BACKGROUND: Carotid angioplasty and stenting (CAS) has increasingly been used as an alternative to carotid endarterectomy (CEA) in the treatment of carotid artery disease. However, neurological complications following carotid angiography or CAS remain a clinical concern. This study aimed to evaluate whether naturally occurring ABO blood group antigens and hematological parameters are associated with cerebrovascular complications after diagnostic or therapeutic carotid angiography. METHODS: In this single-center retrospective study, patients were classified as blood group O or non-O (A, B, or AB). Cerebrovascular complications were defined as in-hospital amaurosis fugax, transient ischemic attack (TIA), or stroke occurring after carotid angiography or carotid artery stenting (CAS). RESULTS: A total of 316 patients who underwent carotid angiography were included; 106 (33.5%) had blood group O and 210 (66.5%) had non-O blood groups. Cerebrovascular events were significantly more frequent in patients with non-O blood groups. Stroke occurred in 13.8% of patients with non-O blood groups compared with 1.9% in those with blood group O (p < 0.001), while TIA was also more common in the non-O group (11.0% vs. 3.8%, p = 0.033). When stratified by procedure type, this association was predominantly observed in patients undergoing CAS, whereas cerebrovascular event rates were low and comparable between groups in patients undergoing diagnostic angiography alone. In univariable analysis, diabetes mellitus was associated with stroke (OR = 2.392, p = 0.024), while blood group O was associated with lower odds of stroke (OR = 0.120, p = 0.004). In multivariable analysis, blood group O (OR = 0.127, p = 0.007) and contrast volume (OR per 10 mL increase: 1.218, p < 0.001) remained independently associated with stroke, whereas diabetes mellitus was no longer statistically significant. CONCLUSION: Non-O blood groups were associated with a higher risk of stroke and TIA following carotid angiography, particularly in patients undergoing CAS, whereas blood group O was associated with a lower risk of stroke. These findings should be interpreted with caution due to the observational design and potential residual confounding.

Hyperhomocysteinemia (HHcy) is an independent risk factor for thrombotic cardiovascular events. We previously demonstrated that homocysteine (Hcy) amplifies platelet activation by promoting membrane remodeling and enhancing signaling through surface platforms such as integrin αIIbβ3 and G protein-coupled receptors. However, the mechanisms by which Hcy remodels platelet membrane lipid metabolism remain poorly understood. Here, using an integrated proteomic and lipidomic approach, we showed that Hcy disrupted platelet lipid homeostasis by impairing fatty acid β-oxidation (FAO), a metabolic pathway that depends on the coordinated action of peroxisomes and mitochondria. Proteomic profiling showed that Hcy downregulated peroxisome proliferator-activated receptor α (PPARα) and its downstream targets carnitine palmitoyltransferase 1 and 2 (CPT1/2), while lipidomic analysis confirmed the accumulation of medium and long-chain fatty acids, which promoted platelet reactive oxygen species production and mitochondrial dysfunction. Notably, pharmacological activation of PPARα with fenofibrate, a PPARα agonist, restored FAO in a CPT1/2-dependent manner, remodeled the platelet lipid membrane, and attenuated Hcy-potentiated platelet hyperactivation and thrombus formation. Collectively, these findings suggest a previously unrecognized Hcy-PPARα-FAO axis in platelet function and thrombosis, linking impaired peroxisomal and mitochondrial FAO to platelet hyperactivation, and support restoring membrane phospholipid dysregulation as a potential therapeutic strategy for HHcy-promoted thrombotic diseases.

OBJECTIVE: This prespecified analysis of Effect of Evolocumab in Patients at High Cardiovascular Risk Without Prior Myocardial Infarction or Stroke (VESALIUS-CV) evaluated the efficacy of the PCSK9 inhibitor evolocumab for preventing first cardiovascular events in patients with high-risk diabetes. RESEARCH DESIGN AND METHODS: VESALIUS-CV randomized patients with high-risk diabetes (microvascular disease, insulin use, or duration ≥10 years) or qualifying atherosclerosis, but no prior myocardial infarction (MI) or stroke, and LDL cholesterol (LDL-C) ≥90 mg/dL to evolocumab 140 mg or matching placebo every 2 weeks. The dual primary end points were a composite of coronary heart disease death, MI or ischemic stroke (three-point major adverse cardiovascular event [3P-MACE]) and 3P-MACE plus ischemia-driven arterial revascularization (four-point [4P]-MACE). RESULTS: Of the 6,002 patients with high-risk diabetes, 67% were on a high-intensity statin and 24% were on an sodium-glucose cotransporter 2 inhibitor (SGLT2i) or a glucagon-like peptide 1 receptor agonist (GLP-1RA) at baseline. The median LDL-C at 48 weeks was 47 mg/dL and 109 mg/dL in the evolocumab and placebo arms, respectively (P < 0.0001). After a median follow-up of 4.6 years, evolocumab decreased the relative rates of 3P-MACE and 4P-MACE by 29% (hazard ratio [HR] 0.71; 95% CI 0.59, 0.86; P = 0.0004) and 21% (HR 0.79; 95% CI 0.69, 0.91; P = 0.0013), respectively. These findings were consistent regardless of the presence or absence of qualifying atherosclerosis, baseline LDL-C, statin intensity, and SGLT2i or GLP-1RA use (Pint > 0.05 for each). The porportion of patients with all-cause death was 8.8% vs. 11.0% in the evolocumab versus placebo arms (HR 0.79; 95% CI 0.67, 0.93). CONCLUSIONS: Evolocumab reduced the rate of cardiovascular events in patients with high-risk diabetes, regardless of the presence or absence of qualifying atherosclerosis and background use of other cardioprotective agents.

