiographic or wearable rhythm tracking may enable early detection of glycemic and cardiac disturbances and help identify high-risk individuals. Future prospective studies using combined CGM–ECG monitoring, particularly during sleep, are essential to clarify the relationship between hypoglycaemia and arrhythmic events.

Cardiac resynchronization therapy (CRT) is a cornerstone intervention for patients with heart failure (HF) and electrical dyssynchrony, improving quality of life, functional capacity, and survival. Beyond mechanical synchrony, mounting evidence suggests CRT exerts systemic and myocardial cardiometabolic benefits. CRT acutely enhances mechanical efficiency and shifts substrate utilization toward greater oxidation of fatty acids and ketones, effects that correlate with long-term reverse remodeling on cardiac magnetic resonance imaging. Earlier metabolomic profiling demonstrated that CRT normalizes circulating energy metabolites, improving Krebs cycle intermediates and substrate balance between glucose and lipids, while baseline metabolite patterns may differentiate responders from non-responders. These metabolic adaptations accompany favorable changes in diastolic performance, right ventricular function, and ventriculo-arterial coupling. In parallel, improved splanchnic perfusion and reduced congestion may ameliorate gut dysbiosis and endotoxemia, mitigating systemic inflammation. Collectively, these findings position CRT as a therapy capable of both mechanical and metabolic restoration in advanced HF. In this review, we discuss the emerging data on how CRT reconditions myocardial energy metabolism, influences ventricular–arterial interactions, and modulates peripheral and gut-derived metabolic pathways.