Age-related structural and functional remodeling of the heart and vessels increases cardiovascular disease (CVD) risk, yet comprehensive assessments using multimodal imaging and genetic characterization remains limited. We aimed to quantify cardiovascular aging using multimodal biomarkers and evaluate its genetic architecture, lifestyle determinants, and prognostic relevance. From the UK biobank, cardiovascular magnetic resonance (CMR), electrocardiogram, arterial stiffness, and carotid ultrasound biomarkers were integrated to establish a cardiovascular aging measure using machine learning (ML) models. Seven ML models were evaluated to predict cardiovascular age, and cardiovascular age gap (CardioAG) was calculated using the best-performing model. Associations between CardioAG and incident CVD outcomes were assessed, alongside modality-specific analyses to evaluate the incremental value of multimodal integration. Whole-genome sequencing (WGS) analyses were conducted to identify genetic variants associated with CardioAG, and linear regression models were applied to examine relationships between CardioAG and key lifestyle factors. Among 22,452 participants with complete multimodal data, 13,694 individuals free of baseline CVDs (median age 62.6 years [IQR 56.5-68.3], median follow-up 4.8 years [IQR 3.7-6.3]) were selected for model development. With 57 cardiovascular aging biomarkers, the CatBoost model performed best on the test dataset (Pearson r = 0.75; mean absolute error = 3.88 years). CardioAG was independently associated with hypertension, stroke, atrial fibrillation, coronary artery disease, and composite major adverse cardiovascular event (MACE, hazard ratio = 1.08, 95% CI, 1.06-1.10). Incremental and ablation analyses demonstrated complementary contributions across imaging and functional modalities, with multimodal integration enhancing predictive accuracy and providing independent prognostic value for MACE. WGS analysis identified novel common genetic variants associated with interindividual variability in CardioAG, including RN7SKP155, SVIL, and CBFA2T3, highlighting genetic contributions to vascular remodeling, electrophysiological and hemodynamic regulation, and cardiovascular functional reserve. Dietary factors, sleep duration, physical activity level, smoking, and alcohol intake were found to be significantly associated with CardioAG. This study developed a unified multimodal cardiovascular aging metric that integrates cardiac structure and function, vascular remodeling and stiffness, and electrophysiological features into a single biologically grounded, cumulative aging signal, providing incremental prognostic utility for CVD, and broadening the biological and genetic landscape underlying cardiovascular aging.
Background/Objectives: Type 2 diabetes mellitus (DM) and carotid atherosclerosis are established risk factors for cardiovascular disease (CVD). However, their relative and combined prognostic significance in individuals without known CVD remains uncertain. This study aimed to evaluate the independent and combined associations of carotid plaques and DM with cardiovascular events and mortality in a high-cardiometabolic-risk primary prevention cohort. Methods: This prospective cohort study followed 6138 participants (3571 men [57%] and 2567 women [43%]; median age 53 years, IQR 48-58) enrolled in the Lithuanian High Cardiovascular Risk (LitHiR) primary prevention program from 2006 to 2023. All individuals underwent clinical assessment and carotid ultrasonography. Participants were stratified by DM status and the presence of carotid plaques. Associations with cardiovascular events, major adverse cardiovascular events (MACE, including non-fatal ischaemic stroke, non-fatal myocardial infarction, and cardiovascular death), and all-cause mortality were evaluated using Cox proportional hazards models. Results: During follow-up (median 6.5 years, IQR 4.5-9.0), 954 participants (16%) experienced composite cardiovascular events (MACE, including non-fatal ischaemic stroke, non-fatal myocardial infarction, and cardiovascular death). Bilateral carotid plaques were more common in individuals with cardiovascular events (23.3% vs. 19.4%; p = 0.007). Individuals with both DM and carotid plaques had the highest risk of MACE (HR = 1.696; 95% CI: 1.346-2.136; p < 0.001), myocardial infarction (MI; HR = 4.089; 95% CI: 1.590-10.516; p = 0.003), and all-cause mortality (HR = 1.802; p = 0.015). The presence of carotid plaques without DM was independently associated with increased risk of MACE (HR = 1.234; 95% CI: 1.062-1.433; p = 0.006) and MI (HR = 2.492; 95% CI: 1.176-5.278; p = 0.017), but not all-cause mortality (HR = 0.986; 95% CI: 0.689-1.413; p = 0.941). In contrast, DM without carotid plaques was not significantly associated with any outcome examined. Conclusions: In this high-cardiometabolic-risk primary prevention cohort, carotid plaques were independently and more strongly associated with cardiovascular outcomes than diabetes alone. Individuals with both carotid plaques and diabetes showed the highest observed risk of adverse cardiovascular events and all-cause mortality. These findings are associational and apply to a high-risk metabolic syndrome cohort; extrapolation to the general population requires further study. The results support the prognostic value of carotid plaque assessment as an adjunctive tool in cardiovascular risk evaluation.