BACKGROUND: Anti-tachycardia pacing (ATP) that entrains but fails to terminate ventricular tachycardia (VT) provides an opportunity to use post-pacing interval minus tachycardia cycle length (PPI - TCL) as a diagnostic tool. We evaluated whether PPI - TCL from failed ATP could predict the presence of epicardial re-entrant VT circuits in patients with ischemic cardiomyopathies (ICM) vs. non-ischemic cardiomyopathies (NICM). METHODS: A retrospective analysis was conducted of 51 patients who underwent VT ablation at Beth Israel Deaconess Medical Center from January 2020 to March 2025 and had failed ATP episodes recorded by their implantable cardioverter-defibrillators (ICDs). PPI - TCL measurements and critical VT circuit locations (apex, septum, free wall, epicardial) were independently adjudicated. PPI - TCL was stratified by VT location and cardiomyopathy type, with sensitivity analyses for normalized PPI - TCL [(PPI - TCL)/TCL]. RESULTS: Included patients had a median age of 70 years, a median LVEF of 31%, 31 (61%) were infarct cardiomyopathy (ICM) and 20 (39%) were non-infarct cardiomyopathies (NICM). ATP-PPI was significantly longer at locations further from the ICD pacing electrode (i.e: free wall, epicardial) as compared to locations that were closer (i.e: apex, septum) (p = 0.023). This relationship held true for NICM (p = 0.026) but not for ICM (p = 0.085). For patients with non-infarct cardiomyopathies, an optimal ATP-PPI cutoff of 165 ms provided an 86% sensitivity and 77% specificity for predicting epicardial circuits. CONCLUSION: PPI - TCL following failed ATP reliably predicts epicardial VT circuits in NICM with a 165 ms cutoff offering high sensitivity and specificity. This non-invasive tool may guide epicardial access planning in NICM VT ablation, though prospective validation is needed.

AIMS: Better control of modifiable risk factors offers substantial potential to prevent cardiovascular disease (CVD). Risk scores can be used to identify and quantify risk and for health promotion, based on prediction of CVD. We aimed to evaluate and compare the prognostic value of Life's Essential 8 (LE8) and its components, and to contrast LE8 with the established risk prediction tool SCORE2. METHODS: The Akershus Cardiac Examination 1950 (ACE1950) Study is an ongoing prospective birth cohort study including all men and women born in 1950 residing in Akershus County, Norway. Calculation of Life's Essential 8 (LE8) and SCORE2 was performed at the baseline visit (2012-2015). Participants were followed through 2022 for incident major adverse cardiovascular events (MACE). RESULTS: Among 3,706 participants (attendance rate 64%), 2,938 without established CVD and with complete LE8 data were included. Mean age 63.9 years, 53% women, with a mean SCORE2 of 6.1 and a LE8 score of 63.9. Only 9.8% had "Optimal" cardiovascular health (CVH) according to LE8. During a median follow-up of 8.3 years, 6.7% experienced incident MACE. Both LE8 (total score, domains, and number of optimal components) and SCORE2 were significantly associated with MACE, with comparable predictive performance (LE 8 HR 1.53, 95% CI 1.35-1.73; SCORE 2 HR 1.82, 95% CI 1.57-2.10, p for comparison = 0.30). The highest risk was observed among participants with "Poor" CVH. CONCLUSIONS: LE8 can be used in health promotion based on prognostic value comparable to SCORE2, for counselling to a healthier lifestyle to preserve cardiovascular health.

BACKGROUND: Unraveling the potential horizontal transfer of resistance genes/virulence genes (RGs/VGs) in gut microbiota from patients with Crohn disease (CD) is an interesting but poorly characterized issue. METHODS: Quantitative assessment was performed to estimate the relative abundance and diversity of RGs/VGs/mobile genetic elements (MGEs). Differential analysis was applied to identify the CD-specific enriched genetic subtypes. A species-RGs/VGs/MGEs association network was constructed to explore possible co-occurrence patterns of these genetic elements across potential microbial hosts. Integrated with topological metrics and Zi-Pi computational modeling, co-occurrence network analysis was conducted to characterize potential associations among RGs, VGs, and MGEs. RESULTS: Comparative metagenomic analyses indicated that the microbiome in group CD exhibited significantly higher relative abundance of RGs compared to that in healthy controls (HC; P = .040), with 131 specific RG/VG subtypes (eg, acrA/T6SS) exhibiting marked enrichment (P < .05). The co-occurrence network revealed intensified interconnectivity between RGs/VGs and MGEs in group CD, in which MGEs accounted for 71% of network nodes (vs 60.80% in HC), and 99.14% of the edges were positively correlated (vs 93.60% in HC). Network topology and Zi-Pi analysis further suggested reduced modularity (0.709 vs 0.979 in HC) and enhanced intergene connectivity (average degree: 12.288 vs 2.156; average weighted degree: 23.359 vs 3.688 in HC). There were no network hubs (0 vs 5 in HC) but abundant modular hubs (60 vs 25 in HC), peripheral nodes (2317 vs 1549 in HC), and connectors (61 vs 36 in HC), which may reflect conditions favorable for enhanced gene transfer potential. Cross-species transfer events were predicted across clinical-environmental-commensal boundaries, exemplified by tet(M) dissemination between Clostridioides difficile and Bacteroides sp., probably implying progressive erosion of ecological barriers. CONCLUSIONS: Collectively, we inferred that the gut microbiome of CD patients might represent a high-risk reservoir for the horizontal transfer of pathogenic determinants, which may pose a potential threat for public health and biosecurity.

