To assess the effect of preoperative acetylsalicylic acid use on the risk of recurrence and complications in patients undergoing surgical drainage of chronic subdural hematoma (cSDH) in light of the widespread use of acetylsalicylic acid for cardiovascular prevention among the growing elderly population.

A systematic review and meta-analysis were conducted in accordance with PRISMA 2020 guidelines. A comprehensive search was performed on May 31st, 2025, across Pubmed, EMBASE, LILACS, and Web of Science. Eligible studies included cohort studies and randomized controlled trials (RCT) involving patients with cSDH undergoing surgical drainage who were on preoperative acetylsalicylic acid therapy. Outcomes analyzed included mortality, morbidity, perioperative and postoperative complications, and recurrence rates. The risk of bias was assessed using the Newcastle-Ottawa Scale (NOS) for cohort studies and the RoB 2 tool for RCT. Meta-analysis was conducted using a random-effects model, and heterogeneity was evaluated using the I² statistics.

The systematic review included eight cohort studies (seven retrospective, one prospective) and one RCT, comprising a total of 3,209 participants, of whom 1,152 (35.8%) had received acetylsalicylic acid preoperatively. Our meta-analysis of 1556 observations found no significant difference in recurrence risk between acetylsalicylic acid users and non-users [RR: 0.99; 95% CI: 0.68-1.45; p = 0.96; I² = 11.2%]. However, preoperatively acetylsalicylic acid use was associated with a significantly increased risk of thromboembolic events [RR: 2.89; 95% CI: 1.18-7.11; p = 0.02; I² = 0.0%].

Limited evidence suggests that preoperative acetylsalicylic acid use does not significantly increase the risk of cSDH recurrence in patients undergoing surgical drainage. Conversely, these patients may be at increased risk of thromboembolic events. This highlights the importance of careful patient selection and individualized management. Further research is warranted to guide clinical decision-making regarding acetylsalicylic acid therapy in this population.

Right ventricular (RV) dysfunction is a major contributor to mortality in several cardiopulmonary diseases. However, the understanding of RV pathophysiology falls behind its left counterpart, limiting treatment options for conditions associated with discrete RV dysfunction and failure, such as pulmonary hypertension (PH). Accumulating evidence suggests that colchicine (COL) may have therapeutic benefits in multiple diseases, including PH. The mechanisms by which COL improves cardiovascular function are incompletely understood but may be associated with reductions in myocardial tissue viscoelasticity via microtubule depolymerization as demonstrated in prior ex vivo studies. The aim of this study is to investigate the impact of acute COL treatment on healthy and diseased RV organ function. Healthy and PH rats were anesthetized and catheterized for investigation of RV pressure-volume (PV) relationships before and after intramyocardial injections of COL. Marked RV failure was observed secondary to PH, characterized by elevated pulmonary vascular resistance (PVR), RV pressures and end diastolic PV relation (EDPVR) with reduced RV compliance, preload and stroke volume. COL reversed pathological changes in parameters such as EDPVR, and improved RV preload, compliance, stroke volume and ejection fraction in PH rats. COL also reduced RV systolic pressure and heart rate in PH rats, which may be associated with broader effects of COL (improved PVR) in addition to myocardial viscoelastic reduction. In contrast, no significant effect on cardiopulmonary function was observed in healthy rats. These results highlight a potential contribution of RV viscoelasticity to ventricular dysfunction, implicating tissue viscoelasticity as a therapeutic target for RV failure patients.

Chronic kidney disease (CKD) is an established global health problem, with the increased prevalence of vascular inflammation, accelerated atherogenesis, and thrombotic risk all contributing to overall cardiovascular risk. The major CKD-specific risk factor is presumed to be the accumulation of uremic toxins in circulation and tissues, further accelerating the progression of CKD and its co-morbidities, including those of bone mineral disorders and cardiovascular diseases.

In our narrative review, we focused on non-traditional cardiovascular risk factors, as they evolve with declined kidney function and are potentially further modulated by the choice of kidney replacement therapy.

Based on the data from the literature to date, the pre-eminent role of non-traditional risk factors emerges to mediate inflammation and increased cardiovascular mortality. In particular, patients receiving hemodialysis (HD) display dramatically increased CVD-mediated mortality. This intensified state of inflammation may be linked to the direct exposure of the bloodstream to a bio-incompatible environment in HD; for both complement-mediated and non-complement-mediated reactions, the possible contribution of neutrophil extracellular traps and complement activation-related pseudoallergy are reviewed in detail.