The association between moderate-to-severe psoriasis and cardiovascular (CV) risk is well known. No clear link between disease activity, disease duration, and CV risk has been established thus far to identify high CV risk patients with psoriasis without CV symptoms. We aimed to investigate the relationship between moderate-to-severe psoriasis and cardiovascular disease (CVD) by introducing and determining the cutoff value for a new tool, the cumulative duration of severe psoriasis (CDSP), reflecting the total duration of severe psoriasis skin symptoms. Ninety-eight asymptomatic patients with moderate-to-severe psoriasis were enrolled in this cross-sectional study, without cardiac symptoms. CDSP was recorded using a structured questionnaire. CDSP threshold, defined as Coronary Artery Calcium Score (CACS) > 0, was determined using receiver operating characteristic curve analysis. Ultrasound (intima-media thickness (IMT) and carotid, brachial, and femoral artery plaque burden) and cardiac computed tomography (CACS, segment involvement score (SIS), and coronary artery disease-reporting and data system severity (CAD-RADS™)) were performed. Controls (n = 248) were matched for age, sex, body mass index, and, where possible, comorbidities. CACS was significantly higher in psoriasis (mean 159.02, standard deviation 365.60) compared to controls (73.12, 166.08), P = 0.029. The CDSP threshold was 60.5 months. Patients with long-CDSP (> 60.5 months) had significantly higher CACS (214.63, 430.11) than patients with short-CDSP (57.61, 162.53), P = 0.012. SIS and CAD-RADS were also significantly higher in the long-CDSP group compared to the short-CDSP group (4.50, 3.85 vs. 1.39, 2.06), P = 0.002 and (2.06, 1.63 vs. 0.71, 1.08), P = 0.003, respectively. Patients with long-CDSP showed a non-significant trend towards higher IMT and peripheral plaque burden. Patients with long-CDSP had a greater extent and severity of CVD. This innovative predictor is easily determined by dermatologists and assists in the early identification of asymptomatic high CV risk patients with psoriasis. Graphical abstract available for this article. Psoriasis is a common skin disease characterized by inflammation, resulting in itchy, red, and scaly skin lesions. The inflammation also affects the blood vessels. Therefore, patients with severe psoriasis have a higher risk of cardiovascular disease, which affects the heart and blood vessels. We propose that patients with longer periods of severe psoriasis are exposed to inflammation for longer and, consequently, are at a higher risk of cardiovascular disease than those with shorter durations of severe symptoms. This study, conducted in Hungary, aimed to investigate the relationship between cumulative duration of severe psoriasis and cardiovascular disease by performing highly sensitive heart scans and ultrasound of blood vessels. Ninety-eight patients with psoriasis were included and matched with non-psoriasis controls. Our findings showed that patients with psoriasis had a greater cardiovascular disease burden, as assessed by imaging tests. Furthermore, patients with long cumulative duration of severe psoriasis (> 60.5 months) had a greater extent and severity of cardiovascular disease than patients with short cumulative duration of severe psoriasis. In conclusion, patients with a long cumulative duration of severe psoriasis are at higher risk of cardiovascular disease. Dermatologists play a vital role in the early identification of asymptomatic high cardiovascular risk patients with psoriasis and referring them to cardiology in order to prevent potentially life-threatening complications, such as heart attacks.
Cardiovascular and vascular diseases remain major causes of morbidity and mortality worldwide, despite substantial advances in prevention, diagnosis, and treatment. In recent years, cardiovascular imaging has moved beyond the traditional assessment of anatomy and morphology toward a multidimensional evaluation of function, tissue composition, haemodynamics, inflammation, and individualized risk. This evolution has been driven by technological progress in echocardiography, cardiovascular magnetic resonance, computed tomography, nuclear imaging, intravascular imaging, and point-of-care ultrasound, together with the rapid development of artificial intelligence, radiomics, and predictive analytics. Advanced echocardiographic techniques, including contrast stress echocardiography and emerging methods for myocardial scar detection, may improve functional and prognostic assessment in patients with suspected or established coronary artery disease. Cardiac magnetic resonance, through tissue mapping, late gadolinium enhancement, and 4D flow imaging, provides unique information on myocardial fibrosis, perfusion, ventricular remodelling, and vascular haemodynamics. Computed tomography, particularly with the introduction of photon-counting technology, is expanding the non-invasive characterization of coronary plaques, vascular calcification, and thromboembolic disease. Hybrid imaging with PET/CT and PET/MR offers additional insight into vascular inflammation, myocardial metabolism, and active disease processes. At the same time, intravascular ultrasound, optical coherence tomography, and augmented-reality-supported imaging are refining interventional guidance, while point-of-care ultrasound is broadening access to rapid bedside cardiovascular and vascular assessment. The integration of imaging findings with circulating biomarkers, clinical scores, lipid profiles, coagulation parameters, and machine-learning models represents a promising strategy for personalized risk stratification, particularly in complex conditions such as coronary artery disease, venous thromboembolism, pulmonary embolism, and bleeding risk during antithrombotic therapy. This review summarizes current advances in cardiovascular imaging, discusses their translational implications, and highlights future directions for integrating imaging, artificial intelligence, and precision medicine into daily clinical practice.
