Search Results for: Intervalli di sorveglianza per Aneurisma Aorta Addominale (AAA)

Stroke, Volume 56, Issue Suppl_1, Page AWP187-AWP187, February 1, 2025. Introduction:3 to 5% of patients undergoing endovascular thrombectomy present impossible catheter access to the occlusion site from transfemoral access (TFA), largely attributed to complex arterial anatomy. Radial access can be an effective bailout strategy, but intraprocedural delays may negatively impact outcomes. Novel image processing algorithms allow for advanced characterization of vascular pathways from baseline neuroimaging, enabling the exploration of predictive models of impossible TFA before arterial puncture.Methods:A retrospective cohort of patients with an anterior large vessel occlusion who received thrombectomy from TFA between 2017 and 2023 were included in this study. A previously described automatic vascular analysis software was used to generate centerline graphs from the aorta to the intracranial occlusion site from baseline CTA. ArterialGNet, a graph neural network based on graph attention designed to integrate descriptors of centerline pathways extracted at three different distance scales, was trained for impossible TFA prediction. Five-fold cross validation was used for model derivation. The method was compared to a previously introduced random forest ensemble model with extreme gradient boosting (XGBRF) based on six vascular tortuosity descriptors of the aortic and supra-aortic regions.Results:A total of 745 patients (aged 78 years IQR 68-85, 56% women) were included in this study. Patients treated between 2017 to 2022 (n=568, 3.2% with impossible TFA) were used for model training and validation. Patients treated in 2023 (n=177, 3.4% with impossible TFA) were held out for testing. In validation, the best-performing configuration of ArterialGNet achieved a C-statistic of 0.82 (95%CI 0.74-0.90), similar to the baseline model (0.82, 95%CI 0.77-0.88). Comparable outcomes were observed in the final testing for ArterialGNet (0.84, 95%CI: 0.82–0.86). In contrast, the XGBRF model exhibited signs of overfitting (0.65, 95% CI: 0.53–0.78). In final testing, ArterialGNet predicted impossible TFA with a sensitivity of 0.80 (95%CI 0.66-0.94) and a specificity of 0.84 (95%CI 0.76-0.91). Median processing time for ArterialGNet was below 4 min.Conclusions:A novel model for impossible TFA prediction was validated with a large dataset. Impossible TFA prediction before arterial puncture may assist in decision support for initial access selection in thrombectomy, reducing intraprocedural delays and potentially improving clinical outcomes.

Stroke, Volume 56, Issue Suppl_1, Page ATP238-ATP238, February 1, 2025. Introduction:Cerebral blood flow (CBF) is a major determinant of when and where within the brain stroke occurs. The brain’s demand for oxygen and nutrients makes it sensitive to pulsatility propagating from the heart. The contribution of cardiac flow to CBF is poorly understood. We present a pilot study using 4D flow MRI to sequentially measure both aortic blood flow and CBF in the same individual and our initial findings comparing blood pressure (BP), cardiac flow, and CBF in healthy volunteers.Methods:We acquired both 4D flow brain MRI and 4D flow cardiac MRI in a single session using a Siemens 3T Magnetom Vida scanner in 5 volunteers (4 male, 1 female) 31.2 ± 10.4 years old. Using a compressed sensing protocol (R=7.7) each 4D flow scan was acquired in under 15 minutes. Brain and cardiac MRI respectively used a 1.4 mm3and 2.1 mm3voxel size; velocity was encoded in 3D at 120 cm/s and 200 cm/s, with 15-25 cardiac phases. 4D flow brain coverage included the ICA, BA, MCA, ACA, and PCA (Fig 1). 4D flow cardiac coverage included the ascending and descending thoracic aorta (Fig 2). 4D flow data were reconstructed using Tempus Pixel (Tempus, IL) and regions of interest were defined to measure volumetric flow rate (Q). Blood flow pulsatility over the cardiac cycle was quantified using pulsatility index (PI). Pearson’s correlation coefficient (r) was calculated for statistical analysis.Results:Aorta Q correlated strongly with cerebral Q, in the ICA and BA (r=0.90), in the MCA, ACA, and PCA (r=0.70). Aorta Q correlated with PI in both the ICA and BA (r=0.81), but not within the MCA, ACA, and PCA (r=0.12). Aorta PI was moderately anticorrelated with PI throughout the cerebral arteries (r=-0.52). Brachial systolic and diastolic BP both correlated with cerebral PI (r=0.68, 0.99, respectively), while moderately anticorrelated with aorta PI (-0.66, -0.52). Pulse pressure correlated strongly with cerebral Q (r=0.85), and less with aorta Q (r=0.59). Heart rate was strongly anti-correlated with aorta PI (r=-0.82) and moderately correlated with cerebral PI (r=0.61).Conclusion:These initial findings demonstrate that flow characteristics Q and PI are similar between the aorta and major arteries feeding the brain (ICA, BA), but the effects of BP and heart rate appear to invert at more distal vessels (MCA, ACA, PCA). We plan to expand this technique to investigate the connection between cardiac and cerebral flow in patients with neurovascular disease.

