Non-acute subdural hematomas (naSDH), encompassing subacute and chronic subdural hematomas, are a common neurosurgical condition in older adults with substantial recurrence rates after treatment. Management has become increasingly multimodal, combining surgical and endovascular strategies; however, the influence of clinical, radiological, surgical and technical factors on recurrence and reintervention remains under investigation. We conducted a retrospective multicenter cohort study including patients from six high-complexity neurosurgical and neurointerventional referral centers in Colombia between January 2023 and June 2025. Adult patients with symptomatic non-acute subdural hematoma confirmed by CT were included. Hematomas were managed with surgery alone, combined surgery and middle meningeal artery embolization, or embolization alone. Recurrence and reintervention were evaluated as outcomes. Univariable and multivariable logistic regression analyses were performed to identify factors associated with the primary outcomes. A total of 247 naSDH were analyzed. Recurrence occurred in 51 hematomas (20.6%) and reintervention in 44 (17.8%). In multivariable analysis, smoking (OR 9.59, 95% CI 1.93-47.52), hypertension (OR 5.23, 95% CI 1.14-23.93), increasing age (OR 1.07, 95% CI 1.00-1.16), and greater hematoma thickness (OR 1.20, 95% CI 1.05-1.37) were independently associated with recurrence. Combined surgery with embolization was associated with reduced recurrence (OR 0.44, 95% CI 0.22-0.88). Among surgical variables, post-drain pneumocephalus significantly increased recurrence risk (OR 13.32, 95% CI 2.83-62.65), whereas longer durostomy drainage duration reduced the recurrence (OR 0.51, 95% CI 0.30-0.85). Endovascular technical factors were not independently associated with recurrence. Clinical factors showed the strongest association with recurrence. Combined surgery and embolization showed a protective association, while postoperative pneumocephalus and drainage duration significantly influenced possible outcomes.

Over the past decades, the approach to cardiomyopathies has deeply evolved. It has progressively transitioned from one predominantly based on clinical evaluation and conventional imaging towards an integrated and multidimensional approach that incorporates advanced imaging techniques, tissue characterization, and comprehensive genetic testing. In this perspective, the current classification of cardiomyopathies, from the European Society of Cardiology, has introduced the new entity of non-dilated left ventricular cardiomyopathy (NDLVC) that encompasses a spectrum of diseases from hypokinetic non-dilated forms [formerly called dilated cardiomyopathies (DCMs)] to non-hypokinetic non-dilated forms, characterized by left ventricular scar (previously called arrhythmogenic cardiomyopathies). However, the pivotal principle of the new classification is that the phenotype should be considered the starting point of a dynamic diagnostic pathway rather than its ultimate definition. Contemporary evaluation of patients with DCM and NDLVC requires a longitudinal and integrative perspective in which clinical features, imaging markers, and molecular data converge to refine disease characterization. Stated that, several aspects warrant further refinement. Arrhythmic risk stratification of DCM and NDLVC remains incompletely delineated, reflecting the complex and heterogeneous nature of the underlying arrhythmogenic substrate and its variable expression across different stages of the diseases. In addition, a proportion of patients remain genetically elusive despite extensive testing, underscoring the need for deeper molecular insights. At the same time, the expanding recognition of genotype-positive/phenotype-negative individuals introduces clinical scenarios that are not yet fully delineated, particularly with regard to surveillance strategies and preventive decision-making. This review paper aims to provide a structured and evidence-informed framework to guide personalized management of DCM and NDLVC, starting from the phenotype towards precision medicine.

Approximately 750 million people worldwide suffer from chronic kidney diseases (CKD)-a leading cause of cardiovascular morbidity and premature mortality-but early identification of progressive kidney function decline in patients at risk is still a challenge. CKD diagnosis relies on estimated glomerular filtration rate (eGFR) and albuminuria screening, primarily reflecting glomerular injury. Nevertheless, in a substantial proportion of affected subjects progressive CKD initially remains undetected, since kidney function deteriorates through ongoing tubulointerstitial injury without significant albuminuria, a condition known as 'non-albuminuric' CKD. Urinary Dickkopf-3 (uDKK3) has emerged as an innovative biomarker of progressive CKD, which is expressed by proximal tubular epithelial cells as a response to continuing injury. It is secreted into the urine, where it signals ongoing fibrogenic activity within the kidney. Clinical studies across a broad range of CKD etiologies-in adults and children alike-have shown that elevated uDKK3 significantly improved detection and prediction of progressive CKD after adjustment for established CKD risk markers including albuminuria. Moreover, in primarily non-albuminuric populations, e.g. those with type 2 diabetes and patients with heart or lung diseases, uDKK3 identifies high-risk individuals for future decline of kidney function. These findings support the hypothesis that CKD progression follows different pathways of mainly glomerular or tubulointerstitial injury. It is therefore plausible to use complementary biomarkers for CKD screening-albuminuria and uDKK3-each reflecting a distinct biological dimension of kidney injury. We discuss the limitations of albuminuria screening and propose a framework for integrating tubular markers like uDKK3 into future CKD screening strategies.