Cardio-renal-metabolic syndrome (CRMS)-characterized by the pathological interplay of visceral adiposity, insulin resistance, chronic kidney disease, and cardiovascular disease-affects over 90% of US adults across its staging spectrum, yet its multi-organ burden remains difficult to assess non-invasively at the point of care. This narrative mini review examines whether multiparametric ultrasound within a single examination can serve as an integrated imaging biomarker set complementary to established molecular markers of CRMS. A narrative search of PubMed (2015-2026) was conducted using PICO-structured queries. The hepatic controlled attenuation parameter and liver stiffness measurement correlate directly with Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), CRP, and adipokine dysregulation, with pooled CAP cutoffs of 268-313 dB/m and elastography thresholds of 8.2-13.6 kPa for fibrosis staging in MASLD. Epicardial adipose tissue thickness correlates with circulating IL-17A (r = 0.308), hs-CRP (r = 0.666), and HOMA-IR (r = 0.567-0.580), independently predicting left ventricular diastolic dysfunction beyond BMI. Carotid intima-media thickness tracks eGFR decline longitudinally and predicts cardiovascular mortality in CKD populations. Renal resistive index, with a validated threshold of ≥0.70, independently predicts GFR decline and cardiovascular mortality across diabetic and hypertensive populations. Renal shear wave elastography distinguishes fibrotic from non-fibrotic parenchyma, with 93.1% sensitivity against biopsy. Cross-compartmental correlations and composite imaging-biochemistry models consistently outperform single-parameter approaches. Two critical gaps remain: specific ultrasound values have not been associated with AHA/ACC CKM stages, and no outcome study has validated a multiorgan protocol. Multiparametric ultrasound provides a clinically feasible, evidence-based CRMS assessment that remains to be validated in prospective trials.
Background: Cardiovascular disease (CVD) remains the leading cause of mortality across the European Union (EU), with a fourfold to fivefold east-west gradient in standardized circulatory-disease mortality. Romania ranks second highest in the EU (787 per 100,000 inhabitants in 2023). Primary-prevention practice is organized around two quantitative frameworks-the 2021 European Society of Cardiology (ESC) SCORE2/SCORE2-OP system and the 2018/2019 American College of Cardiology/American Heart Association (ACC/AHA) Pooled Cohort Equations (PCE)-which converge on therapy but diverge on patient selection. Methods: We conducted a structured narrative review (SANRA-compliant) of contemporary primary-prevention guidelines, validation studies, key trials of risk-modifier interventions, and Romanian epidemiological data through April 2026. On this basis, we developed ROMA-CV (Risk Of Multifactorial Atherosclerosis-CardioVascular) as a conceptual, country-specific risk-stratification framework anchored to existing Class I/IIa recommendations or Level A/B evidence, rather than as a fully developed, ready-to-use clinical tool Results: Four structural limitations of SCORE2 are clinically consequential in Romania: (i) an age floor of 40 years that excludes the population in which premature myocardial infarction is most preventable; (ii) a country-level calibration coefficient applied to individuals; (iii) permissive treatment of lipoprotein(a) [Lp(a)]; and (iv) an under-emphasis of subclinical-atherosclerosis imaging. We propose ROMA-CV (Risk Of Multifactorial Atherosclerosis-Cardiovascular), a four-step algorithm retaining SCORE2 as the quantitative spine while embedding once-in-a-lifetime Lp(a) measurement, a mandatory amplifier checklist, and selective coronary artery calcium (CAC) or carotid/femoral ultrasound imaging. Conclusions: ROMA-CV is a hypothesis-generating proposal that operationalizes existing evidence-based recommendations into a deterministic Romanian pathway aligned with the 2025-2030 Romanian National Plan for Non-Communicable Diseases and the EU Cardiovascular Health Plan. The algorithm is not a validated clinical decision tool and requires prospective external validation in Romanian cohorts-alongside feasibility, cost-effectiveness, and implementation studies-before any consideration of routine clinical adoption.