Aifa-Iss: “Serve sorveglianza, più rischi con mobilità e clima”

Circulation, Volume 151, Issue 4, Page 289-291, January 28, 2025.

In questi grandi raduni internazionali serve una sorveglianza epidemiologica per monitorare eventuali focolai di contagio di virus respiratori

Objectives
Ascending aorta dilatation (AAD) has been suggested as a surrogate marker for vascular organ damage in the hypertensive population. However, limited data are available on AAD in normotensive individuals. This study aims to preliminarily explore the correlation between ascending aorta (AAO) and other established clinically significant target organ damage parameters and to investigate the possible risk factors of AAD in the non-diabetic normotensive individuals.

Design
Our study has a cross-sectional design.

Setting
All participants were recruited from the inpatient and outpatient departments of our hospital.

Participants
We recruited 634 normotensive participants (52.26±16.22 years, 39.43% male) who underwent both ambulatory blood pressure monitoring (ABPM) and echocardiography. The whole study population was divided into AAD and non-AAD groups according to age-gender-specific criteria. The baseline mean blood pressure (BP) of the two groups was 126.92/77.72 and 124.16/77.61 mm Hg, respectively.

Primary and secondary outcome measures
The relationship between AAO and other acknowledged cardiac damage indicators, as well as the associations of AAD with ABPM indexes in the non-diabetic normotensive individuals.

Results
We observed that AAO exhibited a significant correlation with left ventricular mass index (β=1.905, p

‘Necessaria la sorveglianza delle infezioni nelle strutture sanitarie’

Circulation, Volume 150, Issue Suppl_1, Page A4141445-A4141445, November 12, 2024. Introduction:Bicuspid aortic valve (BAV) is associated with progressive ascending aorta (AAo) dilation, often leading to aneurysms, dissections, and ruptures. Thus, current guidelines recommend preventive surgery for AAo dilation. Recent 4D flow MRI studies show that BAV morphology causes abnormal transvalvular flow patterns, increasing wall shear stress (WSS), a trigger of aortic growth. Further studies have delineated areas of abnormally high WSS by comparing to estimates of matched controls, and show promise in detecting risk for aortic growth. However, since the long-term prognostic significance of this marker is unclear, we aimed to quantify WSS in BAV patients to assess its value in predicting the need for aortic surgery up to 10 years post-4D flow MRI acquisition.Methods:BAV patients without prior surgical intervention scanned before April 1, 2014 were identified. Using medical records, patients were categorized as ‘operated’ if they underwent aortic surgery post-scan and ‘non-operated’ if they were surgery-free for at least 10 years post-scan. 4D flow MRIs were processed with an AI pipeline, including 3D segmentation of the aorta, followed by peak velocity (PV) and WSS quantification in the AAo (Fig. 1A-C). Patient-specific WSS heatmaps were computed relative to a map based on the WSS of 10 or more sex and age-matched controls. Relative areas of elevated WSS in the AAo were then calculated (Fig. 1D-F).Results:115 patients were included, with 73 non-operated (age: 42.5±11.5y, 49M) and 42 operated patients (age: 53.5±12.1y, 34M). The mean baseline mid-AAo diameters for non-operated and operated patients were 3.8±0.6 cm and 4.1±0.5 cm, respectively. Among operated patients, the mean scan to surgery time was 5.7±3.3y. All three 4D flow metrics were significantly higher in operated compared to non-operated patients: PV: 2.6±0.6 vs. 1.7±0.4 m/s (p

