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The objective was to investigate the prevalence of abdominal aortic aneurysms (AAAs) and the diameters of the aorta and common iliac arteries (CIAs) in a Korean cohort and secondly to analyze the differences in aortic diameter by comparison with a European cohort. The Korean cohort included participants ≥ 50 years who consented to AAA screening and data were analysed retrospectively. Aortic and common iliac diameters were measured using the outer-to-outer diameter method and prevalence rates were calculated. Common risk factors such as smoking, body mass index, pulmonary disease, hypertension, diabetes, hyperlipidaemia, ischaemic heart disease, and cerebrovascular disease were reported in association with AAA occurrence and AAA development. The aortic diameters were then compared with those in a Belgian cohort of 2487 participants identified in the Liège AAA Screening Program. An aortic size index (ASI) was also calculated to account for the potential size differences in the Belgian and Korean populations. A total of 3124 Korean participants were examined using ultrasound. The prevalence of AAAs in this cohort was 0.7%. The combined prevalence of subaneurysmal dilatation and AAA was 1.5%. The prevalence in male smokers older than 65 years was 2.7% (19/715). The mean infrarenal aortic diameter was 17.3 ± 3.1 mm in men and 15.7 ± 2.7 mm in women; the corresponding values in Belgian participants were 19.4 ± 3.0 mm in men and 17.9 ± 2.4 mm in women. The median aortic size index was 0.99 (interquartile range 0.88–1.12). The mean infrarenal aortic diameter was significantly smaller in the Korean cohort than in the Belgian cohort. Considering the observed prevalence of AAAs in different age groups, the age groups which would contribute to most cases was male persons above 66 years in both cohorts.

Purpose Aortic endograft infection (EI) can result in potentially life-threatening vascular complications. Unfortunately, it is difficult to obtain a correct diagnosis at an early stage in many patients. This report aims at validating the use of [18F] FDG PET/CT imaging for suspected endograft infections in a prospectively collected cohort of patients treated with EVAR and TEVAR. Materials and methods During a 14-year period, 366 patients required aortic stent graft. All procedures were performed electively, except for one patient. Among these 366 patients, eleven patients (3%) were suspected to have aortic EI. Contrast-enhanced CT and FDG PET/CT were performed in all 11 patients. Medical charts and imaging were analysed for these 11 cases, with initial positive CT. Results The final diagnosis of EI was established in seven (1,9%) based on clinical features, laboratory investigations and a significant [18F] FDG uptake in the aortic graft as well as the aortic wall. The median time from the initial EVAR/TEVAR to diagnosed infection was 180 days. During follow-up, the seven patients had a second PET/CT that was compared with the initial evaluation, decreased uptake was correlated with clinical improvement. Conclusions Contemporary diagnostic imaging for a potentially lethal endograft infection lacks precision, this observational study illustrates the potential clinical value of [18F] FDG PET/CT in the management of aortic EI. [18F] FDG PET/CT constitutes an imaging modality able to confirm the diagnosis, monitor disease progression as well as the effect of pharmaceutical treatment and detect relapse.

BACKGROUND Isolated pulmonary artery vasculitis is an uncommon cause of pulmonary artery aneurysm with very few reported cases in the literature. PATIENTS AND METHODS We hereby present the case of a 70-year-old man with occasional episodes of exertional chest discomfort. Our investigations revealed an expanding aneurysm of the main pulmonary artery extending to the proximal portion of the right branch. The patient successfully underwent replacement of the main pulmonary artery with a homograft. RESULTS Histopathological examination revealed images of vasculitis with numerous multinucleated giant cells. The patient's postoperative course was uneventful. CONCLUSION Management of pulmonary artery aneurysm secondary to isolated pulmonary artery vasculitis is not well studied, and no clear guidelines currently exist in the literature.

Background There are limited data on Coronavirus disease 2019 (COVID-19) in solid organ transplant patients, especially in heart transplant recipients, with only a few case reports and case series described so far. Heart transplant recipients may be at particular high risk due to their comorbidities and immunosuppressed state. Case presentation This report describes the clinical course and the challenging management of early COVID-19 infection in two heart transplant recipients who tested positive for the SARS-CoV-2 virus in the perioperative period of the transplant procedure. The two patients developed a severe form of the disease and ultimately died despite the initiation of an antiviral monotherapy with hydroxychloroquine coupled with the interruption of mycophenolate mofetil. Conclusions These two cases illustrate the severity and poor prognosis of COVID-19 in the perioperative period of a heart transplant. Thorough screening of donors and recipients is mandatory, and the issue of asymptomatic carriers needs to be addressed.

