Refractory hypotension may aggravate cerebral hypoperfusion in acute ischemic stroke, but occult coronary artery disease is often overlooked.

A 67-year-old man presented with sudden right-sided weakness. Within 24 hours, he developed persistent hypotension (approximately 90-100/50-60 mm Hg) and neurological worsening.

Brain magnetic resonance imaging revealed an acute left frontoparietal watershed infarction. Despite fluid resuscitation and vasopressors, hemodynamic instability persisted. Hypovolemia, endocrine disorders, and cervico-cephalic stenosis were excluded. Although cardiac biomarkers and ejection fraction were normal, electrocardiography showed inferior Q waves. Coronary angiography confirmed critical left anterior descending (LAD) artery stenosis with distal occlusion.

Fluid resuscitation and vasopressor support failed to stabilize blood pressure. Balloon angioplasty was performed for the left anterior descending artery lesion.

After intervention, blood pressure normalized without vasopressors, and neurological function improved.

In acute ischemic stroke patients with unexplained refractory hypotension and watershed infarction, occult coronary ischemia should be considered even when troponin is normal. Early coronary evaluation and timely revascularization may improve cerebral perfusion and outcomes.

The most common complication of atrial fibrillation is cerebral embolism, while abdominal aortic embolism is relatively rare. This case highlights the need for heightened clinical awareness of systemic embolic complications associated with atrial fibrillation.

A 76-year-old male patient presented with sudden onset of bilateral lower limb weakness lasting 12 hours, accompanied by numbness and pain in both legs. Symptoms have persisted without improvement and are associated with gross hematuria.

Computed tomography angiography of the chest and abdomen reveals occlusion of the lower abdominal aorta (below the renal arteries) and bilateral lower extremity arteries; thrombus formation in the descending aorta; incidental findings of low-density areas in both renal parenchyma.

Administer enoxaparin for anticoagulation. Recommend transferring the patient to an intensive care unit or a higher-level hospital for treatment. The patient and their family are aware of the associated risks and have declined further treatment.

During a subsequent follow-up phone call, it was reported that the patient had passed away.

This case demonstrates that complications of atrial fibrillation are not limited to common cerebral embolism; embolism involving other organs can also be fatal.

Left main coronary artery (LMCA)-related acute myocardial infarction with cardiogenic shock (CS) carries >80% mortality without immediate revascularization.

Thrombolysis often fails in such cases with LMCA and CS, necessitating salvage percutaneous coronary intervention, which typically requires stenting and mechanical circulatory support.

LMCA and CS.

We report a unique case successfully managed with drug-coated balloon (DCB)-only angioplasty amid resource constraints during the pandemic. This report presents a high-risk case of LMCA acute myocardial infarction with CS following unsuccessful TNK thrombolysis at the local hospital, successfully revascularized with DCB-only angioplasty without stenting, intravascular ultrasound (IVUS), intra-aortic balloon pump, or extracorporeal membrane oxygenation, because of pandemic-related medical resource limitations (IVUS/intra-aortic balloon pump unavailable) and extracorporeal membrane oxygenation not yet implemented at our hospital at that time.

Post-procedural TIMI 3 flow was achieved immediately. Postoperatively, the patient's CS gradually resolved. After 1 month, IVUS performed at a tertiary hospital confirmed no need for further intervention for LMCA. Six months later, cardiac function had recovered to normal.

This case demonstrates that in resource-limited settings, when safe stent implantation cannot be guaranteed for thrombotic left main occlusion, the DCB-assisted rapid reperfusion strategy may represent a viable, life-saving option. It offers a new approach for primary care hospitals managing such critical emergencies.

Clinical investigations have demonstrated that blood and immune cells are involved in the pathophysiological processes of dilated cardiomyopathy (DCM) and hypertrophic cardiomyopathy (HCM). However, the causal relationships between these cellular components and the development of DCM and HCM remain uncertain. A two-sample Mendelian randomization analysis was performed to evaluate the causal effects of blood cells and immune cells on DCM and HCM. The primary analytical method was inverse variance weighting, supplemented by Mendelian randomization-Egger, weighted median, and MR-PRESSO approaches. Furthermore, immune cells were examined as mediators to assess their intermediary roles in the causal pathways linking blood cells with DCM and HCM. Significant causal associations were observed between red blood cells, monocytes, eosinophils, and platelets and DCM and HCM (P < .05). CD127 on CD8br, naive CD8br %CD8br, CD16- CD56 on natural killer cell, CD45 on T cell, and lymphocyte AC were identified as mediators in the causal pathways connecting various blood cell types to DCM and HCM. This study provides robust evidence for the causal roles of specific blood cell and immune cell phenotypes in the development of DCM and HCM. These findings open new avenues for investigating the hematological immune system in cardiomyopathy and present novel opportunities for therapeutic interventions targeting DCM and HCM.