De novo aortic insufficiency (AI) is a recognized complication in patients supported with continuous-flow durable left ventricular assist devices (LVADs), carrying important clinical consequences including heart failure progression and increased device-related morbidity. We report the case of a HeartMate 3 (Abbott Inc., Chicago, Illinois, USA) patient, previously supported with a micro-axial flow pump (mAFP), who developed severe AI within the first year of LVAD support and ultimately underwent urgent heart transplantation. Intraoperative inspection and histopathological analysis revealed mechanical injury of the aortic valve, likely initiated during mAFP implantation and subsequently exacerbated by LVAD-related turbulent flow. These findings suggest that even subtle valve trauma may evolve into clinically significant AI under continuous-flow support. This case underscores the need for a proactive strategy to minimize the risk of aortic valve micro-lesions during mAFP placement, including meticulous preprocedural assessment of aortic root and valve anatomy and careful intraprocedural technique.

INTRODUCTION: Imaging-based cerebral small vessel disease (CSVD) summary scores quantify CSVD burden. This study characterized CSVD scores and assessed their cognitive associations in older adults with various neurodegenerative diseases and cognitive profiles. METHODS: Baseline data from 958 Comprehensive Assessment of Neurodegeneration and Dementia (COMPASS-ND) study participants were analyzed (19.4% cognitively normal, 14.9% subjective cognitive decline, 40.3% mild cognitive impairment, 25.4% dementia). MRI markers of cerebral vascular injury (lacunes, microbleeds, white matter hyperintensities [WMHs], and enlarged perivascular spaces) were visually rated, and a cumulative CSVD score was generated. Cognition was measured using the Montreal Cognitive Assessment (MoCA), Clinical Dementia Rating-Sum of Boxes (CDR-SB), and a composite neuropsychological battery test z-score. RESULTS: Higher CSVD scores were associated with greater Hachinski ischemic scores, poorer MoCA performance, worse CDR-SB, and lower composite z-scores. Associations were strongest for cognitive domains of executive function, attention, and learning. DISCUSSION: CSVD burden may further contribute to poorer cognition across neurodegenerative conditions and cognitive profiles.

BACKGROUND Pulmonary arteriovenous malformations (PAVMs) are rare structural vascular abnormalities that create communications between pulmonary arteries and veins, resulting in right-to-left shunts. PAVMs are often asymptomatic; however, patients may exhibit a range of clinical symptoms, including dyspnea, hemoptysis, chest pain, and cyanosis. Common serious complications include cerebrovascular events (eg, paradoxical embolism resulting in stroke or transient ischemic attack) and infectious complications (eg, brain abscess). PAVMs do not always require treatment; management should be guided by factors such as feeding artery size and patient symptoms. When intervention is indicated, percutaneous transcatheter embolization is the primary treatment and demonstrates efficacy in most cases. This report describes a case of recurrent cerebral embolism attributed to an undiagnosed PAVM, which was treated with percutaneous transcatheter embolization. CASE REPORT A 67-year-old man lacking prior medical history or medication use experienced recurrent cerebral embolism within 3 months despite therapeutic anticoagulation. The paradoxical embolism was attributed to a PAVM diagnosed by contrast-enhanced chest computed tomography. Subsequent transcatheter embolization of the PAVM was successfully performed. No recurrence was observed at the 4-year follow-up. CONCLUSIONS In cases of unexplained cerebral embolism, PAVMs should be considered a potential underlying etiology. Hemorrhagic transformation requires careful risk assessment but is not an absolute contraindication to percutaneous transcatheter embolization. Timely diagnosis and embolization are essential to prevent disabling recurrent events.

