Advances in fetal cardiac magnetic resonance imaging (CMR) have expanded its role as an adjunct to expert fetal echocardiography in the prenatal evaluation of complex cardiopulmonary anomalies. This review outlines an evidence-based framework for integrating fetal CMR when it provides diagnostic or prognostic information that can informs counseling, delivery planning, or postnatal management.

Fetal CMR offers high-resolution, multiplanar imaging with superior soft-tissue contrast and wide field of view, enabling improved assessment of cardiopulmonary structures where echocardiography is limited by technical or physiologic factors, or when expert echocardiography raises clinically relevant questions. MRI enables improved delineation of aortic arch and pulmonary venous anatomy, characterization of pulmonary parenchymal changes, and quantify lung and ventricular volumetry without relying on geometric assumptions. Emerging flow-based techniques allow evaluation of fetal hemodynamics and cardiovascular physiology beyond static imaging. These technologies provide diagnostic and prognostic information in select, often critical, congenital heart diseases.

Fetal cardiac CMR serves as a complementary modality to expert echocardiography when applied selectively to address clinically meaningful diagnostic or prognostic questions. However, limited availability, technical complexity, and the need for specialized expertise currently constrain widespread adoption. Continued technical refinement and outcome-based validation are required before fetal CMR can be routinely integrated into clinical practice.

Predictive blood testing for outcomes of out-of-hospital cardiac arrest (OHCA) remains unclear in childhood.

We retrospectively analyzed < 15 years old patients with OHCA who entered Kyushu University Hospital between 2006 and 2021. Pediatric Cerebral Performance Category Scale (PCPC) and ΔPCPC score (post-arrest PCPC 30 days minus pre-arrest value) classified them into intact survival (ΔPCPC = 0) or poor survival (ΔPCPC = 1-4), and death or brain-death (PCPC = 6). Initial laboratory data on admission were studied focusing on outcomes and time from detection of CA to emergency room (ED).

Eligible 115 patients included 38 (15 intact-, 23 poor-) survivors and 77 deaths. Serum transaminase, lactate dehydrogenase, and potassium levels were higher in death cases than survivors, but did not differentiate poor from intact survivors. Blood gas data showed better levels in intact survivors than others, but did not differentiate poor survivors from deaths. In 41 witnessed cases including 16 (8 intact-, 8 poor-) survivors, no one survived with > 40 min of time from detection of CA to ED. In 28 witnessed cases with < 40 min of time from CA to ED, no biochemical variables discriminated the three groups of patients, but three blood gas parameters (pH, HCO₃ ^-, and BE) differentiated intact survivors from the other two groups. Furthermore, pH and BE were correlated with the duration of CA before hospital arrival in the analysis of witnessed OHCA patients.

Initial blood gas data on admission provide valuable information for estimating the duration of CA before hospital arrival and reflect survivors' outcomes in pediatric OHCA patients.

To develop a quantitative bias analysis approach based on realistic assumptions reflective of the complexities of healthcare data.

We describe a 'plasmode' simulation-based bias analysis for residual confounding from unmeasured variables by leveraging granular information from a subset of cohort members. We generated 500 simulated cohorts based on individual-level claims and linked electronic health record (EHR) data identifying new users of varenicline and bupropion from the Mass General Brigham site of the FDA Sentinel Real World Evidence Data Enterprise. Two adverse outcomes were simulated: (1) neuropsychiatric hospitalizations and (2) major adverse cardiovascular events (MACE), and measured confounding factors, identified from information available in claims including demographics, comorbid conditions, and comedications, were tailored to each outcome. Residual confounding was simulated using potential confounders measured in EHRs but unmeasured in claims including suicidal ideation for the neuropsychiatric outcomes and body mass index (BMI), blood pressure (BP), and smoking pack-years for the MACE outcome. These simulations retained the correlation between claims and EHR-based confounders observed in empirical data for realistic reflection of proxy adjustment of unmeasured confounders. Analyses were conducted in simulated data with and without adjustment for the EHR-based covariates to evaluate the extent of residual confounding in claims-only analyses.

After 500 simulations, the median absolute standardized mean difference (ASMD) between treatment groups in the unadjusted sample was 0.16 for suicidal ideation; while < 0.1 for BMI, BP, and smoking pack-years. For both outcomes, adjustment using claims-based variables provided relative bias close to 0, leading to the conclusion that EHR-measured confounders that were unmeasured in claims were unlikely to result in strong residual confounding within realistic simulations informed by empirical data.

The proposed approach provides a method for quantifying bias in non-randomized studies threatened by the unavailability of potentially important confounding variables.

