Abstract: Tumor angiogenesis contributes to tumor growth, metastasis, and treatment resistance, but the newly formed vessels are often structurally abnormal and functionally inefficient. Antiangiogenic therapy, particularly inhibition of Vascular Endothelial Growth Factor (VEGF) signaling, is now used in the treatment of multiple cancers. Its vascular effects depend strongly on the extent of angiogenic inhibition. Moderate inhibition may temporarily improve the structure and function of abnormal tumor vessels. This vascular normalization can improve perfusion, oxygenation, immune cell infiltration, and drug delivery in selected tumor types and treatment settings. More extensive vessel pruning can have the opposite effect, reducing perfusion, worsening hypoxia, and favoring adaptive resistance. VEGF inhibition also affects normal vessels because physiological angiogenic signaling is required for endothelial homeostasis. Disruption of this signaling contributes to hypertension, thromboembolism, renal injury, cardiovascular complications, and cerebrovascular events. In this narrative review, the mechanisms that shape tumor vascular remodeling and compare the vascular effects of anti-angiogenic and other vascular-modulating anticancer therapies in tumors and normal tissues are examined. Particular attention is given to the distinction between tumor-vessel normalization and vascular injury in normal tissues, as well as treatment scheduling, combination strategies, targeted delivery, and vascular-response biomarkers.
Introduction/Objective: Migraine is a primary headache disorder that affects more than a billion people worldwide and can severely impact quality of life. Inflammation and endothelial dysfunction in the trigeminovascular system are the suggested underlying mechanisms. Statins, beyond their lipid-lowering effects, exhibit pleiotropic properties including anti-inflammatory, antioxidative, and endothelial-modulating effects, which may be relevant to migraine pathophysiology. This narrative review evaluates current evidence on the efficacy of statins in migraine prophylaxis, treatment, and prevention of associated vascular events. Methods: A literature search was conducted using MEDLINE (via PubMed) for English-language articles published between 1997 and June 2026 using the terms "migraine," "statins," "pathophysiology of migraine," "neuroinflammation," and "migraine treatment". Results: The majority of studies endorse the use of statins in individuals with migraines, noting that their positive impact on migraines and cardiovascular risk outweighs any adverse effects. Discussion: Considering the increased cardiovascular risk in migraine sufferers compared with those without migraine, statins may play a beneficial role in both migraine management and cardiovascular risk reduction. It is surprising that the role of statins in a common disease like migraine, which is also associated with an increased risk of vascular events, does not include definitive evidence. Conclusion: Statins might be considered for migraine treatment and prevention in individuals with chronic migraine, aura, hyperlipidemia, hypertension, a family history of cardiovascular disease, or other cardiovascular risk factors. We hope that the present article will encourage further research to establish if statins have a definite role in the treatment of migraine.
Abstract: Hemodialysis (HD) remains the cornerstone of renal replacement therapy for patients with End-Stage Kidney Disease (ESKD). Over the past two decades, conventional HD has been followed by more advanced dialysis modalities, including online hemodiafiltration (HDF) and expanded hemodialysis (HDx). These have been introduced to improve solute clearance and clinical outcomes. Yet cardiovascular events, mortality, and symptom burden remain unacceptably high, and it remains unclear which modality is optimal. Studies so far have shown that HDF, which combines diffusive and convective transport, is associated with lower all-cause and cardiovascular mortality than conventional HD. This is particularly the case when HDF achieves adequate convection volume and in patients with certain characteristics. HDx, which employs medium cut-off membranes, enables the clearance of larger middle molecules and may reduce inflammation, hospitalization, and symptom burden, data on hard cardiovascular and survival endpoints remain limited. Across modalities, studies assessing quality of life, symptom relief, and treatment tolerability are few and often underpowered, leaving important patient priorities underexplored. In parallel, the implementation of resourceintensive modalities such as HDF raises concerns about water, energy, and plastic use. This underscores the need for overall environmental sustainability in a growing dialysis population. Current evidence supports an individualized, outcome-driven approach to prescribing HD, HDF, and HDx, balancing potential cardiovascular and survival advantages of high-volume HDF and HDx against feasibility, cost, and environmental impact. This narrative review synthesizes evidence from randomized controlled trials and large observational cohorts comparing conventional low- and high-flux HD with post-dilution HDF and HDx, highlighting key clinical and methodological controversies.