Stroke is a leading cause of death and disability worldwide, with ischemic strokes accounting for the majority of cases. Huangjing Wan (HJW) is a classical Chinese herbal formula used in the treatment of stroke, but the precise mechanisms of action remain unclear. We retrieved the active components of HJW, along with their related targets and the targets associated with middle cerebral artery occlusion (MCAO), by conducting a search across relevant databases. The common targets obtained from the intersection of the 2 target sets were used to establish both a compound-target interaction network and a protein-protein interaction (PPI) network. A Kyoto Encyclopedia of Genes and Genomes (KEGG) bioinformatic analysis was ultimately performed to identify the potential signaling pathways associated with HJW in the treatment of MCAO. Through searching and screening a series of databases, we identified 129 active ingredient-associated targets of HJW and 1246 therapeutic targets for MCAO. The intersection of the 2 sets yielded 40 overlapping targets. Based on these 40 common targets, a compound-target interaction network and a PPI network were constructed. Finally, KEGG pathway enrichment analysis revealed that the key signaling pathways potentially involved in HJW treatment of MCAO primarily include the Hepatitis B pathway, the lipid and atherosclerosis pathway, and the Apoptosis pathway. This study reveals that HJW primarily exerts its therapeutic effects on MCAO through the Hepatitis B virus pathway, the lipid and atherosclerosis pathway, and the apoptosis pathway, providing a theoretical basis for further in-depth research.

Extracellular vesicles (EVs) are non-replicating, lipid membrane-bound nanoparticles released by most eukaryotic cells into the extracellular space. When derived from platelets, a subset of EVs can exhibit remarkable anti-inflammatory and antioxidant properties, making them attractive candidates to attenuate sterile inflammatory states such as limb skeletal muscle ischaemia-reperfusion injury (IRI). Peripheral extremity IRI complicating acute limb revascularisation procedures, replantation of major traumatic amputations and limb allotransplants can trigger a life-threatening reperfusion syndrome that leads to multi-organ system failure and death. In this study, we used a platelet-derived EVs-enriched preparation as a therapeutic strategy for extremity IRI. To allow for a clinically translatable drug delivery strategy, we established and validated a catheter-directed regional intra-arterial limb infusion (RLI) delivery approach that permitted selective and effective targeting of pEVs to limb skeletal muscles and soft tissues in the vascularly isolated rodent extremity simulating pre-reperfusion preservation and revascularisation conditions of the ischaemic or amputated extremity. In addition to being safe and feasible, we demonstrated robust retention of EVs by skeletal muscles of the operative limb during the early critical phase of reperfusion injury following RLI. We also show that pretreatment of ischaemic skeletal muscles using an pEVs-enriched formulation just before reestablishing extremity blood flow alleviated metabolic derangements and suppressed the systemic and localised proinflammatory cytokine response associated with skeletal muscle reperfusion and reduced histologic markers of myofibre injury without adverse effects on serum chemistries. This work opens a new perspective to investigate novel approaches for regional delivery of therapeutic pEVs to skeletal muscle to mitigate limb IRI in vivo, and to achieve both in situ and ex vivo targeted delivery of nanocarriers to the isolated limb tissue for other therapeutic applications.

As a widely used anticancer drug for the treatment of chronic myeloid leukemia, ponatinib is known to cause severe cardiovascular toxicities. Cardiomyocytes are the major functional units in the myocardium, and impairment of their viability and function plays a crucial role in cardiotoxic responses. Previous studies have indicated direct toxicity of ponatinib on cardiomyocytes, but the effect of ponatinib on adult human primary cardiomyocytes (hPCMs) remains unknown, largely due to sample scarcity and the technical challenges associated with the adult human cardiomyocyte model. Based upon our previous work establishing hPCMs as a pharmacologically competent model, we tested the direct toxicity of ponatinib on these cells. We reveal suppression of AKT, but not ERK, phosphorylation upon ponatinib treatment. Treatment of hPCMs with AKT inhibitor MK-2206 phenocopied ponatinib, while restoration of AKT signaling with UCL-TRO-1938 or insulin partially rescued hPCMs from cell death, suggesting a potential protective effect.