This study evaluates the association between baseline left ventricular (LV) peak strain dispersion (PSD) and 3-to-5-year cardiovascular outcomes in patients undergoing maintenance hemodialysis (MHD). This single-center retrospective cohort study screened 586 adult patients undergoing MHD at a tertiary renal unit between January 2018 and December 2020, with follow-up through June 2024. Patients were stratified by baseline PSD at the prespecified cutoff of ≥65 ms. One-to-one propensity score matching (nearest neighbor, caliper: 0.02) using 24 covariates was applied to minimize confounding. The primary outcome was major adverse cardiovascular events (MACE)-a composite of cardiovascular death, nonfatal myocardial infarction, hospitalization for heart failure, nonfatal stroke and sustained ventricular arrhythmia. Secondary outcomes included cardiovascular and all-cause mortality. Survival was analyzed using Kaplan-Meier curves, matched-pair robust Cox proportional hazards models and competing-risk sensitivity analyses. After matching, 336 patients (168 per group) were analyzed, with excellent covariate balance (all standardized mean differences <0.10). Over a median follow-up of 46.8 months, MACE occurred in 64 patients (38.1%) with high PSD and 34 patients (20.2%) with low PSD. High PSD was associated with a higher hazard of MACE (adjusted hazard ratio [aHR]: 2.05, 95% confidence interval [CI]: 1.48-2.84; p < 0.001), cardiovascular mortality (aHR: 2.18, 95% CI: 1.08-4.40; p = 0.030) and all-cause mortality (aHR: 1.58, 95% CI: 1.02-2.45; p = 0.041). Subgroup analyses demonstrated directionally consistent associations, with a stronger association in patients with impaired global longitudinal strain (interaction p = 0.03). Baseline LV PSD was associated with adverse cardiovascular outcomes in patients receiving MHD. Incorporating PSD into echocardiographic risk stratification may refine risk assessment, but multicenter prospective validation is required before threshold-based clinical implementation.
Arterial stiffness, as a biomarker of cardiovascular diseases, is most often described by a surrogate global stiffness index, pulse pressure wave velocity (PWV), a measure of the time for pressure pulses to transit to sensors normally placed on different arteries. However, local arterial elasticity also influences the transient response of an artery to an impulse of flow, as characterized by the local pulsatile flow velocity waveform. Such transient response to pulsatile flow has not previously been analyzed as an indicator of arterial stiffness and a biomarker of cardiovascular disease. The objectives of this exploratory study were to identify physical relationships between arteries' pulse flow velocity (PFV) transient response characteristics and the elasticity of central arteries, and to provide preliminary evidence of a match between measured arterial pulse flow response characteristics and those predicted by physical relationships. A transmission line model is applied to the analysis of transient blood flow velocity waveforms, a new analytic approach, offering a new measure of arterial elasticity, that of natural frequency, which is shown to be directly related to arterial stiffness. Specific flow velocity values, as measured at specific points on damped oscillation transient flow velocity waveforms, enable the determination of the natural frequency associated with the artery's transient response to an impulse of flow from the left ventricle. The damped oscillation transient flow velocity waveforms, as measured by pulse Doppler ultrasound, is shown to match the damped oscillation flow velocity waveforms measured on the thoracic aorta and on the femoral artery. Such matching includes Bland-Altman analysis of waveform match using zero, one and two reflection sites. Also, the local stiffnesses of central arteries determined from the pulse Doppler ultrasound measurement of natural frequency are shown to match global stiffness reported for the same arteries using established PWV measurement approaches, providing an initial indicator of the validity of this new sonographic arterial elasticity measurement technique. This new arterial elasticity measurement technique, Doppler ultrasound measurement of vascular natural frequency, potentially offers advantages over established pulse pressure wave velocity measurement techniques as follows: a The measurement of elasticity at specific arterial locations; b The measurement of the elasticity of deeply set central arteries, and; c The potential for measuring central artery elasticity in clinical settings. This study is exploratory in that the application of pulse flow transient velocity waveform analysis to the determination of arterial elasticity is a novel departure from established pulse pressure wave analysis approaches. The study's preliminary findings, specifically the match between predicted transient flow velocity waveforms and those measured, and also the match between predicted PWVs to those measured using established pulse transit time techniques, are both sufficiently close that further independent verification and more extensive formal validation initiatives are indicated and justifiable.
