Coronary artery disease (CAD) remains the leading cause of morbidity and mortality worldwide. Echocardiographic assessment of left ventricular (LV) asynchrony may provide additional value for detecting ischemia or infarction.

To assess the systolic and diastolic mechanical dispersion (MD) by 3D-echocardiography and its correlation with left ventricular ejection fraction (LVEF) and ischemia or infarction by myocardial perfusion study (MPS) gated 99m-Tc Sestamibi-SPECT.

Cross-sectional study of patients with angina. Systolic and diastolic MD were defined as the standard deviation (SD) of the time to reach minimum ventricular volume, corrected for the R-R interval. Association with LVEF was assessed with correlation and linear regression. ROC curves identified ischemia or infarction and compared with E/A ratio, TRIVI, and E/e' ratio.

205 patients were studied with median age 62 (IQR: 54-69) years. 51% (n = 104) presented ischemia or infarction. We observed a negative correlation with systolic (r = -0.343, 95% -0.459 to -0.215; p < 0.001) and diastolic (r = -0.184, 95% -0.314 to -0.047; p < 0.01) MD and MPS-LVEF, which contributes to 8.9% and 11.8% of variance, respectively. Both parameters displayed an area under the curve (AUC) of 0.634 (95% 0.559-0.709, p < 0.001) and 0.604 (95% CI 0.527-0.679, p < 0.001) are shown to detect ischemia/infarction. In patients with transmural infarction the AUC for systolic MD improved to 0.691 (95% 0.582-0.801, p < 0.05).

Systolic and diastolic MD are useful and simple parameters for assessment of LV function and ischemia or infarction.

Mycotic aneurysms (MA) are a potentially fatal complication following intestinal transplantation (ITx). Their occurrence arises from several factors, such as chronic abdominal sepsis, potential for contamination of the vascular grafts during enteric anastomoses and the heightened burden of immunosuppression.

A retrospective review of a prospectively maintained database of all adult ITx from December 2007 to June 2025 was conducted.

Among 168 ITx, six patients (3.6%) experienced eight MA episodes. MA occurred bimodally, early post-transplant (2-8 weeks) or in a later phase (55-377 weeks). Recurrence occurred in two patients, averaging 132.4 weeks after initial diagnosis. A history of hollow viscus perforation or anastomotic leak was present in 83.4%. Diagnosis was peri-operative in two cases due to rupture, while others were detected electively via angio-CT. Recurrences were subtler, identified incidentally or with mild symptoms. Apart from targeted antibiotic and antifungal treatment, management strategy pivoted around endovascular stent grafting (ESG) followed by an aneurysmectomy and creation of a new conduit. Post-operative mortality at first presentation occurred in 66.6% of patients, with 50% within a week. Two patients survived recurrence, with one remaining alive 6.5 years post-diagnosis.

MA in ITx is rare but commonly fatal, often linked to bowel perforation or anastomotic complications. Diagnosis relies on angio-CT or intraoperative identification at the time of emergency laparotomy. Management involves ESG and conduit resection. Early aggressive control of potential contamination sources after ITx is crucial, though general conclusions are limited by low incidence.