Heart failure (HF) remains a leading cause of morbidity and mortality worldwide and frequently coexists with Philadelphia-negative myeloproliferative neoplasms (MPNs), which share thrombo-inflammatory pathways that increase cardiovascular risk. HF is often underestimated in this population, and current risk models rarely include variables specific to this complex cardio-hematologic setting. From a cardio-oncology perspective, MPNs represent a prototypical at-risk cancer population in whom chronic inflammation, clonal hematopoiesis, and cancer therapy converge to accelerate cardiovascular damage.This narrative review summarizes current evidence on diagnostic and prognostic biomarkers, imaging parameters, and validated HF and MPNs risk scores, and proposes a pragmatic hybrid framework for integrated HF-MPNs cardiovascular risk assessment. PubMed, Embase, and Web of Science were searched up to December 2025 using combinations of terms related to HF, MPNs, biomarkers, imaging, and risk models. In HF, natriuretic peptides and cardiac troponins remain central for diagnosis and short-term prognosis, whereas emerging biomarkers such as galectin-3, soluble ST2, and GDF-15 refine long-term risk prediction. Advanced imaging tools, including global longitudinal strain, left atrial strain, and cardiac magnetic resonance tissue characterization, provide prognostic value beyond the left ventricular ejection fraction. Multidimensional HF models (e.g., MAGGIC, SHFM, BCN Bio-HF, H2FPEF, 3A3B, GWTG-HF, ADHERE, and EHMRG) combine different variables to estimate mortality and hospitalization risk. In MPNs, blood counts, driver mutations (JAK2, CALR, MPL), inflammatory markers, and scores such as IPSET-thrombosis, DIPSS/DIPSS-plus, and MIPSS stratify thrombotic risk, survival, and leukemic transformation but seldom incorporate HF-specific variables.No single biomarker or score fully captures the bidirectional cardiovascular risk in patients with HF and coexisting MPNs. We propose a simple 0-8-point composite algorithm that combines key HF and MPNs variables (natriuretic peptides or troponins, HF risk scores, driver mutations, leukocytosis/thrombocytosis, LDH) to identify high-risk HF-MPNs phenotypes across ACC/AHA HF Stages A-C, suitable for structured cardio-oncology follow-up. Prospective validation of this hybrid algorithm in dedicated cardio-oncology cohorts and the development of MPNs-adapted HF guidelines are key future priorities.

Atherosclerosis, a chronic inflammatory disease of the arterial wall, is a leading cause of cardiovascular diseases worldwide. The complex pathogenesis of atherosclerosis involves genetic predisposition, environmental factors, and immune responses. N-Methyl-d-aspartate receptors (NMDARs), a subclass of glutamate receptors, are critical for synaptic plasticity, learning, and memory in the central nervous system (CNS). Non-neuronal NMDARs are poorly understood compared to neuronal receptors, but there is a developing consensus that they have distinct structural and functional properties when activated by glutamate and NMDARs co-agonists. Emerging evidence indicates that non-neuronal NMDARs may participate in an array of physiological and pathophysiological processes, including but not limited to driving macrophage polarization, lipid dysregulation in macrophages, inflammation response, vascular smooth muscle cells phenotype switching and endothelial dysfunction, thereby fueling atherogenesis. This review discusses the association between NMDARs genes and atherosclerosis risk, molecular mechanisms underlying NMDARs-mediated regulation of atherosclerosis-related cells, and potential therapeutic implications. Besides, we introduce some pharmacological tools that can be used for studying NMDARs outside the CNS, which reflect modern subunit-selective agents to provide more precise insight into NMDARs mediate the various effects. Overall, the study of NMDARs may provide insights into the pathogenesis of atherosclerosis and lead to the development of more effective therapeutic strategies.

BACKGROUND: Ensuring equitable access to essential medicines is fundamental to universal health coverage, yet disparities in availability, pricing, and affordability persist in many low- and middle-income countries. OBJECTIVES: This study assessed the availability, prices, and affordability of essential cardiovascular and antidiabetic medicines across public and private healthcare sectors in Pakistan using the WHO/Health Action International (WHO/HAI) methodology. METHODS: A cross-sectional survey of 32 essential medicines was conducted across selected study areas (Rawalpindi, Muzaffargarh, Vehari, Gujranwala, Islamabad, and Azad Jammu & Kashmir). Medicine availability was measured as the percentage of facilities stocking medicines on the survey day. Prices were analyzed using median price ratios (MPRs) against international reference prices, and affordability was calculated as the number of days' wages required by the lowest-paid unskilled government worker to purchase a standard 30-day treatment. Sectoral and regional differences were evaluated using chi-square tests. RESULTS: The availability of the 32 cardiovascular and antidiabetic medications was generally poor, especially in government facilities; originator brands (OBs) and lowest-priced generics (LPGs) were consistently more readily available in private pharmacies (χ²=180.6, p < 0.001). There were notable geographical differences, with rural areas exhibiting very poor access (χ²=202.8, p < 0.001) and Gujranwala exhibiting the greatest availability. While certain OBs, particularly insulin analogs, were noticeably more expensive than LPGs, prices and affordability favored LPGs across all medications. Public and private sectors continued to have insufficient supplies of insulin and emergency medications, falling short of WHO objectives. CONCLUSION: This study reveals persistent inequities in the availability and affordability of essential medicines across the selected districts in Pakistan. While these findings specifically reflect the studied regions, they provide actionable evidence to strengthen Pakistan's public-sector supply systems, promote generic medicines, and inform national access policies.