Arterial stiffness is an independent predictor of cardiovascular mortality, with localized compliance variations providing key insights for vascular disease assessment. In our previous studies, we implemented a PINN-based inverse approach integrating Pulse Wave Imaging (PWI) and Vector Flow Imaging (VFI) data with 1D PDEs of pulse wave propagation and was trained to minimize mismatch between measured data and physics constraints for in silico and phantom-mimicking stenotic vessels. This study evaluates the performance of the previously-reported PINN framework for noninvasive, spatially resolved estimation of arterial compliance and lumen pressure from the high-frame-rate ultrasound (PWI and VFI) data in a clinical setting. The framework was applied on common carotid artery high-frequency ultrasound frames (3 kHz frame rate) in five subjects: one healthy and four with carotid stenosis (low to medium occlusion). The proposed model estimated spatially varying compliance in all subjects: healthy subjects showed uniform compliance, while stenotic subjects exhibited focal compliance variation correlating with plaques/occlusion on ultrasound B-mode images. The model reconstructed wall motion (% difference <0.2% in healthy, <0.48% in carotid stenosis patients) and flow velocity (% difference <0.2% in healthy). In stenotic cases, the model adapted to unreliable flow data by using the wall motion data only. The computation time ranged from 20 minutes to 1.5 hour depending on the spatial lateral resolution; lateral resolution of 16-elements data (instead of full 128-elements data of L7-4 transducer) considered for healthy cases required 20 minutes runtime, whereas, for the stenotic cases, 1.5 hours was needed due to the required full resolution (all 128-elements data). In conclusion, this study demonstrates the effectiveness of the PINN-based framework for non-invasive, patient-specific mapping of localized arterial compliance variation as well as luminal pressure. These findings presented in this feasibility study support clinical translation for non-invasive atherosclerotic plaque risk evaluation and personalized cardiovascular assessment.
Conventional ultrasound-based assessment of aortic stiffness relies on two-point distension metrics using maximum and minimum vessel diameters within a cardiac cycle, which may not fully reflect time-resolved aortic wall dynamics. This retrospective pilot study investigated the feasibility and clinical relevance of a time-series-based stiffness parameter, termed pulsatile stiffness-β, derived from automated segmentation of archived aortic M-mode ultrasound images. Seventy-nine cases with available aortic M-mode images were analyzed. Automated image processing was used to segment the anterior and posterior aortic walls and reconstruct diameter waveforms. Conventional stiffness-β, pulsatile stiffness-β, and wall asymmetry-related parameters were calculated and compared with demographic, tonometry-derived, hemodynamic, coronary burden, cardiovascular risk, and echocardiographic variables. Conventional and pulsatile stiffness-β were strongly correlated and showed directionally consistent associations with established vascular functional parameters, including systolic blood pressure, pulse pressure, augmentation pressure, age, and cardiovascular risk burden. Pulsatile stiffness-β demonstrated association patterns broadly comparable to conventional stiffness-β, suggesting its role as a waveform-informed extension rather than a superior alternative. Wall asymmetry-related parameters were associated with the Syntax score. Automated analysis of archived aortic M-mode images may provide feasible time-resolved vascular biomarkers for stiffness and wall motion assessment.
Inflammation contributes to atherosclerosis and vascular remodeling, but the immune pathways associated with distinct carotid ultrasound phenotypes, including carotid intima-media thickness (cIMT), maximal plaque thickness (MPT), and arterial stiffness remain incompletely characterized. We investigated associations between circulating immune biomarkers and carotid ultrasound measures in a stroke-free, multi-ethnic cohort. We analyzed data from 1,134 stroke-free participants (mean age 70 ± 9 years, 59% women, 66% Hispanic) in the Northern Manhattan Study (NOMAS) who underwent high-resolution B-mode carotid ultrasound. cIMT and MPT were measured using automated edge-detection software, while arterial stiffness was assessed via systolic and diastolic diameter measurements, strain, and β-stiffness. Plasma levels of 60 immune biomarkers were quantified using a multiplex immunoassay. Biomarker selection was performed using LASSO, Random Forest, and XGBoost; markers selected by ≥ 2 methods were prioritized. Associations were tested using multivariable linear regression adjusted for age, sex, race/ethnicity, and cardiovascular risk factors (hypertension, hyperlipidemia, diabetes, and smoking). Machine-learning analyses identified partially distinct candidate biomarker profiles for cIMT, MPT, and arterial stiffness. In fully adjusted regression models, greater cIMT was associated with higher IL-4 and leptin levels and lower IL-10, VCAM-1, and SerpinE1 levels. None of the machine-learning-selected biomarkers was independently associated with MPT at the conventional p < 0.05 threshold. Greater arterial stiffness was associated with higher SCF levels, while CXCL10 demonstrated a nonsignificant inverse trend. Models incorporating the selected biomarkers had modestly higher adjusted R² values than models containing clinical covariates alone (cIMT, 0.072 versus 0.109; MPT, 0.134 versus 0.147; arterial stiffness, 0.063 versus 0.075). In a stroke-free, multiethnic cohort, machine-learning analyses identified distinct and overlapping candidate immune biomarker profiles across cIMT, plaque thickness, and arterial stiffness. However, only a subset of selected biomarkers demonstrated independent associations in fully adjusted regression models. These findings support a hypothesis-generating role for inflammatory and immunometabolic pathways in subclinical carotid disease and vascular aging and require validation in longitudinal studies.