VEGFA plays a pivotal role in angiogenesis and is known to affect clinical phenotypes related to the vasculature in various diseases, such as cancer or stroke. However, it is still unclear how the VEGFA genotype influences the clinical phenotype of moyamoya disease (MMD). This study included 137 Japanese MMD patients (84 adult and 53 pediatric patients) carrying either the heterozygous RNF213 p.R4810K or the RNF213 wild-type genotypes. Patients with homozygous RNF213 p.R4810K genotype or the other rare RNF213 variants were excluded because these genotypes are already known to affect the clinical phenotype. After genotyping VEGFA rs2010963 (NM_001171623.2, c.-634G > C, also known as c.+405G > C), we statistically analyzed the genotype-phenotype correlation. Genotyping and clinical data collection were both blinded. 110 (80.3%) patients carried the heterozygous RNF213 p.R4810K genotype. For VEGFA rs2010963 genotypes, 36 (26.3%) patients had the G/G genotype, 86 (62.8%) had the C/G genotype, and 15 (10.9%) had the C/C genotype. In the subgroup analysis, the VEGFA rs2010963 C/G + C/C genotype was significantly associated with a higher incidence of bilaterality and PCA involvement in pediatric MMD patients (p = 0.032 and 0.0399, respectively). Furthermore, a multivariate regression analysis confirmed the significant association for them (p = 0.0391 and 0.0271, respectively). This genotype-phenotype association study suggests that the VEGFA rs2010963 CG + CC genotype may be associated with a higher rate of bilaterality and PCA stenosis in pediatric MMD patients, in addition to the well-known association of RNF213. These findings suggest that both RNF213 and VEGFA genotypes may be useful in the clinical assessment of MMD patients.

While exercise training is an established cornerstone for the prevention and treatment of cardiovascular diseases (CVDs), the underlying molecular mechanisms remain incompletely understood. Recent studies have identified long non-coding RNAs (lncRNAs) as critical epigenetic modulators that dynamically respond to physical activity and drive cardiovascular adaptation. This review provides a comprehensive overview of how exercise training reshapes lncRNA transcriptomic landscape to exert cardioprotective effects. Central to this discussion is the elucidation of lncRNA-associated competitive endogenous RNA (ceRNA) networks, which serve as pivotal regulatory axes in exercise-induced cellular responses. Additionally, we highlight the emerging significance of exercise-derived exosomal lncRNAs in mediating inter-organ communication and promoting systemic vascular health. Ultimately, this synthesis delineates current knowledge gaps and future research directions, offering a robust molecular rationale for the development and implementation of personalized exercise prescriptions in clinical cardiology.

Di(2-ethylhexyl) phthalate (DEHP) is a widespread plasticizer, but its role in subarachnoid hemorrhage (SAH) remains unclear. Integrating network toxicology, machine learning, transcriptomics, immune infiltration, molecular docking/dynamics, single-cell RNA sequencing, and in vivo/ in vitro experiments, we identified 264 DEHP-SAH overlapping targets enriched in PI3K-Akt/MAPK pathways. Three core genes (ADORA1, PDGFRA, PTGS2) were screened, with ADORA1 specifically upregulated in astrocytes under SAH. Chronic DEHP exposure exacerbated neurological deficits, neuronal damage, astrocyte proliferation/activation, apoptosis, and inflammatory cytokines in SAH mice, while reducing antioxidant enzymes. In primary astrocytes, DEHP suppressed viability, activated PI3K-Akt/MAPK, and induced oxidative stress and inflammation, synergizing with Hemin. An adverse outcome pathway framework was constructed. These findings reveal that DEHP aggravates SAH neurotoxicity via ADORA1-mediated astrocyte inflammation and oxidative stress through the PI3K-Akt/MAPK axis, providing new insights into environmental pollutant neurotoxicity.