BACKGROUND: Familial hypercholesterolaemia (FH) is a common but underdiagnosed genetic condition that leads to high low-density lipoprotein cholesterol and premature cardiovascular disease. Cascade genetic testing remains underutilised as a screening approach. Implementation strategies can increase the diffusion of innovations such as genetic medicine into non-genetic specialty settings more rapidly through dissemination networks. This study aimed to evaluate the success of a multifaceted implementation strategy to increase cascade testing for relatives of a person diagnosed with FH using a primary-tertiary shared care model. METHODS: A multisite effectiveness-implementation hybrid type III pre-post study was conducted between 2022 and 2024 to compare the implementation of a new shared care model for FH cascade testing in NSW, Australia. During the control period, cascade testing of relatives was offered to FH index cases by a genetic counsellor at the lipid clinic. In the implementation strategy period, FH index cases were offered a cascade testing expression of interest form to provide to their relatives. Relatives were contacted by a genetic counsellor and provided with a pre- and post-cascade testing package, which was also provided to their general practitioner. RESULTS: A total of n = 25 index and n = 6 cascade cases were included in the control period and n = 81 index and n = 56 cascade cases in the implementation period. The number of cascade genetic tests per index case increased significantly from 0.24 in the control period to 0.52 in the implementation strategy period (incident rate ratio = 4.62; 95% CI: 0.39, 8.84; p = 0.032). Among relatives tested, there was no difference in the proportion with a confirmed FH gene change per index case (IRR = 2.15; 95% CI: 0.65, 7.01; p = 0.207). There was no difference in the proportion of index cases with at least one cascade test (OR = 1.49; 95% CI: 0.53, 4.19; p = 0.442). CONCLUSIONS: Implementation of our model increased FH cascade testing compared to previous standard care. These findings suggest a greater role for cascade testing in primary care settings. This opens new opportunities for integrating genetic screening into routine general practice, particularly for autosomal dominant conditions such as FH.

BACKGROUND: Cardiovascular-kidney-metabolic (CKM) syndrome represents a composite disease state driven by glucose and lipid metabolic dysregulation. The Cholesterol, High-density lipoprotein, and Glucose (CHG) index reflects the composite burden of these metabolic factors. However, its impact on the onset, stage-wise progression, and prognosis of CKM syndrome remains unclear. METHODS: This study utilized data from two large-scale prospective cohorts. In the UK Biobank (UKB) cohort, Fine-Gray proportional subdistribution hazards models were employed to investigate associations between CHG levels and the risk of incident cardiovascular disease (CVD), chronic kidney disease (CKD), and type 2 diabetes mellitus (T2DM), as well as the risk of progression from CKM Stage 0-1 to 2-3 and Stage 1-3 to 4. In the Beijing Anzhen Hospital cohort, Cox regression models assessed the impact of CHG on major adverse cardiovascular and cerebrovascular events (MACCE) in patients with CKM Stage 4 (established coronary artery disease). A causal forest algorithm was used to identify high-value subpopulations, and restricted cubic splines (RCS) characterized dose-response relationships. Sensitivity analyses were conducted to verify result robustness. RESULTS: The study included 370,916 participants free of CKM diseases from UKB (median follow-up: 16.5 years) and 8,494 patients with CKM Stage 4 from Beijing Anzhen Hospital (median follow-up: 645 days). In the general population, each 1-SD increase in the CHG index was significantly associated with an increased risk of incident T2DM (HR: 1.47; 95% CI: 1.40-1.53), CVD (HR: 1.07; 1.06-1.09), and CKD (HR: 1.07; 1.04-1.10). Furthermore, elevated CHG significantly accelerated CKM progression from Stage 0-1 to 2-3 (HR: 1.16; 1.11-1.23) and from Stage 1-3 to 4 (HR: 1.06; 1.05-1.08) per 1-SD increase. In patients with established CAD (Stage 4), a 1-SD increase in CHG was associated with a higher risk of MACCE (HR: 1.12; 1.05-1.19). Machine learning analysis revealed that this prognostic impact was particularly pronounced in patients with low systemic inflammation and elevated HbA1c. CONCLUSIONS: The CHG index demonstrates significant predictive value for the onset of component diseases, stage-wise progression, and adverse prognosis across the entire CKM syndrome continuum.

BACKGROUND: Horseshoe lung (HL) and scimitar syndrome are rare congenital cardiopulmonary anomalies that may coexist, posing complex diagnostic and management challenges. The following case presents the clinical manifestation of repeated hemoptysis episodes and syncope, a combination that has rarely been reported in this context. Moreover, there were treatment challenges regarding the utility of minimally invasive techniques in the iatrogenic occlusion of aberrant vessels, which has more recently been suggested in the literature to yield comparable outcomes compared with open surgeries. CASE PRESENTATION: We described the case of a 15-year-old Iranian boy who presented with syncope and hemoptysis following physical activity. Imaging findings were consistent with concomitant HL, partial anomalous pulmonary venous return (PAPVR), right lung hypoplasia, and scimitar syndrome. The patient successfully underwent transcatheter arterial embolization (TAE); however, another episode of hemoptysis occurred after three weeks. This recurrence indicated the failure of TAE and necessitated a right lower lobe segmentectomy. After the surgical excision, the patient showed improvement in respiratory status, with no further episodes of hemoptysis. He was discharged on postoperative day seven. At the 2-month follow-up, there were no signs of recurrence or complications. Nonetheless, the patient was scheduled for subsequent open-heart repair of the PAPVR defect. CONCLUSIONS: This case highlights that when HL or scimitar syndrome is identified, clinicians should be aware of associated congenital cardiopulmonary and vascular anomalies and perform a comprehensive clinical exam and multimodality imaging. Moreover, although TAE may yield outcomes comparable to open surgery with faster recovery and fewer postoperative complications, its effectiveness is questionable in patients with complex underlying conditions. Therefore, although the choice between the minimally invasive and invasive managements requires a multidisciplinary approach, it is recommended that patients with complications such as infections, bronchiectasis, large lumen aberrant vessels, multiple aberrant vessels, or unusual anatomies be planned for surgical resection of sequestrated lung tissue to avoid potentially less effective interventions.