Circulation, Volume 150, Issue Suppl_1, Page A4148073-A4148073, November 12, 2024. Case Description:A 26 yo woman with Marfan Syndrome (MFS,FBN1), ectopia lentis, aortic dilation and no family history of MFS or aortic dissection was evaluated for preconception counseling. She was asymptomatic, and the size of her aortic root (~4cm) and ascending aorta (~3.5cm) had been stable for over 5 years. She was counseled that risk of cardiac events during her pregnancy is high, but lower compared to those with aortic sizes >4.5cm. Once pregnant, she was followed closely with imaging every trimester (MRA at 25 weeks gestation showed stable aortic sizes). Cardio-obstetric recommendations included: CARPREG II score: 2, mWHO class: III, consideration of assisted second stage due to aortic root dilation. She was counseled on symptoms of aortic dissection and to seek emergency care should those symptoms arise. At 27 weeks gestation, she presented to the ED with intense chest and neck pain, shortness of breath, and headache. Emergent CT showed aortic root (4.1cm) and proximal ascending aortic dissection with propagation into the left main coronary artery(Figure 1).She underwent emergent C-section followed by aortic root and ascending aorta replacement and mechanical aortic valve replacement due to severe regurgitation. She was discharged in stable condition 8 days after an uncomplicated post-operative recovery. Her baby is recovering in the NICU.Discussion:While risk of aortic dissection in women with MFS is higher during pregnancy, recent studies suggest relative safety with aortic root diameters up to 4.5cm. Our case highlights that even at “lower risk” aortic sizes, aortic dissection remains an important risk for such women. Educating patients and providers about the acute symptoms of aortic dissection and forming an action plan for timely intervention can be lifesaving. Furthermore, some genetic mutations (e.g.TGBR1/2orSMAD3) and sequence variants within theFBN1gene may pose a higher risk of aortic dissection at smaller aortic diameters. Our patient’s pathogenicFBN1mutation (-c.2114-5T >G, previously classified as a VUS) highlights the importance of genetic testing: prophylactic surgery at sizes

Circulation, Volume 150, Issue Suppl_1, Page A4144548-A4144548, November 12, 2024. Introduction:Turner syndrome (TS) is caused by the partial or complete absence of one sex chromosome and affects 1 in 2500 liveborn infants. Hypertension, bicuspid aortic valve (BAV), and thoracic aortic aneurysms (TAAs) are more prevalent in TS compared to the general population and predispose to aortic dissections, which may occur in young adults with TS. We hypothesize that adults with TS who have TAAs experience a high rate of adverse cardiovascular outcomes.Methods:Adults with TS who had Healthy Heart Project (HHP) echocardiograms at national conferences between 2003 and 2023 were contacted for enrollment in descending order of the aortic size index (ASI, cm/m2), defined as the ratio of the maximum ascending aortic diameter to body surface area. After informed consent, clinical characteristics and outcomes (as numbers of participants or median and interquartile range) were abstracted from questionnaires and medical records.Results:Sixty-four of 704 total HHP participants were contacted and 19 (with 10 of the 20 highest ASI values) were enrolled with complete data. The baseline ASI was 2.19 (0.48), compared to 1.51 (0.36) for all other HHP participants. The median age was 59 (13) years. The most prevalent characteristics were 45,X (10) or 45,X/46,XX (6) karyotypes; BAV (9), coarctation (4), or no congenital lesions (6); and hypertension (12). A mean of 10 serial aortic images were available for each participant over a follow up period of 14 (9.8) years. The median increase in aortic diameter was 0.09 (0.29) mm/yr at the sinuses of Valsalva and 0.26 (0.44) mm/yr at the ascending aorta. Seven participants underwent aortic operations due to enlarging TAAs when the median ascending diameter was 3.83 (0.67) cm (ASI 2.58 (0.11) cm/m2). In 3 cases, operations were urgent due to cardiovascular symptoms or rapid aortic dilation, but there were no acute aortic dissections. The median time between the index image and subsequent repair was 3.5 (7.0) years. Three HHP participants with the 8th, 15th, and 42nd largest ASI values died prior to follow up. One death was caused by complications after surgical aortic valve replacement at age 20.Conclusions:In a cohort of adults with TS and TAAs, 40% (7/19) developed progressive aortic enlargement requiring aortic repairs and there were 3 deaths. These observations underscore the importance of lifelong surveillance and timely intervention to prevent deaths due to cardiovascular disease in TS.

