Background: The glymphatic system is a perivascular cerebrospinal fluid (CSF)–interstitial fluid (ISF) exchange pathway that supports brain homeostasis by clearing metabolic waste and neurotoxic proteins. Across central nervous system diseases, converging evidence indicates that glymphatic dysfunction represents a shared pathophysiological axis linking vascular, astroglial, inflammatory, and sleep‐related disturbances to impaired solute clearance. Results and Conclusion: In this review, we synthesize mechanistic and clinical evidence for glymphatic impairment in acute brain injury (ischemic and hemorrhagic stroke, traumatic brain injury) and chronic neurological disorders (Alzheimer's disease, Parkinson's disease, cerebral small vessel disease, multiple sclerosis, idiopathic normal pressure hydrocephalus, idiopathic intracranial hypertension, epilepsy, and headache disorders). Major mechanisms include (i) aquaporin‐4 (AQP4) depolarization/mislocalization at astrocytic endfeet, reducing perivascular water transport; (ii) perivascular space compression or obstruction from cytotoxic/vasogenic edema, blood‐derived products, protein aggregates, or altered extracellular matrix; (iii) loss of arterial pulsatility and vascular stiffening, weakening the driving forces for convective exchange; (iv) blood–brain barrier disruption and neuroinflammation, which remodel perivascular architecture and amplify clearance failure; and (v) sleep and autonomic dysregulation, including altered noradrenergic tone, which suppresses glymphatic activity during periods when clearance is normally maximal. Clinically, glymphatic dysfunction can be probed using diffusion tensor imaging–analysis along the perivascular space (DTI‐ALPS), contrast‐enhanced MRI approaches, and structural surrogates such as enlarged perivascular spaces, with emerging associations to cognition, mood, and disease severity. Finally, we discuss translational strategies aimed at restoring clearance, including sleep/circadian optimization, vascular risk control, anti‐inflammatory approaches, AQP4‐ and TRPV4‐oriented targets, and neuromodulation. Mechanism‐guided, standardized imaging and longitudinal interventional studies are needed to establish glymphatic biomarkers as actionable therapeutic and prognostic tools.

Hyperuricemia, characterized by elevated serum uric acid levels, has been linked to cardiovascular diseases such as hypertension, atrial fibrillation, chronic kidney disease, heart failure, metabolic syndrome, and coronary artery disease. This relationship, however, is complex; while some studies indicate a strong association, others suggest that it may be influenced by confounding factors. The rising global prevalence of hyperuricemia underscores the necessity for a deeper understanding of its cardiovascular implications. Hyperuricemia results from an imbalance in uric acid production and excretion, driven by dietary factors, obesity, insulin resistance, and other conditions. Elevated uric acid levels contribute to cardiovascular risk through mechanisms such as inflammation, oxidative stress, endothelial dysfunction, and activation of the renin-angiotensin-aldosterone system. This review highlights the importance of ongoing research to clarify hyperuricemia’s role in cardiovascular disease and suggests that urate-lowering therapies, such as xanthine oxidase inhibitors, may confer cardiovascular benefits; however, evidence remains conflicting. The Cardiovascular Safety of Febuxostat and Allopurinol in Patients with Gout and Cardiovascular Morbidities (CARES) trial indicated an increased risk of cardiovascular and all-cause mortality with febuxostat compared with allopurinol, raising safety concerns. In contrast, the Febuxostat versus Allopurinol Streamlined Trial (FAST) demonstrated that febuxostat was noninferior to allopurinol, with even lower all-cause mortality. These opposing findings emphasize the complexity of treatment decisions and the need for individualized management strategies for hyperuricemia. Clinical decisions should consider individual patient risks and characteristics. Ultimately, this comprehensive analysis aims to enhance prevention and management strategies for cardiovascular diseases related to hyperuricemia. The overview includes discussions on major studies such as the Framingham Heart Study, CARES, FAST, PRIZE, and FREED trials, examining their results. It explores whether hyperuricemia is a causal factor versus an associated risk factor and whether it serves as a marker or mediator of disease. Additionally, the review addresses novel biomarkers and predictive models, the management of hyperuricemia in the context of cardiovascular risk, the role of urate-lowering therapies in cardiovascular disease, variability in guidelines and recommendations, and the impact of hyperuricemia in special populations such as those with diabetes and chronic kidney disease. The cardiovascular risk associated with hyperuricemia across various demographics is also discussed. Furthermore, the review suggests that existing risk scores might be modified to include uric acid levels in patients with hyperuricemia.