We report on the case of a pediatric patient with homozygous familial hypercholesterolemia (HoFH) who developed significant coronary artery disease (CAD). Percutaneous coronary intervention (PCI) guided by intravascular ultrasound (IVUS) was performed. A 6-year-old female patient was diagnosed with HoFH following the identification of cutaneous xanthomas. Genetic test identified a homozygous mutation in the LDLR gene. Cardiovascular assessment including a coronary CT angiography revealed a severe (70-90%) stenosis of the ostium of the left main coronary artery (LMCA) without significant lesions in other coronary branches. Given the severity of the lesion, PCI was indicated. The patient underwent PCI via the right femoral artery. The LMCA lesion was confirmed (70-90% stenosis, TIMI 3 flow) and a drug-eluting stent was deployed. Intravascular ultrasound (IVUS) played a crucial role in guiding the intervention, ensuring optimal stent expansion and apposition. Post-procedure, dual antiplatelet therapy (aspirin + clopidogrel) was initiated, clopidogrel was stopped after six months. A six-month follow-up CT angiogram demonstrated satisfactory stent positioning, despite metallic artifacts limiting full assessment. Two years after angioplasty, there have been no clinical, electrocardiographic, or echocardiographic signs of myocardial ischemia. This case highlights the feasibility and safety of LMCA stenting in pediatric patients with HoFH. Given the challenges of coronary interventions in pediatric patients, IVUS should be considered a critical adjunct to angiography in complex cases of early-onset coronary artery disease.
Patients undergoing distal diabetic foot surgery commonly have diabetic peripheral neuropathy and substantial systemic comorbidity. This study evaluated the association between preoperative glycated hemoglobin (HbA1c) level and ultrasound-guided ankle block onset. Prospective observational study. Adults with diabetic peripheral neuropathy undergoing wound debridement or toe amputation were grouped according to HbA1c level (<8.0% or ≥8.0%). The primary outcome was sensory block onset time. Postoperative pain, opioid consumption, and patient satisfaction were also evaluated. Forty-two patients were analyzed. Sensory block onset was shorter in the HbA1c ≥8.0% group than in the HbA1c <8.0% group (4.9 ± 1.1 versus 7.4 ± 2.8 minutes; mean difference, -2.43 minutes; 95% confidence interval, -3.67 to -1.19; p < 0.001). Among patients who developed a measurable motor block, motor onset was also shorter (13.0 ± 3.4 versus 16.9 ± 3.5 minutes; mean difference, -3.89 minutes; 95% confidence interval, -6.36 to -1.43; p = 0.003). Postoperative pain, opioid consumption, and satisfaction were comparable between groups. Higher HbA1c remained associated with shorter sensory onset after covariate adjustment. Poor glycemic control was associated with modestly faster ultrasound-guided ankle block onset in patients with diabetic peripheral neuropathy. The clinical importance of this finding and the potential effect of glycemic control on block duration require further investigation. 3.
Cardiovascular disease (CVD) is the leading threat to human health and has the highest morbidity and mortality rates worldwide. Compared with drug-eluting stents (DES), drug-eluting balloons (DEB) could offer better safety and efficacy in the treatment of in-stent restenosis (ISR) and small vessel disease (SVD), due to the ability to homogeneously transfer the drug into the vessel wall without leaving permanent stents in the coronary vessel. However, the high drug loss and low drug utilization limit the DEB use in clinical. The smart response technology can improve the drug delivery and targeting ability of DEB to achieve controlled drug delivery and release processes, which could address the shortcoming of DEB such as high drug loss and low drug utilization. There have been studies using light-driven, gas-driven, ultrasound (US)-responsive, reactive oxygen species (ROS)-responsive, and microneedle (MN) smart response technologies to construct smart DEB developing. This paper reviews the research progress of DEB in recent years from the smart DEB, aiming to address their limitations in clinical applications and provide guidance for the development of DEB.
Background: Trisomy 21 (T21) is strongly associated with congenital heart disease, particularly atrioventricular septal defect (AVSD), ventricular septal defect (VSD), atrial septal defect (ASD) and selected conotruncal and arch anomalies. First- and second-trimester ultrasound, Doppler and fetal cardiac MRI enable increasingly early and detailed characterization of these lesions, while advances in molecular cardiogenesis have linked specific phenotypes to dosage-sensitive genes on chromosome 21. Methods: This narrative review synthesizes contemporary evidence on structural and functional cardiovascular anomalies in T21 fetuses in the first and second trimester, integrating fetal echocardiography, Doppler assessment and fetal cardiac MRI with embryologic and molecular insights, and summarizing trimester-specific detectability and pathophysiologic links to candidate genes in the Down syndrome-critical region. Approximately one quarter to one third of T21 fetuses have major congenital heart disease on high-quality prenatal echocardiography, with AVSD representing about half of all lesions and VSD, tetralogy of Fallot (TOF), arch anomalies, venous return abnormalities and functional markers (increased nuchal translucency, tricuspid regurgitation, ductus venosus abnormalities) comprising the remainder. Results: First-trimester detection relies on functional markers and early four-chamber and outflow-tract views, whereas second-trimester studies refine anatomic definition and hemodynamics, with MRI reserved for complex cases. Overexpression of genes such as DSCAM, COL6A1/COL6A2, DYRK1A and RCAN1 perturbs endocardial cushion, conotruncal and vascular development. Conclusions: Early, protocol-driven cardiac imaging in T21 supports timely diagnosis, risk stratification and multidisciplinary counselling, and links fetal imaging phenotypes with chromosome 21 gene dosage to advance personalized management and future genotype-phenotype research.