The 11th Cardiovascular Outcome Trial (CVOT) Summit: Congress on Cardiovascular, Kidney, and Metabolic Outcomes was held virtually on November 20-21, 2025. The Summit provided a multidisciplinary forum to review and discuss recent outcome trials investigating emerging pharmacological therapies targeting diseases of the cardiovascular-kidney-metabolic (CKM) continuum. This report highlights the unique developments of 2025 discussed during the Summit, including the first head-to-head CVOT (SURPASS-CVOT), the growing evidence base for combination therapies across the disease spectrum, new insights into the inflammatory component of the CKM syndrome, and relevant policy developments. The first part of this report summarizes pioneering clinical trials addressing combination therapy with finerenone and empagliflozin (CONFIDENCE), the oral glucagon-like peptide-1 (GLP-1) receptor agonists orforglipron (ATTAIN-1), and the aldosterone synthase inhibitor (ASI) baxdrostat (BaxHTN). The second part presents recent guideline and policy developments discussed by experts in endocrinology, diabetology, cardiology, nephrology, hepatology, and general practice. In addition, advances in medical technology, particularly in continuous glucose and ketone monitoring, are highlighted, as well as emerging therapies for diseases of the CKM continuum. These include pharmacological agents for a broad spectrum of metabolic disorders such as metabolic liver disease and type 1 Diabetes (T1D) alongside emphasis on the importance of early detection and innovative treatment strategies. The 12th Cardiovascular Outcome Trial Summit will be held virtually on 19-20 November 2026 ( http://www.cvot.org ).

Current evidence does not support superiority of one cardioplegia type over another, but stems from low-risk populations. Therefore, we compared outcomes of multimorbid, high-risk infective endocarditis (IE) patients receiving Custodiol^®crystalloid or Calafiore blood cardioplegia during cardiac surgery.

We retrospectively analyzed 553 patients (mean EuroScore II 22.7 ± 21.1) who underwent surgery for IE between 2009 and 2023 and received either cold crystalloid (Custodiol^®, n = 335) or warm blood (Calafiore, n = 218) cardioplegia. The primary endpoint was 1-year mortality. Secondary endpoints included 30-day mortality, postoperative stroke, and new-onset dialysis. Propensity score matching (1:1, 14 covariates) resulted in 175 matched pairs. Statistical analysis included nonparametric and exact tests.

In the overall cohort, patients receiving Custodiol^® were higher risk and had higher mortality and morbidity. After matching, there was no significant difference in 1-year mortality between patients receiving Custodiol^® and Calafiore (37.1% vs. 28.6%, p = 0.09). 30-day mortality trended to be lower in the Calafiore group without reaching statistical significance (22.9% vs. 14.9%, p = 0.057). However, stroke was less frequent (4.6% vs. 10.9%, p = 0.029), ICU stay was shorter (3[1-8] vs. 6[3-12.5] days, p < 0.001) and postoperative dialysis was numerically less common (13.7 vs. 20.6%, p = 0.091). These differences were most evident in procedures with shorter cross-clamp times, such as isolated mitral or aortic valve surgery, where mortality and recovery parameters consistently favored Calafiore.

In high-risk endocarditis patients warm blood cardioplegia may be superior to cold crystalloid, although differences did not reach statistical significance. However, propensity matching may not have accounted for all differences, which warrants further discussion and investigation.

Previous studies have found that the pathology of post-stroke aphasia might be related to abnormalities in the white matter connectivity. However, it is still unclear about the neural mechanism of white matter impairment in the post-stroke aphasia. The present study attempted to detect the alteration of the brain white matter structural network in the post-stroke aphasia. We recruited 16 PSA patients who suffered from post-stroke aphasia and 14 healthy controls and acquired their diffusion-tensor imaging data. We performed a deterministic white matter fiber tracking to construct white matter structural network and estimated network topological properties by using graph theory. We also assessed the between-group differences in these parameters and estimated the correlations between the abnormal parameters and clinical assessments in the patients. The patients showed higher shortest path length, higher normalized clustering coefficient, and lower global efficiency than the controls. We found abnormal nodal parameters in the frontal, parietal, basal ganglia, and limbic regions in the patient group. From the rich-club analysis, we found that the patient group showed higher rich-club connections and lower feeder connections than the control group, and had a new rich-club region, the right fusiform gyrus. In summary, this study detected the abnormal both nodal and global parameters of the brain white matter structural network in the post-stroke aphasia. These findings may provide insights into understanding the abnormal brain network and impairment of language function in the post-stroke aphasia.

Peripheral nerves are increasingly recognized as regulators of vascular pathology, shaping arterial tone, inflammation, and structural remodeling. This review delineates how neural circuits interface with the aortic wall, considers sympathetic and sensory pathways in atherosclerosis and aneurysm pathophysiology, and discusses emerging experimental approaches and therapeutic strategies.