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease, is increasingly recognized as a multisystem disorder with significant cardiovascular implications, particularly in its association with atrial fibrillation (AF). As the most common sustained cardiac arrhythmia, AF contributes to substantial morbidity and mortality, making it essential to explore its links with MASLD. The relationship between these conditions is underpinned by shared pathophysiological mechanisms, including systemic inflammation, insulin resistance, oxidative stress, and activation of the renin-angiotensin-aldosterone system. These processes drive atrial remodeling and electrical instability, predisposing individuals with MASLD to AF. Epidemiological studies further support this connection, showing an independent association between MASLD and an increased risk of AF, particularly in those with metabolic comorbidities such as obesity and type 2 diabetes. Beyond increasing AF susceptibility, MASLD may also influence disease progression and response to treatment, affecting anticoagulation safety, rhythm-control strategies, and the success of catheter ablation. Given these clinical implications, therapies targeting metabolic dysfunction—such as statins, renin-angiotensin-aldosterone system inhibitors, and structured lifestyle modifications—may offer dual benefits in mitigating both MASLD and AF risk. However, significant knowledge gaps remain regarding the causal direction of this association, the impact of MASLD severity on AF burden, and the most effective management strategies for patients with both conditions. Future research should prioritize longitudinal studies, mechanistic investigations, and randomized controlled trials to deepen our understanding of this relationship, ultimately guiding more personalized and integrated treatment approaches. Incorporating MASLD screening into cardiovascular risk assessment may enhance early detection and improve outcomes for at-risk populations.

Background: Nonalcoholic steatohepatitis (NASH) is a severe form of nonalcoholic fatty liver disease (NAFLD) that can progress to cirrhosis and hepatocellular carcinoma (HCC). Obesity is a major risk factor for NASH, and metabolic interventions such as bariatric surgery (BS) and glucagon‐like peptide‐1 receptor agonists (GLP‐1 RAs) have been explored for their impact on liver‐related outcomes. This study evaluates the comparative effectiveness of BS and GLP‐1 RAs in reducing the incidence of new‐onset NASH and related hepatic complications.Methods: This was a large, population‐based, retrospective cohort using data from the TriNetX platform. Adult patients with a body mass index (BMI, of 35 or greater and without a history of NAFLD/NASH (without cirrhosis) who underwent BS versus GLP‐1RA between January 1, 2014 and December 31, 2019, were included. Patients in the BS group were matched with patients in the GLP‐1RA group according to age, demographics, comorbidities and medication by using 1:1 propensity matching.Results: Among 180,022 eligible adults, 143,404 underwent BS, while 36,618 received GLP‐1 RA therapy. Following propensity score matching, 33,594 patients in the BS group (mean age 49.1 ± 13.2 years; 72.73% female) were matched to an equal number of individuals in the GLP‐1 RA group (mean age 48.9 ± 14.0 years; 72.41% female). Compared to those receiving GLP‐1 RA therapy, patients who underwent BS had a significantly lower risk of HCC (HR, 0.304; 95% CI, 0.099–0.931), which showed the strongest protective effect, followed by a substantial reduction in NASH (HR, 0.509; 95% CI, 0.469–0.551). The reduction in liver cirrhosis risk was not statistically significant (HR, 0.865; 95% CI, 0.696–1.075). These associations remained across follow‐up periods of 1, 3, 5 and 7 years.Conclusions: These findings suggest that BS was significantly associated with lower risk of new onset of NASH/NAFLD.

Background: Atrial fibrillation (AF) is a frequent and serious cardiovascular complication in oncology patients, driven by shared pathophysiological mechanisms of inflammation, thrombosis, and cardiac remodeling. Cancer and its therapies significantly increase AF risk, impacting survival, quality of life, and management complexity. Methods: This narrative review synthesizes current evidence on the epidemiology, pathogenesis, and management of AF in cancer, emphasizing inflammatory and prothrombotic pathways, treatment-related cardiotoxicity, and cardio-oncology strategies. Literature was retrieved from PubMed and recent cardio-oncology guidelines to provide an integrated overview of mechanistic insights and therapeutic implications. Results: Cancer patients exhibit up to a 10-fold higher risk of AF than the general population, particularly with esophageal, lung, and hematologic malignancies. Mechanistically, the NLRP3 inflammasome, neutrophil extracellular traps, and hypercoagulability promote atrial fibrosis and electrical instability. Cancer therapies—including anthracyclines, platinum agents, tyrosine kinase inhibitors, immunotherapies, and thoracic radiation—further potentiate AF. Management is challenging due to drug–drug interactions, bleeding risks, and altered pharmacokinetics. Evidence supports the use of direct oral anticoagulants when feasible and emphasizes multidisciplinary cardio-oncology collaboration. Personalized anticoagulation, vigilant rhythm monitoring, and shared decision-making are key to optimizing outcomes. Conclusion: AF in cancer arises from a convergence of inflammation, thrombosis, and therapy-induced injury. A structured, multidisciplinary cardio-oncology approach integrating early risk stratification, tailored anticoagulation, and preventive strategies is essential. Future research should focus on oncology-specific risk prediction tools, biomarker-guided management, and randomized trials to refine evidence-based care for this high-risk population.