Background: The progressive aging of the global population has been accompanied by a parallel increase in both dementia and atrial fibrillation (AF), two conditions that frequently coexist and are linked through complex cerebrovascular and systemic mechanisms. Beyond overt ischemic stroke, AF has been increasingly associated with subclinical brain injury and cognitive decline. Objective: This review examines the relationship between AF, oral anticoagulation, and cognitive outcomes, with a particular focus on elderly patients and those with cognitive impairment. Methods: Study Design and Literature Search Strategy: This article is a narrative review based on a structured literature search conducted in PubMed/MEDLINE, Scopus, and relevant guideline databases. The search focused on studies addressing atrial fibrillation, oral anticoagulation, cognitive decline, dementia, silent cerebral infarction, cerebral microbleeds, and neurovascular injury. Priority was given to systematic reviews, meta-analyses, randomized controlled trials, observational cohort studies, and current international guidelines. Relevant English-language articles published up to 2025 were considered. We performed a narrative synthesis of the current evidence addressing the biological pathways connecting AF and neurodegeneration, as well as clinical studies evaluating the impact of oral anticoagulant therapy on cognitive trajectories. Results: Oral anticoagulation remains central to stroke prevention in AF, yet its role in modulating cognitive decline remains incompletely defined. Observational data suggest that direct oral anticoagulants (DOACs) may be associated with a lower incidence of dementia, potentially through the reduction of microembolism and silent cerebral ischemia. However, these findings are not conclusive and should be interpreted with caution. Concerns regarding bleeding risk, particularly intracerebral hemorrhage, continue to influence treatment decisions, especially in frail and cognitively impaired populations. Conclusion: Managing anticoagulation in patients with AF and cognitive impairment requires a careful balance between preventing blood clots and minimizing bleeding risk. A comprehensive, patientfocused approach, supported by multidisciplinary collaboration, may improve clinical decisionmaking. More research is needed to understand the long-term cognitive effects of anticoagulant treatments in this vulnerable group.
Pericarditis is a common disease caused by various factors such as viral infections, systemic diseases, or drugs. A diagnosis of pericarditis is rendered in up to 5% of Emergency Room (ER) visits for non-ischemic chest pain. It is diagnosed when pleuritic chest pain is present, accentuated in the supine position, accompanied by ECG changes comprising new extensive ST-segment elevation and PR depression, a pericardial friction rub, and new or increased pericardial effusion on echocardiography. In North America and Western Europe, the most common causes of acute pericarditis are idiopathic or viral, followed by post-procedural (iatrogenic) pericarditis, radiation therapy, and cardiac surgery. Tuberculosis is the most common cause of pericarditis in endemic areas and is managed with antituberculosis therapy, with corticosteroids used when there is concurrent constrictive pericarditis. New diagnostic techniques have aided the sampling and analysis of pericardial fluid and in determining its cause. Treatment of pericarditis comprises high-dose Non-Steroidal AntiInflammatory Drugs (NSAIDs) for uncomplicated cases, with doses tapered when symptoms have subsided and C-reactive protein level has normalized, typically over several weeks. Colchicine (often a 3-6-month course) is needed to both alleviate symptoms and decrease recurrences, while glucocorticoids and newer therapies with interleukin-1 blockers are reserved for recurrences and/or failures of prior therapies. Integrated use of new imaging methods facilitates more precise detection and better management of complications such as pericardial effusion or constriction. The diagnostic yield of extensive laboratory evaluation and pericardiocentesis remains low; hence, invasive procedures should be limited mostly to patients in whom a therapeutic intervention is needed. The majority of pericardial effusions can be safely drained with an echo-guided percutaneous technique. Pericardiectomy remains the definitive treatment for constrictive pericarditis and provides symptomatic relief in most cases. Importantly, differentiation of constrictive pericarditis from restrictive cardiomyopathy remains a clinical challenge, but is facilitated by tissue Doppler and colour M-mode echocardiography. All these issues are reviewed herein.