BACKGROUND AND OBJECTIVE: The atherogenic index of plasma (AIP) reflects atherogenic dyslipidemia and insulin resistance, whereas the frailty index (FI) quantifies cumulative physiological deficits across multiple organ systems. Although both the AIP and FI are independently associated with cardiometabolic multimorbidity (CMM), the joint impact of the atherogenic index of plasma-frailty index (AIPFI) on the risk of CMM remains unclear. In this study, the associations between baseline levels, cumulative AIPFI and longitudinal changes of AIPFI and the incidence of CMM were evaluated. METHODS: Data were obtained from the China Health and Retirement Longitudinal Study (CHARLS). A total of 7995 participants were included in the baseline analysis, and 4,483 participants with repeated biomarker measurements in 2012 and 2015 were included in the longitudinal analysis. AIPFI was calculated via the following formula: AIPFI = AIP × FI. Multivariate Cox proportional hazards models and restricted cubic splines were applied to evaluate the associations of AIPFI with the incidence of CMM. K-means clustering characterized longitudinal AIPFI patterns. The clinical prediction model was performed in both the training and validation cohorts, as validated by receiver operating characteristic curve analysis, calibration curve analysis, and decision curve analysis. The shapley additive explanations (SHAP) method was employed to provide further explanation. RESULTS: A total of 7995 participants were included and followed for a median of 9.0 years, during which 747 (9.3%) incident CMMs occurred. Across quartiles of the AIPFI, the risk of CMM increased progressively, with adjusted HR of 2.46 (95% CI 1.77-3.43) for Q4 compared with those for Q1. In longitudinal analyses (n = 4,483), participants in cluster 2, with persistently high and increasing AIPFI values, presented increased risks of CMM (HR 1.54, 95% CI 1.19-2.01). An elevated cumulative AIPFI was associated with an increased incidence of CMM (HR 1.01, 95% CI 1.01-1.01). The RCS revealed a significant positive nonlinear relationship between the baseline AIPFI and cumulative AIPFI with the risk of CMM (all P < 0.05, and all P for nonlinear values < 0.05). SHAP model analysis revealed hypertension, heart disease, and AIPFI as the most influential predictors. CONCLUSIONS: Both baseline and longitudinal changes in the AIPFI were independently associated with the risk of CMM. The incorporation of longitudinal monitoring of the AIPFI into routine health evaluations may enhance population-level CMM risk prediction and support more effective prevention strategies.

BACKGROUND: Hypertension and dyslipidemia are major global risk factors for cardiovascular diseases, with their prevalence increasing annually. In China, hypertension and dyslipidemia exhibit a "dual high" epidemic characteristic. To contribute to the reduction of their prevalence, this study analyzes factors related to dyslipidemia in hypertensive patients from a clinical perspective. METHODS: This study analyzed data from 5,018 hypertensive patients recruited from 110 hospitals across China. Participants were categorized into a dyslipidemia group and a non-dyslipidemia group based on diagnostic criteria. Variables selected based on clinical relevance and univariate associations were included in a multivariate logistic regression model to determine independent factors associated with the co-occurrence of hypertension and dyslipidemia. RESULTS: Analysis of the dyslipidemia group and non-dyslipidemia group revealed that the dyslipidemia group exhibited significantly higher proportions (p < 0.05) in multiple disease conditions (stroke, angina pectoris, atrial fibrillation), medication use (beta-blockers, antiplatelet agents, etc.), and family histories of certain diseases (hypertension, coronary heart disease, diabetes) compared to the non-dyslipidemia group. Regression analysis further identified BMI, family history of hypertension, stroke, angina pectoris, atrial fibrillation, obstructive sleep apnea, and family history of coronary heart disease as significant correlates of hypertension combined with dyslipidemia. CONCLUSIONS: Hypertension comorbid with dyslipidemia demonstrates significant correlations with body mass index (BMI) and familial predisposition (family histories of hypertension and coronary heart disease). Furthermore, individual medical histories and pharmacological regimens exhibit substantial associations with disease progression. These findings suggest potential targets for a three-tier prevention approach. With appropriate validation in prospective studies, prioritized screening and early intervention for high-risk individuals may contribute to halting or delaying disease progression.

Heart failure (HF) affects over 64 million people worldwide, with prevalence projected to reach 3% by 2030. In advanced stages, when medical therapy fails and transplantation is limited by organ shortages, left ventricular assist devices (LVADs) represent a viable alternative. This retrospective, single-center study reports 10-year outcomes from the first Chilean LVAD program using the HeartWare (HVAD) device. Between 2013 and 2015, nine patients with advanced HF received HVAD implants. The mean age was 42.2 ± 15.8 years, with a left ventricular ejection fraction of 22% ± 4.1%. One-year survival was 77.8%, and 10-year survival for those using LVAD as destination therapy was 62.2%. All patients experienced at least one infection, with driveline infections being most common (55.5%). Bleeding events affected 77.7%, including gastrointestinal bleeding and severe epistaxis (both 22.2%). Neurological complications occurred in 33.3% of patients. Despite these events, four patients remained on LVAD support after 10 years, with no mechanical device failures requiring replacement. This case series highlights the feasibility, durability, and clinical relevance of long-term LVAD support in low-donation settings. Findings support LVADs as a destination therapy in selected patients and emphasize the importance of multidisciplinary care and structured follow-up.