Our narrative review emphasizes key elements of a bio-incompatible HD environment that may contribute to increased cardiovascular mortality in patients receiving HD. Summarizing these results may provide conceptual opportunities to develop new therapeutic targets.

Background and Clinical Significance: Ventricular septal defect (VSD) is a rare but serious complication following myocardial infarction (MI) that can lead to cardiogenic shock and carries a high mortality rate. Acute mitral regurgitation (MR) is another severe complication of MI with additional risks of mortality. The optimal timing of surgical intervention for VSD with MR is still being debated, and delaying surgery in medically manageable patients has been associated with improved survival. However, managing these patients in the intensive care unit (ICU) presents unique challenges. Case Presentation: In this paper, we present the case of a 52-year-old male with comorbidities who developed post-MI VSD with severe MR and underwent successful delayed surgical repair and mitral valve replacement. Our aim is to highlight the clinical characteristics, diagnostic approach, and management strategies of this rare complication in the critical care setting. The patient presented in cardiogenic shock and acute pulmonary edema. After stabilization using an intra-aortic balloon pump, pre- and afterload reducing pharmacotherapy and non-invasive mechanical ventilation, a watchful waiting strategy was employed, and surgery was performed on day 21 after hospital admission. Surgery was performed under general anesthesia, and the patient did not develop any complications related to the intra-aortic balloon pump or novel organ dysfunction. Conclusions: This case highlights the importance of a multidisciplinary approach to managing post-MI VSD with MR and emphasizes the need for careful patient selection and timing of surgical intervention in the critical care setting. Clinicians should be aware of the potential benefits of delaying surgical intervention in medically manageable patients, while also considering the unique challenges of managing these patients in the ICU.

Background and Clinical Significance: Scimitar Syndrome is a rare congenital cardiopulmonary anomaly characterized by partial anomalous pulmonary venous return, often requiring early surgical correction. It may coexist with other congenital or acquired cardiovascular anomalies, including valvular diseases such as mitral regurgitation. When surgical correction of Scimitar Syndrome is combined with mitral valve annuloplasty, the proximity to the atrioventricular node may potentially predispose patients to late-onset conduction disturbances, although causality remains speculative. Case Presentation: We describe the case of a 53-year-old male who developed paroxysmal atrial fibrillation, atrial flutter, and intermittent second-degree AV block decades after undergoing surgical correction of Scimitar Syndrome with concomitant mitral annuloplasty. Multimodal echocardiographic evaluation revealed preserved left atrial volume, normal intra-atrial conduction time, mildly reduced strain, and maintained atrial synchrony. The patient was treated with direct oral anticoagulants and beta-blockers and underwent the implantation of a ventricular leadless pacemaker. Conclusions: This case highlights the supportive role of atrial function imaging in assessing atrial health and informing rhythm management and procedural choices in surgically corrected congenital heart disease.

Cardiomyopathies represent a heterogeneous group of myocardial disorders, traditionally classified by phenotype into hypertrophic, dilated, and arrhythmogenic. Historically, these conditions have been attributed to high-penetrance rare variants in key structural genes, consistent with a classical Mendelian pattern of inheritance. However, emerging evidence suggests that this model does not fully capture the full spectrum and complexity of disease expression. Many patients do not harbor identifiable pathogenic variants, while others carrying well-known disease-causing variants remain unaffected. This highlights the role of incomplete penetrance, likely modulated by additional genetic modifiers. Recent advances in genomics have revealed a broader view of the genetic basis of cardiomyopathies, introducing new players such as common genetic variants identified as risk alleles, as well as intermediate-effect variants. This continuum of genetic risk, reflecting an overall genetic influence, interacts further with environmental and lifestyle factors, likely contributing together to the observed variability in clinical presentation. This model offers a more realistic framework for understanding genetic inheritance and helps provide a clearer picture of disease expression and penetrance. This review explores the evolving genetic architecture of cardiomyopathies, spanning from a monogenic foundation to intermediate-risk variants and complex polygenic contribution. Recognizing this continuum is essential for enhancing diagnostic accuracy, guiding family screening strategies, and enabling personalized patient management.