BACKGROUND: Periodontitis is a chronic inflammatory disease characterized by Gram-negative bacteria responsible for the degradation of tissues surrounding tooth. Moreover, periopathogens can invade the bloodstream, disseminate and promote cardiovascular disease, such as the link between Porphyromonas gingivalis and atherosclerosis. The aim of this study was to explore the relationship between the severity of periodontitis and of abdominal aortic aneurysm (AAA). METHODS: This cross-sectional study compared patients with stable AAA (n = 30) and patients with unstable AAA (n = 31) based on aortic diameter, growth rate, and eligibility for surgical intervention. Periodontal clinical parameters were recorded as well as the Periodontal Inflamed Surface Area and the Periodontal Index for Risk of Infectiousness (PIRI). Microbiological analyses were performed on saliva and supragingival and subgingival plaque. Quantification of Tannerella forsythia (Tf), Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (Aa), Fusobacterium nucleatum (Fn), and Prevotella intermedia (Pi) was done by quantitative polymerase chain reaction. RESULTS: The two AAA groups were homogeneous for age, sex, and most risk factors except hypertension and chronic obstructive pulmonary disease. Periodontal parameters were comparable but the proportion of patients with high PIRI scores was greater in those with unstable AAA (51.6% versus 23.3%). The probing depth (PD) and the proportion of PD >6 mm were positively correlated with AAA size and thrombus volume. Several associations were found between periopathogens such as Pg and AAA diameters and volumes, but no difference could be evidenced between stable and unstable AAA groups. CONCLUSIONS: Periodontitis was highly prevalent in both stable and unstable AAA patients. Severe and progressive periodontitis (stage IV and grade C) tended to be more frequent in the group of patients with unstable AAA. Moreover, Pg was observed in all the samples (saliva, supragingival, and subgingival plaque) and was correlated with AAA diameters and volumes. The study evidenced potential relationships between periodontitis severity and size of AAA. ispartof: JOURNAL OF PERIODONTOLOGY vol:91 issue:11 pages:1453-1464 ispartof: location:United States status: published

The improvement in survival rates for heart transplant recipients (HTRs) has increased their risk of developing extracardiac diseases such as abdominal aortic aneurysms (AAAs). The purposes of this study were to evaluate the prevalence and to describe the clinical features and natural history of AAA in HTRs.A retrospective review of all patients (375) who underwent heart transplantation (HT) at our center over a 32-year period (1983-2015) was carried out.We identified 20 patients (5.3%) with AAA. All but one patient were male (95%), and most of them (80%) had a history of ischemic heart disease (IHD) prior to transplantation. The mean age of the patients with AAA at transplant was 57.2 ± 7.3 years (range: 42-62 years). Seven of the 20 patients with AAA already had an AAA (30-55 mm) prior to transplantation. The average aneurysm size at the time of diagnosis was 40.9 ± 9.6 mm, and the average patient age at the time of diagnosis was 62.2 ± 8.3 years. The mean linear expansion rate was 10.6 ± 2.12 mm/y, and the exponential expansion rate was 0.220 ± 0.040 yearThe natural history of AAA in HTR is characterized by an increased expansion rate. Male HTR with end-stage IHD are particularly at risk and should be closely followed-up after HT.

BACKGROUND Heart transplantation (HT) from donation after circulatory death (DCD) has yet to achieve wide clinical application despite the encouraging resultsreported recently. In this study we describe 2 cases of successful adult DCD HT performed at our institution using an original protocol. METHODS Our local abdominal DCD protocol was updated to allow DCD heart procurement, and was accepted by the institutional ethics committee. The main features of the protocol include: pre-mortem insertion of peripheral venoarterial extracorporeal membrane oxygenation cannulas ; thoracoabdominal normothermic regional perfusion (NRP) by clamping the 3 aortic arch vessels to exclude cerebral circulation ; and in-situ heart resuscitation. The retrieved hearts were directly transplanted into recipients located in an adjoining operating room. RESULTS The procurement warm ischemic time was 25 minutes for the first donor, and 26 minutes for the second donor. The cold ischemic time was 16 minutes for the first recipient and 17 minutes for the second recipient. The suture time was 30 minutes for the first recipient, and 53 minutes for the second recipient. Both recipients were easily weaned off cardiopulmonary bypass in sinus rhythm and inotropic support. Post-operative evaluation of cardiac function was excellent and the patients were subsequently discharged home. CONCLUSIONS Transplantation of hearts from DCD donors is now a clinical reality.NRP is a useful tool for resuscitation, reperfusion, and preservation of transplanted hearts. It also offers the opportunity to assess the function and viability of organs before transplantation. However,due to ethical issues, some may object to ante-mortem intervention.