Green spaces and their biodiversity seem to improve the urban life quality. However, a wide range of descriptors were associated with multiple health outcomes, which limits the comparability of existing evidence. The objective of this systematic review was to organise this knowledge, investigating the relationship between biodiversity in urban green spaces and health outcomes in adults. Following PRISMA guidelines and a registered protocol (PROSPERO: CRD42025636281), a search of PubMed, Scopus, Web of Science identified studies published between January 2014 and July 2025. The search strategy ("biodiversity" AND "human health" AND "urban green space") yielded 147 eligible studies. Most were published between 2017 and 2020 (57%) and predominantly relied on medium-sized cohorts of 101-10,000 participants (55%). Health outcomes fell into four categories: (i) general health, mental health, and well-being; (ii) drug prescriptions; (iii) chronic diseases (cardiovascular disease, T2 diabetes, obesity); and (iv) birth outcomes. Green exposure was primarily assessed through vegetation-based indicators: 66.1% of studies used green-exposure metrics (tree canopy or vegetation cover), 34.0% NDVI, and 22.4% percentage green area. Only a minority incorporated composite ecological indices or fauna-based metrics (bird or insect richness). Across all health domains, findings were predominantly favourable. Between 70% and 90% of studies on general health, mental health, and well-being reported beneficial associations with green exposure, including improved self-rated health, reduced depressive and anxiety symptoms, lower stress, and increased life satisfaction. All studies using drug prescription data found inverse associations between green exposure and antidepressant or anxiolytic prescriptions. Evidence for chronic diseases consistently indicated protective associations: reduced cardiovascular and respiratory disease risk, prevalence of T2 diabetes, and all-cause mortality. Birth outcomes demonstrated more variability, with half of the studies reporting positive associations, largely influenced by socioeconomic and contextual factors. Socioeconomic status frequently modified associations, with stronger positive effects observed among lower-SES populations. The overall evidence indicates that richness of urban green spaces is associated with health benefits. However, the role of biodiversity remains unclear and understudied, mostly due to inconsistent measurements and ambiguous associations with health outcomes. Integrating ecological quality into urban planning may therefore represent an important strategy for promoting healthier and more equitable urban environments.

PURPOSE: Hypoxia is a consequence of diseases such as obstructive sleep apnea (OSA) and can be detrimental to tissue function, with in vitro platforms commonly used to study the associated impacts. However, to create a realistic experimental simulation of hypoxia, the dissolved oxygen concentration at the in vitro cell layer must mimic in vivo values. Considering the limitations associated with mass transfer and continuous oxygen monitoring in standard hypoxia chambers, mathematical modeling can be leveraged to inform experimental design for more accurate and clinically relevant in vitro representations. METHODS: A model of oxygen transfer in a standard hypoxia chamber with a cell culture set-up was calibrated and validated using experimental data. To demonstrate a direct application with clinical data, the validated model was coupled with a novel optimization approach to create a "patient-specific" gas controller protocol capable of reproducing a model-derived OSA patient profile at the in vitro cell layer. RESULTS: The validated model was successful in independently capturing the effect of endothelial cell oxygen consumption in the media. Furthermore, the predicted "patient-specific" gas controller protocol resulted in an in vitro oxygen profile which mimicked the oxygen values and fluctuation timings seen in a model-predicted arterial oxygen pattern for an OSA patient. Combining the analyses of this study, media height, evaporation, and spatial position were determined to be important factors in experimental design. CONCLUSION: This work demonstrates the utility of applying mathematical modeling for experimental design and presents a means to bridge the gap between the clinical and experimental fields with a "bedside to bench" approach.

Patients with chronic kidney disease (CKD) are at increased risk for masked and nocturnal hypertension, conditions best identified through ambulatory blood pressure (BP) monitoring (ABPM) and associated with adverse cardiovascular outcomes. We evaluated associations between antihypertensive medication classes and ABPM profiles by conducting a cross-sectional analysis of participants from the Chronic Renal Insufficiency Cohort (CRIC) with ABPM data. Antihypertensive medications were categorized as renin-angiotensin system inhibitors (RASis), beta-blockers, calcium channel blockers (CCBs), and thiazide/loop diuretics. We used multinomial logistic regression to evaluate the independent association between each medication class (accounting for simultaneous use of multiple classes) and ABPM phenotype: controlled hypertension, white coat effect, sustained hypertension, and masked uncontrolled hypertension (MUCH). Secondary outcomes included nocturnal hypertension, nocturnal non-dipping, and BP variability. Analyses were Bonferroni-corrected for multiple comparisons. Among 1499 eligible participants, 66% used RASis, 52% beta-blockers, 43% CCBs, and 50% thiazide/loop diuretics. RASi use was associated with lower odds of sustained hypertension (OR 0.60, 95% CI 0.42 to 0.84), while beta-blocker use was positively associated with MUCH (OR 1.48, 95% CI: 1.12 to 1.96). For secondary outcomes, RASi use was associated with lower odds of nocturnal hypertension (OR 0.71, 95% CI: 0.55 to 0.91), whereas beta-blocker and CCB use were both associated with nocturnal hypertension (OR for beta-blockers 1.33, 95% CI 1.04 to 1.70; OR for CCBs 1.36, 95% CI 1.07 to 1.73). Overall, we identified several associations between specific antihypertensive classes and abnormal ABPM profiles. Longitudinal studies are needed to evaluate reproducibility and potential mechanisms of these findings.