Metabolic dysfunction-associated fatty liver disease (MAFLD) and carotid artery plaque (CAP) are both linked to circulatory lipid and lipoprotein metabolism. However, the shared lipidome-wide mechanisms underlying these diseases remain unexplored. To identify plasma lipid species associated with both MAFLD and CAP to uncover their shared metabolic pathways. We analyzed data from the Young Finns Study cohort from the 2007 and 2018 follow-ups (n = 1496, aged 41-56 years, 56.3% females). Ultrasound was used to determine the prevalence of both CAP and MAFLD during the 2018 follow-up. The participants were categorized into three mutually exclusive groups: participants with CAP without MAFLD (n = 257), participants with MAFLD without CAP (n = 150), and a control group free from both diseases (n = 436). Lipidomic profiling of 437 lipid species from plasma was performed during the 2007 follow-up (aged 30-45 years) via liquid chromatography‒tandem mass spectrometry. Logistic regression models, both unadjusted and adjusted for age, sex, physical activity, alcohol consumption, and smoking, were used to assess lipid associations with both disease outcomes separately. Odds ratios (ORs) and confidence intervals (95% CIs) were calculated for each lipid species, and multiple testing corrections were performed via the false discovery rate (FDR) method (< 0.05). Additionally, we performed a hypergeometric enrichment analysis to determine whether certain lipid classes appear more often than expected among the lipids associated with disease. In the unadjusted models, there were a total of 51 significant (FDR < 0.05) overlapping lipids between the CAP and MAFLD groups. In the adjusted models, four lipids were significantly associated with CAP, and 202 lipids were significantly associated with MAFLD. Notably, only one lipid-phosphatidylcholine (PC) 40:4-was significantly associated with both diseases. PC 40:4 was associated with an increased risk of CAP (OR 2.59; 95% CI, 1.57-4.32) and MAFLD (OR 5.26; 95% CI, 2.81-9.85). Our findings highlight PC 40:4 as a novel shared lipid signature for both MAFLD and CAP. This dual association suggests that overlapping metabolic disturbances and potentially common lipid-based pathogenic mechanisms link liver and vascular health. PC 40:4 may serve as a promising early biomarker or therapeutic target for metabolic-vascular comorbidities.

Despite improved survival, patients with advanced heart failure receiving long-term left ventricular assist device (LVAD) support remain at risk of serious complications, including pump thrombosis, ischemic stroke, and bleeding. LVAD therapy may contribute to persistent alterations in the hemostatic system, the impact of which on adverse clinical events remains unclear. The aim of the study was to characterize longitudinal alterations in coagulation in patients supported with continuous-flow LVADs, assessed using the Calibrated Automated Thrombogram (CAT) assay. Basic coagulation parameters were assessed at baseline, 3-4 months, 6-12 months, and every 6 months thereafter. Only patients completing all four scheduled follow-up visits were included in further analyses. Eighty-five patients were recruited; 22 met the inclusion criteria. Significant shift toward a hypocoagulable state was observed: increase in thrombin generation lagtime, decrease in endogenous thrombin potential and peak thrombin concentration (P < 0.001). Markers of persistent fibrinolytic activity were observed. LVAD support was associated with increased albumin and hemoglobin levels, decreased bilirubin, creatinine, and NT-proBNP concentrations (P < 0.05). No significant differences were observed between CAT parameters and adverse events in the investigated group. Long-term LVAD therapy was associated with progressive changes in coagulation parameters, despite a stable anticoagulant and antiplatelet treatment regimen.

This review evaluates the antihypertensive potential of next-generation incretin-based therapies, including GLP-1 receptor agonists and dual GLP-1/GIP receptor agonists. It examines their effects on blood pressure reduction, underlying mechanisms, clinical benefits, and implications for future guidelines.

Recent large-scale trials demonstrate that incretin-based therapies such as semaglutide and tirzepatide significantly reduce body weight, blood pressure, and cardiovascular outcomes. Mediation analyses indicate that weight loss explains a substantial proportion of blood pressure reduction, while direct effects on vascular function, renal sodium handling, and neurohumoral pathways also contribute. These effects are consistent across diverse populations, including individuals without overt hypertension. Incretin-based therapies represent a promising approach in hypertension management, combining metabolic and cardiovascular benefits. Despite the lack of trials with blood pressure as a primary endpoint, current evidence supports their use in selected high-risk populations and suggests an emerging role in future guideline recommendations.

The special AT-rich sequence-binding protein 2 (SATB2) is associated with human cognitive ability. Mutations in the SATB2 gene lead to SATB2-associated syndrome (SAS), characterized by severe intellectual disability. SATB2 is mainly expressed in pyramidal neurons in the cerebral cortex and hippocampus, playing a crucial role in cognitive processes. However, the function of SATB2 in the adult hippocampus remains unclear. In this study, we deleted Satb2 in the CA1 region of the adult mouse hippocampus and observed cognitive impairments along with significant changes in soma and dendrite morphology. Additionally, we identified the growth factor pleiotrophin (PTN) as a downstream target of Satb2, essential for mediating its impact on cognitive functions. Importantly, increasing PTN expression mitigated the morphological and behavioral deficits resulting from Satb2 deletion in CA1. Our findings highlight the importance of hippocampal Satb2 in regulating cognitive function in adult mice through PTN modulation.