Visceral artery pseudoaneurysms (VAP) develop following inflammatory pathology or trauma. Endovascular management remains the gold standard as per the Cardiovascular and Interventional Radiological Society of Europe (CIRSE) standards. However, when endovascular therapy is not feasible, other modalities like percutaneous or endoscopic ultrasound (EUS)-guided embolization have also been utilized. Lately, EUS-guided procedures have been reported increasingly in the literature. We report a case of post-laparoscopic cholecystectomy cystic artery pseudoaneurysm complicated by associated biliary injury. It was initially managed with EUS-guided glue and coil embolization, but the patient developed recurrent bleeding with formation of a pseudoaneurysm-duodenal fistula. This complication was successfully salvaged with emergency surgery. Coexistent biliary injury was subsequently repaired with hepaticojejunostomy. We have performed a systematic review of the available literature to assess the current status of the EUS-guided endotherapy for VAP. A systematic review has been conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) and Cochrane Handbook for Systematic Reviews and Interventions guidelines. Literature search showed 30 studies with 122 patients in whom VAP was managed by EUS-guided intervention. Studies primarily included case reports (n = 15), case series (n = 8), videos (n = 4), images (n = 2), and abstracts (n = 1). Most of the patients (108, 88.5%) were male, mean age of the cohort was 41.9 years (range: 18-73 years), chronic pancreatitis was the most common etiology, reported in 85 (69.7%) cases, splenic artery was the most commonly involved vessel, seen in 76 (61.8%) cases, and upper gastrointestinal bleeding was the most common presentation, reported in 83 (68%) cases. Unfavorable anatomy for angioembolization was the most common indication for EUS-guided endotherapy, reported in 26 (21.3%) cases, followed by failed angioembolization, which was reported in 19 (15.6%) cases. A combination of cyanoacrylate glue with coil was used in 70 (57.4%) patients during endotherapy. Pooled clinical success rate of EUS-guided endotherapy for VAP was 94.25% (95% confidence interval: 88.43-97.40%), with technical success rates approaching 100%. Pooled complication rate was 11.54% (95% CI: 6.11-19.29%), with recurrent bleeding in four (3.85%, 95% CI: 1.19-9.79%), and solid organ complications (infarct/abscess involving spleen and/or liver) in five (4.8%, 95% CI: 1.79-11.04%). Recanalization of pseudoaneurysm was noted in two patients (recurrence rate: 1.64%, 95% CI: 0.08-6.15%) on follow-up. Post-cholecystectomy cystic artery pseudoaneurysm is a rare complication. EUS-guided intervention is an evolving technique for the management of visceral artery pseudoaneurysm. There is limited and low-level evidence available at present to clearly define the role of EUS-guided endotherapy in the overall management of visceral artery pseudoaneurysm. EUS-guided intervention is a rescue therapy only for VAP at present; its first-line use (as in this case) is not supported. Endovascular management of visceral artery pseudoaneurysm remains the standard of care. Surgery remains the rescue intervention in cases where other interventions have failed.
Background: Despite therapeutic advances, many patients with metastatic lung cancer still lack access to comprehensive molecular profiling, often due to inadequate biopsy samples. Percutaneous ultrasound-guided needle aspiration biopsy (US-NAB) from both lung and metastatic sites has shown promise in improving diagnostic and molecular profiling accuracy. However, data regarding its real-world utilization, diagnostic performance, and contribution to comprehensive molecular profiling in unselected patients with advanced lung cancer remain limited. Methods: We performed a secondary (post hoc) analysis of prospectively collected data from the Propheta Pro study, a prospective observational cohort of patients with advanced lung cancer. The aim of the present analysis was to assess patterns of invasive sampling procedures, with a particular focus on the prevalence of US-NAB utilization across histologic subtypes. We also assessed the diagnostic yield of US-NAB for cancer diagnosis, comprehensive genomic profiling, and PD-L1 expression. Results: Among the 348 patients enrolled, 123 (35.3%) underwent US-NAB, making it the most frequently utilized sampling technique overall and across individual histologic subtypes. Biopsy of metastatic sites was significantly more common than primary lung tumors (113, 91.9% versus 10, 8.1%; p < 0.001), with superficial metastases being the primary target (110, 89.4%). US-NAB demonstrated high diagnostic yields: 97% for histological diagnosis, 91.1% for comprehensive genomic profiling, and 95.8% for PD-L1 testing. Only two minor, self-limiting complications were observed. Conclusions: US-NAB is a highly effective yet underrecognized diagnostic option for advanced lung cancer, particularly given the high prevalence of accessible superficial metastases. Integrating US-NAB into interventional pulmonology services could enhance diagnostic and molecular profiling yields.