We aimed to examine the prevalence of frailty in older adults with hypertension and its association with suboptimal blood pressure (BP), with a particular focus on differences by sex. The study was conducted at two major hospitals in Vietnam from 2023 to 2024. Frailty was defined by a Clinical Frailty Scale of ≥ 4. Suboptimal BP was defined as systolic BP ≥ 140 mmHg or diastolic BP ≥ 90 mmHg. There were 1038 participants (326 female, mean age 73 years). The prevalence of frailty was 28.6%, higher in female (35.3%) than male participants (25.6%). The overall rate of suboptimal BP was 26.7%. In female participants, the frail had a significantly higher rate of suboptimal BP (33.9%) compared to the non-frail (20.9%), but no significant differences among male. In the logistic model adjusted for age, education, marital status, physical exercise, falls, coronary heart disease, diabetes, chronic kidney disease, osteoarthritis, heart failure, stroke, atrial fibrillation, osteoporosis, chronic obstructive pulmonary disease, duration of hypertension, monotherapy/combination therapy, and medication adherence score, the odds ratios of frailty on suboptimal BP were 2.01 (95% CI 1.08-3.76) in female participants, 0.92 (95% CI 0.59-1.44) in male, female-to-male ratio of odds ratios 2.18 (95% CI 1.01-4.70). These findings highlight the need for sex-specific approaches in managing hypertension in older populations.

This study aimed to identify aqueous humor (AQ) proteins that correlate with vitreous humor (VH) levels in proliferative diabetic retinopathy (PDR). Using paired VH and AQ samples from 41 patients undergoing vitrectomy for PDR, we measured 92 protein biomarkers via a high-throughput immunoassay. We assessed Spearman correlations between AQ and VH levels for each protein and associations with PDR severity parameters. Thirty-two proteins showed positive AQ-VH correlations. A stepwise selection process, based on detectability, consistency and correlation strength narrowed this down to 21 proteins. An exploratory analysis of associations with disease severity parameters suggested that of these proteins, CXCL-10, IL-8, and MCP-4 were most strongly associated with fibrosis, while GAL-9 and PGF were most strongly associated with the extent of neovascularization, supporting the potential of these proteins as useful biomarkers. In conclusion, 21 AQ proteins show significant correlation with patient-matched VH levels in PDR patients, indicating that relative patient-level differences in AQ reflect relative differences in VH for these proteins. This methodological framework provides a foundation for future studies aiming to identify diagnostic or treatment stratification biomarkers for PDR and related complications such as diabetic macular edema.

Atherosclerosis is a chronic disease which can lead to peripheral vascular occlusion causing cardiovascular, cerebrovascular, and peripheral artery diseases (PAD). Key contributors to PAD include ageing, classical cardiovascular risk factors, diabetes mellitus, and hypertension. For decades, these factors have also been related to arterial tortuosity, potentially indicating vascular fragility or arteriopathies. We aimed to evaluate the association between abdominal aortic tortuosity (AAT) and arteriopathies from other vascular beds and to assess its potential role as a subclinical marker of peripheral vascular disease. Atherosclerosis is a chronic disease which can lead to peripheral vascular occlusion causing cardiovascular, cerebrovascular, and peripheral artery diseases (PAD). Key contributors to PAD include ageing, classical cardiovascular risk factors, diabetes mellitus, and hypertension. For decades, these factors have also been related to arterial tortuosity, potentially indicating vascular fragility or arteriopathies. We aimed to evaluate the association between abdominal aortic tortuosity (AAT) and arteriopathies from other vascular beds and to assess its potential role as a subclinical marker of peripheral vascular disease. We included individuals aged ≥ 50 years and excluded those with dorsolumbar scoliosis. We built a multivariate log-linear regression model to identify factors associated with AAT. The model was adjusted by carotid calcification, stiffness, and stenosis as well as individual clinical characteristics and previously registered vascular diseases. A total of 490 individuals (mean age, 66.92 years; range, 50-98 years; 44.29% of women) from the Ageing Imageomics Study were included in this analysis. We observed that the AAT index was strongly dependent on age and also with diastolic blood pressure and estimated glomerular filtration rate (eGFR), but to a lesser extent. In contrast, other classical cardiovascular risk factors like diabetes mellitus, hypertension, smoking, aortic stiffness, and calcification did not play a significant role. Our results do not support the AAT index as a subclinical marker of cardiac, cerebrovascular, or peripheral vascular disease. AAT was not associated with classical cardiovascular risk factors and comorbidities.