Ischemic stroke remains a leading cause of death and long-term disability worldwide, and effective neuroprotective therapies applicable to a broad patient population are still limited. Although mesenchymal stromal cell-derived exosomes (MSC-EXO) have emerged as promising cell-free therapeutic agents, evidence regarding exosomes derived from human amnion-derived mesenchymal stromal cells (AMSC-EXO) in cerebral ischemia remains scarce.

Human AMSC-EXO were isolated from conditioned media of cultured human amnion-derived mesenchymal stromal cells and characterized by nanoparticle tracking analysis and exosomal marker expression. Male mice were subjected to middle cerebral artery occlusion and randomly assigned to receive intravenous AMSC-EXO or vehicle 24 h after ischemia. Neurological function, motor coordination, and spatial working memory were assessed at 3 and 14 days. Post-ischemic neuroinflammation, neuronal degeneration, and endothelial cell proliferation were evaluated by immunohistochemistry and enzyme-linked immunosorbent assay in a blinded manner.

Systemic administration of AMSC-EXO significantly improved neurological outcomes and motor performance after cerebral ischemia and enhanced spatial working memory. AMSC-EXO treatment markedly suppressed microglial activation and reduced the expression of pro-inflammatory cytokines, including tumor necrosis factor-α, interleukin-1β, and interleukin-6, in the ischemic brain. In addition, neuronal degeneration in the cortical infarct border zone was significantly attenuated. At later stages, AMSC-EXO significantly increased the number of proliferating endothelial cells, suggesting a potential involvement in neurovascular remodeling.

Human AMSC-derived exosomes exert neuroprotective and neurovascular restorative effects after cerebral ischemia by suppressing post-ischemic neuroinflammation, reducing neuronal cell death, and promoting endothelial cell proliferation. AMSC-EXO represents a promising, scalable, and cell-free therapeutic strategy for ischemic stroke.

Ultra-processed foods (UPFs) have increasingly displaced traditional diets globally and have become a significant public health concern, particularly in relation to cardiovascular (CV) diseases. UPFs are defined as food products primarily composed of cheap industrial ingredients, additives, and neo-formed compounds, often with little to no nutritional value. These foods are highly processed and contain additives that can have harmful effects on health. While traditional dietary guidelines have long emphasized the importance of limiting animal-derived fats and promoting the intake of fruits, vegetables, and unsaturated fats, recent evidence suggests that the extent and nature of food processing are also key factors in the relationship between diet and health. Studies over the past decade have highlighted that the consumption of UPFs is associated with increased CV risk, often independent of the overall diet quality. Despite growing evidence linking UPF consumption to major CV risk factors (e.g. hypertension, dyslipidaemia, obesity) and adverse CV outcomes, the role of food processing in CV health remains underrecognized in cardiology. Current dietary counselling in clinical practice tends to overlook the potential adverse impact of UPFs, with patients not receiving comprehensive nutritional guidance. This European Society of Cardiology (ESC) clinical consensus statement, developed by a multidisciplinary group of European experts, is conceived to increase awareness among clinicians about the CV risks associated with UPFs. Starting from a comprehensive review of current evidence, it provides practical, actionable advice to help the general cardiologists incorporate UPF-related assessment and counselling into their routine care. The statement also proposes a stepwise framework focused on CV prevention, including tools designed to enhance patient communication and engagement. Moreover, it discusses these clinical advices within wider strategic and policy frameworks, therefore supporting a more integrated, food-centred approach to improve CV health.

Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, has been implicated in cardiometabolic inflammation; however, the intracellular signaling mechanisms linking TMAO to macrophage polarization remain incompletely defined. This study aimed to investigate whether TMAO promotes macrophage M1 polarization through a Piezo1-Yes-associated protein (YAP) signaling axis. Gain- and loss-of-function approaches were performed in RAW264.7 cells and primary bone marrow-derived macrophages, including Piezo1 overexpression, small interfering RNA-mediated knockdown of Piezo1 or YAP, and pharmacological inhibition of YAP. Macrophage polarization markers were evaluated by immunofluorescence, flow cytometry, real-time quantitative polymerase chain reaction, and Western blot analysis. Intracellular Ca²⁺ levels were assessed using Fluo-4 acetoxymethyl ester fluorescence imaging. TMAO increased inducible nitric oxide synthase expression and reduced arginase-1 levels (P < .01), accompanied by elevated IL-1β and IL-6 and decreased IL-4 and IL-10 (P < .01). Piezo1 overexpression promoted M1 polarization (P < .01), whereas Piezo1 knockdown under TMAO exposure attenuated inflammatory cytokine induction (P < .001). TMAO enhanced intracellular Ca²⁺ influx (P < .001) and reduced inhibitory phosphorylation of YAP (Ser127) (P < .01). Inhibition or silencing of YAP mitigated TMAO-induced M1 marker expression and downstream kappa B/extracellular signal-regulated kinase activation (P < .05). Similar results were confirmed in primary bone marrow-derived macrophages. These findings suggest that TMAO promotes macrophage M1 polarization in association with Piezo1-dependent Ca²⁺ influx and YAP activation, identifying the Piezo1-YAP axis as a potential mechanistic interface linking microbiota-derived metabolites to inflammatory remodeling. SIGNIFICANCE STATEMENT: This study identifies the Piezo1-Yes-associated protein signaling axis as a potential drug target in trimethylamine N-oxide-induced macrophage polarization toward a proinflammatory phenotype. Inhibition of this pathway attenuates inflammatory responses, suggesting a potential pharmacological strategy for microbiota-associated cardiovascular diseases.

Myocardial infarction (MI) is the most severe clinical complication of coronary atherosclerotic heart disease (CHD), representing a leading cause of global morbidity and mortality. Qi-Blood Harmony Formula (QBHF), a traditional Chinese medicine, has shown clinical promise for managing MI; however, its underlying mechanisms remain to be fully elucidated.

This study aimed to explore the therapeutic mechanism of QBHF against MI in the context of CHD, with a specific focus on its role in angiogenesis.

QBHF chemical components were characterized by ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry. Therapeutic efficacy was evaluated in a high-fat diet-fed ApoE^-/- mouse model with left anterior descending coronary artery ligation and in a hypoxia-induced endothelial cell model. Cardiac function and angiogenesis were assessed through histological, functional, and molecular assays, with the underlying mechanisms further investigated using bioinformatics and experimental validation.

Chemical profiling identified 67 compounds in QBHF, with eight major constituents quantified. In atherosclerosis-myocardial infarction (AS-MI) mice, QBHF dose-dependently improved cardiac function, attenuated myocardial injury, and upregulated angiogenic markers. In vitro, QBHF enhanced hypoxia-induced proliferation, migration, and tube formation in EA.hy926 cells. Mechanistically, a specific circular RNA (hsa_circ_0003296) was found to be significantly upregulated in the peripheral blood of AS and MI patients. It directly bound to eukaryotic initiation factor 4A-III (EIF4A3) to promote its ubiquitin-mediated degradation. QBHF suppressed hsa_circ_0003296 expression, thereby preventing EIF4A3 degradation. The stabilized EIF4A3 subsequently prolonged the mRNA half-lives of vascular endothelial growth factor A (VEGFA) and VEGF receptor 2 (VEGFR2), thereby promoting angiogenesis.

These results suggest that QBHF ameliorates MI in CHD by reversing hsa_circ_0003296-mediated inhibition of angiogenesis. This process is executed through the stabilization of EIF4A3, which enhances the mRNA stability of VEGFA and VEGFR2.