Cardiac computed tomography (CCT) plays an established role in the assessment of cardiac patients. In this document, the aim is to demonstrate and clarify the role of CCT in the clinical management of heart disease. This document will cover the clinical indications, prognostic values, and limitations of CCT in the diagnosis and follow-up of heart disease, including ischaemic heart disease, valvular heart disease, cardiomyopathies, cardiac masses, large vessel disease, and adult congenital heart disease. It will provide a basic knowledge of CCT technology and scan protocols. Continuous improvements in CCT technology and reduced radiation exposure will further enhance its clinical utility. Therefore, this document outlines the technical principles of CCT and its use in everyday clinical practice for cardiologists who are not experts in CCT.

Right ventricular (RV) function is closely associated with prognosis in isolated tricuspid regurgitation. Beyond conventional longitudinal indexes, nonlongitudinal RV deformation may provide additional prognostic information.

The authors aimed to evaluate whether 3-dimensional (3D) RV circumferential strain (RV-CS) provides incremental prognostic value in patients undergoing isolated tricuspid valve surgery (ITVS).

Patients scheduled for ITVS were prospectively enrolled and underwent 3D echocardiography 1 day before surgery. 3D RV longitudinal strain, CS, and area strain were derived using commercially available software. The primary endpoint was a composite of all-cause mortality or heart failure hospitalization.

From April 2018 to December 2024, 251 patients were enrolled; 171/251 (68.1%) were women, and the mean age was 57 ± 14 years. During a median follow-up of 495 days, 48/251 patients (19.1%) reached the primary endpoint. Baseline 3D right ventricular circumferential strain (3D RV-CS) was lower in patients with events than in those without events (P < 0.001) and showed modest but had the highest Harrell's C-index for adverse events discrimination (0.695; 95% CI: 0.618-0.774; P < 0.001) among all tested RV function parameters. Patients with impaired 3D RV-CS, defined as |3D RV-CS| < 14%, had lower 1-year event-free survival than those with preserved 3D RV-CS (54.2% vs 92.5%; log-rank P < 0.001). After multivariable adjustment, impaired 3D RV-CS remained independently associated with adverse events. Adding 3D RV-CS improved risk reclassification beyond European System for Cardiac Operative Risk Evaluation II, TRI-SCORE, and Society of Thoracic Surgeons score models.

3D RV-CS provides complementary prognostic information in patients undergoing ITVS and may improve preoperative risk stratification.

Anthracyclines such as doxorubicin remain central to cancer therapy, but their clinical utility is constrained by dose-limiting cardiotoxicity and long-term cardiovascular sequelae. Although traditionally attributed to cardiomyocyte-intrinsic mechanisms, including mitochondrial dysfunction, oxidative stress, and DNA damage, emerging evidence demonstrates that these initial injuries rapidly activate the immune system, transforming doxorubicin-induced cardiotoxicity (DIC) into a multicellular inflammatory process. Release of mitochondrial and nuclear danger signals triggers innate immune pathways and recruitment of neutrophils, monocytes, and lymphocytes, whose sustained activation promotes maladaptive remodeling, fibrosis, and chronic dysfunction. Conversely, specific immune subsets exert context-dependent cardioprotective effects, underscoring the dual role of immune responses in disease progression. This review frames DIC within a cardioimmunology paradigm, highlighting the intersection of mitochondrial stress, sterile inflammation, and adaptive immunity across acute and chronic phases of injury. We discuss emerging therapeutic strategies that extend beyond cardiomyocyte protection, including immune recalibration rather than broad immunosuppression, immune-targeted interventions, and biomarker-guided monitoring, to enable mechanism-based, individualized cardioprotection without compromising anticancer efficacy.

Cardiometabolic multimorbidity, encompassing type 2 diabetes, hypertension, and metabolic dysfunction-associated steatotic liver disease, is closely linked to sympathetic nervous system overactivity and remains suboptimally controlled by pharmacotherapy alone. This state-of-the-art review evaluates the biological rationale, technical feasibility, preclinical evidence, and emerging clinical data supporting combined hepatic and renal denervation as an investigational neuromodulatory strategy for cardiometabolic disease. Preclinical models suggest that multiorgan denervation may modulate sympathetic activity and metabolic pathways, whereas early first-in-human studies of celiac-hepatic denervation indicate feasibility and acceptable short-term safety. However, current human evidence remains limited by small sample sizes, single-arm designs, and the absence of sham-controlled trials, precluding definitive conclusions regarding efficacy, durability, and causal mechanisms. Combined hepatic-renal denervation should therefore be regarded as a translational-stage, hypothesis-generating approach. Rigorous randomized trials are required to define target engagement, safety, durability, and clinical relevance.