Purpose: To assess if aortic 18F-fluorodeoxyglucose (FDG) uptake on positron emission tomography/computed tomography (PET/CT) could play a role in predicting complications after endovascular aneurysm repair (EVAR). Materials and Methods: This study involved 2 cohorts of men with abdominal aortic aneurysm treated by EVAR: those who underwent a PET/CT scan before EVAR (n=17) and those who had a PET/CT during follow-up (n=34). Uptake of FDG was measured as the standardized uptake value (SUV). D-dimer, a marker of fibrinolysis, was measured in blood drawn concomitantly with the PET/CT. Results: A significant uptake of FDG in the aneurysm wall was detected by PET/CT before EVAR in 6 of 17 patients. During the first year after EVAR, type II endoleaks developed in 5 of these FDG+ patients vs 3 of 11 FDG– patients (p=0.04). Two of the FDG+ patients had continued sac growth and required conversion to open repair. A significant association between sac growth rate, SUV, and the presence of endoleak was found in the 34 patients who underwent PET/CT after EVAR. Finally, D-dimer was significantly increased in patients with both endoleak and positive PET/CT in the post-EVAR group. Conclusion: This study suggests that the presence of FDG uptake in the aortic wall might be a useful tool to predict patients at high risk of developing post-EVAR complications.

Improved risk stratification is a key priority for type B aortic dissection (TBAD). Partial false lumen thrombus morphology is an emerging predictor of complications. However, partial thrombosis is poorly defined, and its evaluation in clinical studies has been inconsistent. Thus, we aimed to characterize the hemodynamic pressure in TBAD and determine how the pressure relates to the false lumen thrombus morphology and clinical events.The retrospective admission computed tomography angiograms of 69 patients with acute TBAD were used to construct three-dimensional computational models for simulation of cyclical blood flow and calculation of pressure. The patients were categorized by the false lumen thrombus morphology as minimal, extensive, proximal or distal thrombosis. Linear regression analysis was used to compare the luminal pressure difference between the true and false lumen for each morphology group. The effect of morphology classification on the incidence of acute complications within 14 days was studied using logistic regression adjusted for clinical parameters. A survival analysis for adverse aortic events at 1 year was also performed using Cox regression.Of the 69 patients, 44 had experienced acute complications and 45 had had an adverse aortic event at 1 year. The mean ± standard deviation age was 62.6 ± 12.6 years, and 75.4% were men. Compared with the patients with minimal thrombosis, those with proximal thrombosis had a reduced false lumen pressure by 10.1 mm Hg (95% confidence interval [CI], 4.3-15.9 mm Hg; P = .001). The patients who had not experienced an acute complication had had a reduced relative false lumen pressure (-6.35 mm Hg vs -0.62 mm Hg; P = .03). Proximal thrombosis was associated with fewer acute complications (odds ratio, 0.17; 95% CI, 0.04-0.60; P = .01) and 1-year adverse aortic events (hazard ratio, 0.36; 95% CI, 0.16-0.80; P = .01).We found that proximal false lumen thrombosis was a marker of reduced false lumen pressure. This might explain how proximal false lumen thrombosis appears to be protective of acute complications (eg, refractory hypertension or pain, aortic rupture, visceral or limb malperfusion, acute expansion) and adverse aortic events within the first year.