Circulation, Volume 150, Issue Suppl_1, Page A4140139-A4140139, November 12, 2024. Introduction:The cardio-ankle vascular index (CAVI) is a significant metric for evaluating arterial function. The test measures the stiffness of the arteries from the beginning of the aorta to the ankle, and the algorithm used is not influenced by blood pressure. Recent statistics indicate that a high CAVI score has the potential to predict future cardiovascular disease (CVD) occurrences. However, no research has been conducted in Vietnam to investigate this matter.Methods:A prospective study was conducted on 222 patients. Out of these, 162 patients had chronic coronary artery disease (CAD), while the remaining 62 patients were free of CAD. The study took place between October 2019 and December 2022. Participants who fulfilled the criteria were evaluated using the CAVI baseline measurement and clinical and paraclinical parameters. A total of 162 patients with chronic coronary artery disease (CAD) were monitored for cardiovascular disease (CVD) events over a period of 2 years.Results:CAVI in chronic CAD patients (9.21±0.79) was significantly higher compared to those in free-CAD patients (8.48 ± 0.62) with p

Circulation, Volume 150, Issue Suppl_1, Page A4144473-A4144473, November 12, 2024. Background:We hypothesized that patients with coarctation of aorta (COA) and obesity would have more advanced cardiovascular remodeling and impaired aerobic capacity compared to COA patients without obesity. The purpose of this study was to assess the relationship between obesity, cardiovascular remodeling, and aerobic capacity in adults with repaired COA.Methods:The study comprised of 3 groups: (1) Obese COA group (n=177) (COA patients with body mass index [BMI] >30 kg/m2); (2) Non-obese COA group (n=572) (COA patients with BMI ≤30 kg/m2); (3) Control group (n=59) (subjects without structural heart disease and BMI ≤30 kg/m2). Cardiovascular remodeling was assessed using the following indices: (1) Arterial stiffness – total arterial compliance index (TACI). (2) Left ventricular hypertrophy – LV mass (LVM) and relative wall thickness (RWT). (3) LV diastolic function – Doppler-derived estimated LV end-diastolic pressure (LVEDP) and Tau. (4) Right ventricular-pulmonary artery coupling – RV free wall strain and right ventricle systolic pressure (RVFW/RVSP). Aerobic capacity was assessed using predicted peak oxygen consumption (VO2).Results:The obese COA group had higher LVM, RWT, LVEDP, and Tau, well as lower RVFWS/RVSP, TACI and peak VO2 compared to non-obese COA group and controls. There was a correlation between BMI and LVM (r=0.39, p