Cardiac rehabilitation should be suggested after mitral valve intervention. Physical exercise is associated with improved cardiorespiratory fitness and clinical outcome and reduced rehospitalization and mortality in patients after heart valve surgery. Tailored assessment is the first step before starting a cardiac rehabilitation program. Physical examination, electrocardiogram, echocardiography, and peak exercise capacity stratify the risk of these patients when prescribing appropriate supervised aerobic and resistance exercise training. Cardiac rehabilitation participation impacts physical capacity, psychosocial function, and prognosis in patients after mitral valve surgery and transcatheter edge-to-edge repair. However, further evidence is needed on the efficacy and safety of cardiac rehabilitation programs, as well as standardization. In this review, we provide a contemporary and comprehensive update on the role of cardiac rehabilitation in patients after mitral valve intervention, after both mitral valve surgery and transcatheter mitral valve implantation. Specifically, we focus our review on the tailored assessment and management of these patients from post-operative to cardiac rehabilitation.

The imbalance in the interaction between the autonomic nervous system and the immune system serves as a central mechanism in the onset and progression of cardiovascular diseases. The excessive activation of the sympathetic nervous system and suppression of vagal function contribute to chronic inflammation and cardiac remodeling. Precision medicine, by integrating multidimensional data such as genomics and metabolomics, offers a novel perspective for the personalized design of exercise interventions. This systematic review explores the bidirectional regulatory mechanisms of exercise interventions on the autonomic nervous system-immune axis and examines the potential applications of precision medicine in optimizing exercise prescriptions and clinical translation. Exercise significantly improves cardiovascular function through immunometabolic reprogramming, which includes suppressing sympathetic overactivity, enhancing vagal tone, and modulating the IL-6/IL-10 balance, as well as activating the short-chain fatty acid (SCFA)-Treg axis. Moreover, precision-medicine-driven ACE I/D gene typing provides a basis for selecting tailored exercise prescriptions, thereby significantly enhancing the efficacy of exercise interventions. By leveraging a multi-tiered "neuro-immune-metabolic" regulatory framework, exercise interventions contribute to improved cardiovascular health. The application of precision medicine technology overcomes individual variability constraints, advancing exercise prescription design from generalized recommendations toward personalized and dynamically adaptive strategies.

Based on the notion that inflammation plays a pivotal role in the development and progression of cardiovascular diseases (CV) and that hyperuricaemia is an independent CV risk factor, chronic inflammatory diseases such as gout and rheumatoid arthritis are an interesting case study. Both conditions are burdened by an excess CV risk; they are themselves an independent CV risk factor, and in the case of gout, hyperuricaemia is a hallmark of the disease. Colchicine, a drug historically used for the management of gout, has recently been repurposed for secondary CV prevention in individuals at high CV risk. The purpose of this review article is to discuss evidence on CV diseases and CV prevention in rheumatoid arthritis, gout, and other chronic inflammatory/systemic autoimmune diseases with a focus on inflammation and hyperuricaemia.

Background/Objectives: Transcatheter aortic valve replacement (TAVR) has been introduced as an optimal treatment for patients with severe aortic stenosis, offering a minimally invasive alternative to surgical aortic valve replacement. Predicting these outcomes following TAVR is crucial. Artificial intelligence (AI) has emerged as a promising tool for improving post-TAVR outcome prediction. In this systematic review and meta-analysis, we aim to summarize the current evidence on utilizing AI in predicting post-TAVR outcomes. Methods: A comprehensive search was conducted to evaluate the studies focused on TAVR that applied AI methods for risk stratification. We assessed various ML algorithms, including random forests, neural networks, extreme gradient boosting, and support vector machines. Model performance metrics-recall, area under the curve (AUC), and accuracy-were collected with 95% confidence intervals (CIs). A random-effects meta-analysis was conducted to pool effect estimates. Results: We included 43 studies evaluating 366,269 patients (mean age 80 ± 8.25; 52.9% men) following TAVR. Meta-analyses for AI model performances demonstrated the following results: all-cause mortality (AUC = 0.78 (0.74-0.82), accuracy = 0.81 (0.69-0.89), and recall = 0.90 (0.70-0.97); permanent pacemaker implantation or new left bundle branch block (AUC = 0.75 (0.68-0.82), accuracy = 0.73 (0.59-0.84), and recall = 0.87 (0.50-0.98)); valve-related dysfunction (AUC = 0.73 (0.62-0.84), accuracy = 0.79 (0.57-0.91), and recall = 0.54 (0.26-0.80)); and major adverse cardiovascular events (AUC = 0.79 (0.67-0.92)). Subgroup analyses based on the model development approaches indicated that models incorporating baseline clinical data, imaging, and biomarker information enhanced predictive performance. Conclusions: AI-based risk prediction for TAVR complications has demonstrated promising performance. However, it is necessary to evaluate the efficiency of the aforementioned models in external validation datasets.