Autonomic and sensory neural circuits are increasingly recognized as modulators of arterial disease. In experimental atherosclerosis, neuroimmune crosstalk shapes vascular inflammation and influences plaque stability. Limited available evidence from human and experimental studies suggest increased sympathetic innervation within aneurysm tissue. In preclinical models, aneurysm remodeling was linked with sympathetic input, and interventions that reduce noradrenergic signaling via sympathetic denervation or pharmacological adrenergic blockade attenuated disease severity. Improved understanding of the role for innervation in vascular pathophysiology may open therapeutic opportunities, including neuromodulation and pharmacological interventions. Clarifying sources of heterogeneity between models and clinical data can potentially refine therapeutic targets and patient selection, and advance opportunities for precision interventions. Peripheral neural circuits are integral to vascular homeostasis in health and disease, interfacing with blood vessels and regulating their physiology. Converging human and preclinical evidence implicates sympathetic innervation in disease development, and that dampening adrenergic signaling via denervation or adrenergic blockade may mitigate disease progression. This review discusses mechanistic neuroimmune crosstalk across atherosclerosis and aneurysm biology and outlines some potential translational opportunities. Together, the advances position neurovascular crosstalk as a potentially tractable axis for disease-modifying interventions.

Infectious complications, such as sepsis or catheter-related infections, are common and serious sequelae after trauma. Despite their clinical significance, existing risk-prediction models are limited by reliance on in-hospital data that fail to capture complex physiological interactions. Thus, this study aimed to develop and validate an interpretable ensemble machine learning (ML) model integrating both prehospital and in-hospital clinical data to predict infectious complications after trauma.

We used data from the Korean Trauma Data Bank, comprising patients admitted to all 19 trauma centers from 2017 to 2022 in South Korea (discovery; n = 227,567) and from four additional centers added in 2023 for external validation (n = 8867). Trauma cases were defined utilizing S or T diagnostic codes based on the 7th Korean Standard Classification of Diseases, and infectious complications were defined as a composite outcome of pneumonia, urinary tract infection, catheter-related bloodstream infection, surgical site infection (deep, organ, and superficial), osteomyelitis, or severe sepsis. A total of 33 prehospital and in-hospital features were used in ML model training, and the top-performing models were ensembled to construct the final model. Model performance was evaluated through five-fold cross-validation, internal testing, and external validation. Shapley Additive Explanations (SHAP) were applied to assess predictor importance, and predicted risks were categorized into tertiles (T1-T3) to examine associations with in-hospital mortality and presented adjusted odds ratios (aORs) with 95% confidence intervals (CIs).

Among 88,899 eligible patients with trauma in the discovery cohort, the soft-voting ensemble model integrating logistic regression, categorical boosting, and extreme gradient boosting achieved the best discrimination, with an area under the receiver operating characteristic curve of 0.796 in the discovery cohort and 0.717 in the external validation cohort. SHAP analysis identified age, accident type, Glasgow Coma Scale verbal response, and sex as the most influential variables. Higher tertiles of predicted infection risk were strongly associated with mortality, with aORs of 2.52 (95% CI, 2.12-2.99) for T1, 4.65 (3.96-5.47) for T2, and 6.19 (5.02-7.62) for T3.

This interpretable model, which integrates prehospital and in-hospital data available within the first 24 h of admission, presented robust predictive performance for post-traumatic infectious complications. The proportional association between predicted infection risk and mortality highlights its clinical relevance, as even modest increases in predicted risk may carry meaningful implications for patient outcomes and early intervention strategies.

Aneurysmal subarachnoid haemorrhage (aSAH) results from the rupture of an intracranial aneurysm. The case-fatality after aSAH is approximately 40% and those who survive often have functional, cognitive or emotional sequelae. We prepared guidelines according to Grading of Recommendations, Assessment, Development and Evaluations (GRADE) methodology, using data from meta-analyses, randomised trials, prospective observational and case-control studies, prospective registries with external validation and single-arm cohort studies with > 50 patients with aSAH. Based on high levels of evidence, we recommend oral administration of nimodipine and regular coiling over clipping if both aneurysm treatment options are equally suitable in patients who are in good clinical condition, and recommend against the routine use of antifibrinolytic drugs prior to aneurysm treatment and against the use of tirilazad, statins, magnesium sulphate or endothelin receptor antagonists. Because of lower levels of evidence, no evidence-based recommendations can be made for the prophylactic use of antiplatelet drugs or external lumbar drainage, hypertension induction, treatment of the ruptured aneurysm with endovascular devices other than coils or endovascular treatment of vasospasm. We formulated 37 expert-consensus statements, which include, among others, the suggestions to treat aSAH patients in a dedicated neuro-ICU or high care unit in a centre that treats at least 70 patients with aSAH per year or at least 35 patients with aSAH per year in geographically remote areas, and to treat the ruptured aneurysm within 24 h after ictus provided that the most dedicated team of experts is available. These guidelines present up-to-date recommendations and expert-consensus statements on key aspects in the management of aSAH patients.

In this review, traumatic brain injury (TBI) is found to be a frequent cause of contact in primary and secondary healthcare services. Intracranial haemorrhage associated with TBI occurs when direct or indirect forces to the head damage intracranial vessels. Patients with mild TBI, defined as a GCS of 14-15, seldom require CT imaging unless they were unconscious or had a seizure at the time of injury, are receiving anticoagulant therapy, have coagulopathies, present with focal neurological deficits, have shunt-treated hydrocephalus, or show clinical signs of a skull fracture.