Early applications of fetal Doppler evaluation drew on parameters derived from adult vascular examination, primarily applied to identifying fetuses at risk for growth restriction and hypoxia. The integration of color Doppler into real-time imaging facilitated a shift toward structural-functional correlation, enabling clinicians to visualize fetal cardiac outflow tracts, valve regurgitant jets, and the complex umbilical-venous connections alongside standard grayscale anatomy. Power Doppler extended these capabilities to slow flow and small caliber vascular structures. Doppler modalities have been crucial in delineating the fetal cardiovascular system, increasingly detecting complex congenital heart disease (CHD) prenatally, and illuminating cardiac and non-cardiac vascular structures that previously posed a challenge to visualization, including cerebral, hepatic, and placental capillary beds. Highly sensitive Doppler technologies such as SlowflowHD as well as MV-Flow and LumiFlow, exemplify the convergence of anatomical and physiological imaging, such as fetal venous sinuses and deep cerebral venous return, to allow brain perfusion assessment at earlier gestational stages. Although SlowflowHD has been shown to have added value for diagnosis, it seems to be an underused modality. Here we show several examples drawn from our experience with SlowflowHD, in both routine scanning and anomalous cases spanning various organ systems and stages of gestation. While there is a learning curve in optimizing image acquisition and interpretation of microvascular anatomy, it should not deter practitioners proficient in Doppler techniques. We recommend incorporation of SlowflowHD and comparable microvascular imaging technologies into the sonographic armamentarium.
The progressive nature of cardiovascular-kidney-metabolic syndrome (CKM) allows early intervention during stages 0-3. However, the role of the cardiometabolic index (CMI) across CKM stages 0-3 and its potential synergy with depressive symptoms remain unclear. We followed 5,556 CHARLS participants (aged ≥ 45, CKM stages 0-3) for 7 years. Higher CMI and cumulative average CMI (CumCMI) were independently associated with CVD (HR for Q4 vs. Q1: 1.27, P trend = 0.009; HR for high vs. low CumCMI: 1.28, P trend < 0.001). Nonlinear thresholds were 0.47 (CMI) and 2.08 (CumCMI). Among 2,595 participants with complete depressive symptoms data, those with high CumCMI alone (HR = 1.61) or depressive symptoms alone (HR = 1.43) had elevated risk, whereas those with both factors had the highest risk (HR = 2.08). Baseline AUC was 0.651; adding CMI alone yielded no improvement (0.651), whereas adding depressive symptoms alone raised it to 0.657; both together gave 0.657-0.658. However, additive interaction was not statistically significant, and the AUC improvement from adding depressive symptoms to a model already containing CMI was minimal (ΔAUC ≈ 0.007), suggesting that this combined indicator may be more suitable for population-level risk stratification than individual clinical prediction.
The original intravascular ultrasound (IVUS) calcium score in percutaneous coronary intervention (PCI) applies only to lesions with a maximum calcium angle > 270°, distinguishing it from the optical coherence tomography (OCT) calcium score. We aimed to investigate a new IVUS-derived calcium score to predict stent underexpansion in moderately to severely calcified lesions. We retrospectively analyzed 238 IVUS-guided PCI cases with moderate to severe calcification visible on angiography, including 136 cases with IVUS-guided PCI as a derivation cohort and 102 cases with both IVUS- and OCT-guided PCI as a validation cohort, excluding cases in which atherectomy was used. In the derivation cohort, IVUS-derived maximum calcium angle showed significant area under the curve (AUC) to predict stent underexpansion (< 70%) at the maximum superficial calcium site (cutoff value: 228°, AUC: 0.72). A multivariable linear regression model showed that maximum calcium angle of 225° (regression coefficient: -11.69; p = 0.023) and the presence of calcified nodule (regression coefficient: -4.913; p = 0.004) were associated with stent expansion. A new IVUS calcium score (0-4 points) was defined as 3 points for maximum calcium angle > 225°, and 1 point for presence of a calcified nodule. A cutoff of ≥ 3 showed a good AUC (0.751) and an excellent negative predictive value (0.963) to predict stent underexpansion. In the validation cohort, the incidence of stent underexpansion was 0%, 0%, 8.6%, and 33.3% in patients with the new IVUS calcium score of 0, 1, 3, and 4, respectively (p = 0.004). The new IVUS-derived calcium score can effectively predict stent expansion in moderately to severely calcified lesions.