D-dimer as a mixture of soluble cross-linked fibrin degradation products cleaved by plasmin is a well-established biomarker of in vivo blood coagulation activation with concomitant secondary fibrinolysis that is widely determined in a broad variety of clinical settings. D-dimer interpretation is hampered by the lack of the assay international standard and assay harmonization across laboratories, preanalytical variables affecting the results, multiple assays available with different units, and the impact of heterophilic nonspecific IgG or IgM antibodies, which cause falsely increased or decreased results. Different reactivity of monoclonal antibodies against D-dimer molecule results in a variability of results obtained with different assays within individual patients. Compelling clinical evidence supports a high negative predictive value of age-adjusted D-dimer concentration in ruling out venous thromboembolism, both pulmonary embolism and deep-vein thrombosis. Elevated D-dimer levels are observed in acute myocardial infarction or stroke, aortic aneurysm and acute dissection, atrial fibrillation, heart failure, following invasive procedures, infection. Elevated D-dimer can be found in chronic venous insufficiency, chronic inflammatory diseases, cancer, sepsis, autoimmune disorders, diabetes, advanced age, strenuous physical activity, and pregnancy. Though elevated D-dimer is associated with increased risk of first and recurrent venous thromboembolism, it is no per se indication for anticoagulant treatment and should lead to in-depth diagnostic evaluation to identify mechanisms underlying such abnormality. The current overview summarizes both laboratory and clinical knowledge on D-dimer measurement and interpretation with focus on acute and chronic cardiovascular diseases.

Machine learning (ML) has emerged as a transformative approach for developing high-performance clinical prediction models (CPMs). By leveraging multidimensional patient data, ML enables more accurate disease risk stratification, prognostic assessment, and clinical decision-making. In recent years, research on CPMs has expanded rapidly, with nearly 250,000 publications indexed as of 2024. Despite this remarkable growth, a comprehensive bibliometric analysis of the field is currently lacking.

This study aimed to analyze the global research status, evolutionary trends, and thematic hotspots of machine learning-based clinical prediction models (ML-CPMs) through bibliometric and visualization techniques.

Publications related to ML-CPMs were retrieved from the Web of Science Core Collection and the Scopus database (up to May 9, 2025). Bibliometric analyses were performed using various tools, including R, VOSviewer, and CiteSpace, to generate annual publication trends, collaboration networks, and journal distributions, as well as co-citation, clustering, and keyword analyses.

A total of 8,619 publications (8,000 original articles and 619 reviews) from 118 countries were identified. Since 2015, annual publications have grown exponentially (R² = 0.9919). While China led in total publication volume, the United States maintained the highest academic influence (H-index = 105; Total Citations = 66,788). Harvard University and BMC Medical Informatics and Decision Making emerged as the most productive institution and journal, respectively. Tian J from the Chinese Academy of Sciences led in publication count, while Wynants L from KU Leuven in Belgium recorded the highest citation frequency. Key research hotspots include algorithm optimization, multimodal data integration, and model interpretability, with clinical applications primarily focused on oncology, cardiovascular diseases, and critical care medicine.

Research on ML-CPMs has experienced rapid global growth over the past decade, forming extensive international collaboration networks. However, challenges such as limited interpretability, data heterogeneity, and privacy concerns persist. Future studies should prioritize external validation, clinical applicability, and the integration of human-AI collaborative decision-making to ensure robust implementation in real-world clinical settings.

Cardio-cerebrovascular diseases (CCVDs), notably stroke and coronary heart disease, represent the leading causes of mortality and disability worldwide. The intricate bidirectional feedback between the brain and heart in brain-heart syndrome (BHS) exacerbates clinical outcomes and imposes a significant economic burden on patients. The cytokine tumor necrosis factor-like apoptosis weak inducer (TWEAK) and its receptor fibroblast growth factor-inducible 14 (Fn14) are overexpressed in cerebral injury and cardiac dysfunction. Elevated levels of TWEAK and Fn14 contribute to the development of various brain diseases, including blood-brain barrier damage, brain edema, neuroinflammation, neuronal apoptosis, and neurodegeneration. Additionally, the TWEAK-Fn14 axis is implicated in numerous pathophysiological events in the heart, such as cardiomyocyte proliferation, inflammation, apoptosis, hypertrophy, fibrosis, contractile function disruption, and ventricular dilatation. Given its significant contributions to CCVDs, the TWEAK-Fn14 axis has also emerged as a promising therapeutic target for BHS. In this review, the critical roles of TWEAK-Fn14 in CCVDs and its potential interplay between the brain-heart axis in BHS were updated and discussed, which shed a new light on co-treatment of brain and heart and brain-heart syndrome.