Circulation, Volume 150, Issue Suppl_1, Page A4140048-A4140048, November 12, 2024. Background:Myocardial fibrosis is a key indicator of cardiac remodeling caused by pressure overload, involving a complex interplay of mechanical, inflammatory, and neurohormonal factors. Our recent studies reveal a harmful interaction between visceral adipose tissue (VAT) and the heart during aging, where profibrotic proteins from VAT and plasma contribute to heart fibrosis. We hypothesize that transverse aortic constriction (TAC)-induced pressure overload induces VAT remodeling and VAT profibrotic secretome that aggravates cardiac fibrosis and compromises heart function.Purpose:- To determine the interaction between VAT and heart-To assess the time course of TAC-induced transcriptomic changes in presence or absence of VATMethods:We divided wild-type male mice (5-month-old, n=10/group) into four groups: a visceral Lipectomy group and a Sham group two weeks before either a moderate TAC (26G; i.e. gradient between left ventricle and aorta of 30mmHg) or a sham surgery. We sacrificed the mice at 1- and 8-week after TAC. We performedin vivometabolic tests, echocardiography, and invasive hemodynamics, followed byex vivotissue analysis. We subsequently examined cardiac transcriptomic changes in TAC versus control groups, as well as the effect of visceral lipectomy through RNA-seq followed by Partial Least Squares Regression and Over-Representation Pathway Analysis.Results:TAC-induced cardiac pressure overload initiates a pathological heart-VAT crosstalk stimulating a senescence-like profibrotic (TGFb, Spp1) and proinflammatory secretory phenotype (TNFa, IL6, PAI1) in VAT as early as 1 week after TAC. Importantly, we demonstrate that VAT lipectomy reverses TAC-induced cardiac remodeling and restores normal heart function. Transcriptomic analyses show the powerful effect of TAC on gene expression, notably profibrotic (MMP9, TGFb1, Col1a1) and prohypertrophic genes (Nppa, Nppb) increase. After 1 week, TAC had a stronger effect than lipectomy, while 8 weeks post-TAC, lipectomy could reverse all the transcriptomic changes induced by TAC with a transcriptomic profile of TAC+lipectomy similar to sham group.Conclusion:This study highlighted the exacerbation by VAT of the detrimental impact of TAC on the heart. Our findings show a dynamic crosstalk between the heart and VAT orchestrated by the secretome of the adipose tissue resulting in transcriptomic and physiological heart changes.

Circulation, Volume 150, Issue Suppl_1, Page A4120623-A4120623, November 12, 2024. Introduction:Defective elastic lamellae and smooth muscle cell (SMC) accumulation are characteristics of diverse obstructive arterial diseases (e.g., atherosclerosis, pulmonary hypertension, and supravalvular aortic stenosis [SVAS]) as well as physiological closure of the ductus arteriosus (DA). Mechanistic links between defective elastin and SMC proliferation are not well elucidated.Methods:Immunostaining for proliferation marker Ki67 was performed on wild-type (WT) andEln(-/-)mouse aortas at embryonic day (E) 13.5 and E15.5 because elastin (ELN) is expressed in the mouse aorta from E14. Bulk RNA-seq was conducted on mouse aortic SMCs isolated from WT orEln(-/-)embryos at E15.5. As sphingosine kinase 1 (SPHK1) was found as a highly promising candidate, its expression was evaluated in human SVAS patient aortas and in mouseEln(-/-)aortas and WT DA. S1P receptor 1 (S1PR1) activity was assessed in aortic SMCs fromS1pr1(knock-in/knock-in), H2B-GFPmice. Genetic deletion ofSphk1in SMCs was performed on the elastin mutant background. Pharmacological SPHK1 inhibition was evaluated on both elastin mutants and WT embryos. Regulatory mechanisms of SPHK1 were assessed by mRNA stability assay and TRANSFAC database analysis.Results:SMC hyperproliferation was first observed inEln(-/-)aorta at E15.5, prior to morphological differences. Bulk RNA-seq revealed that Sphk1 is the most upregulated transcript inEln(-/-)aortic SMCs at E15.5. Reduced ELN increases SPHK1 levels in SMCs of human patient aortas and mouse aorta and DA. S1PR1 expression and activity are increased by elastin insufficiency. SMCSphk1deletion attenuates SMC proliferation and muscularization in the elastin-defective aorta, leading to extended viability ofEln(-/-)mice. Similarly, pharmacological SPHK1 inhibition ameliorates elastin aortopathy but leads to patent DA in WT mice. mRNA stability assay indicated Sphk1 is upregulated by enhanced transcription. TRANSFAC and bulk RNA-seq data suggested that transcription factor early growth response 1 (Egr1) induces Sphk1 transcription. Indeed, EGR1 was upregulated in elastin mutant aortas and DA.Conclusions:Elastin deficiency upregulates SPHK1 transcription, leading to SMC proliferation and hypermuscularization in elastin aortopathy as well as during physiological DA closure. Inhibiting SPHK1 is a promising therapeutic strategy for elastin aortopathy and for select congenital heart diseases in which patent DA maintains circulation.