Background Abdominal aortic aneurysm (AAA) rupture is a serious condition that results in extremely high mortality rates. Some improvements in outcome have been reported during the last 2 decades. The objective of the present study was to determine the overall and operative (by open repair) mortality related to ruptured AAA in the contemporary era and to identify preoperative, intraoperative, and early postoperative parameters associated with poor outcomes. Methods We performed a retrospective review of all consecutive patients admitted to our single institution with a diagnosis of ruptured AAA between 2004 and 2013. A total of 103 parameters, including demographic characteristics, medical history, clinical and biological parameters, cardiovascular risk factors, emergency level, diagnostic modalities, time from symptoms to diagnosis and treatment, type of operative procedure and postoperative complications, were analyzed. The primary endpoint considered in this study was the cumulative incidence rate of mortality. The secondary endpoint was the identification, by logistic regression methods, of risk factors for overall mortality as well as for operative, and postoperative mortality. Results Within our study period, 104 patients were admitted for a ruptured AAA. The majority of patients (84.6%) were male, and the AAA was known in 34.6% of the patients. Rupture occurred for a maximal diameter lower than 55 mm in 25% of the female population, compared to 5.7% of the male population (P = 0.030). The proportions of admitted patients who died before (preoperative mortality), during (intraoperative mortality) or after (postoperative hospital mortality) surgery was 17.3%, 16.3%, and 18.3%, respectively, yielding a cumulative in-hospital mortality of 51.9%. In the multivariate analysis, age ≥ 80 (P = 0.001), myocardial ischemia on the admission ECG (P = 0.046), and management by the physician response unit (P = 0.002) were the only preoperative parameters associated with a higher risk of hospital mortality. Four risk factors were found to be associated with a higher risk of postoperative mortality in the multivariate analysis, and all patients presenting with 3 or more of these risk factors (n = 5) died. Conclusions The overall mortality of ruptured AAA in a contemporary cohort of patients who underwent open repair remains high and does not seem to have decreased during recent decades. Ruptures occur at smaller diameters in women than in men, supporting a lower threshold for intervention in women with known AAA. We developed risk scores to predict the mortality of patients with rAAA at different times of their hospital course. The validity of these scores should be assessed in prospective clinical studies.

Additional file 3: Fig. 7-suppinfo Total confirmed COVID-19 deaths and cases in Belgium. ( https://www.ecdc.europa.eu/en/covid-19-pandemic ). The blue arrow represents the date of the two transplant procedures. The confirmed counts shown here are lower than the total counts. The main reason for this is limited testing and challenges in the attribution of the cause of death (Source: European CDC-Situation update Worldwide-Last updated 29th June, 11).

Additional file 1: Fig. 5-suppinfo Evolution of the viral load and the absolute lymphocyte count in recipient 1

Item does not contain fulltext Progressive dilatation of the thoracic aorta leads to thoracic aortic aneurysm (TAA), which is often asymptomatic but predisposes to lethal aortic dissections and ruptures. TAA is a common complication in patients with bicuspid aortic valve (BAV). Recently, rare loss-of-function SMAD6 variants were shown to contribute significantly to the genetic aetiology of BAV/TAA. Intriguingly, patients with craniosynostosis have also been reported to be explained molecularly by similar loss-of-function SMAD6 variants. While significantly reduced penetrance of craniosynostosis has been reported for the SMAD6 variants as such, near-complete penetrance is reached upon co-occurrence with a common BMP2 SNP risk allele. Here, we report on the results of a SMAD6-variant analysis in 473 unrelated non-syndromic TAA patients, of which the SMAD6-positive individuals were also studied for the presence of the BMP2 risk allele. Although only 14% of the TAA patients also presented BAV, all novel likely pathogenic SMAD6 variants (N = 7) were identified in BAV/TAA individuals, further establishing the role of SMAD6 variants to the aetiology of BAV/TAA and revealing limited contribution to TAA development in patients with a tricuspid aortic valve. Familial segregation studies confirmed reduced penetrance (82%) and variable clinical expressivity, with coarctation of the aorta being a common comorbidity. None of our six BMP2+/SMAD6+ patients presented with craniosynostosis. Hence, the proposed digenic model for craniosynostosis was not supported in the presented BAV/TAA cohort, suggesting that additional factors are at play. Finally, our data provide improved insights into the clinical spectrum of SMAD6-related BAV/TAA and has important implications for molecular diagnostics.

There is some evidence that periodontitis increases the risk of atherothrombosis. Abdominal aortic aneurysm (AAA) is a cardiovascular disease with specific risk factors and physiopathological mechanisms that can lead to rupture in the absence of treatment. The aim of the present systematic review was to explore the influence of periodontitis on the progression of AAAs as a specific disease. A systematic search in PubMed/MEDLINE and Embase databases was performed. Human and animal studies exploring the influence of periodontal pathogens on the progression of AAA were considered for inclusion. After systematic screening, 5 articles were included in the review. Due to the heterogeneity of the selected studies, a meta-analysis could not be performed. The descriptive analyses of the studies emphasized that periodontal pathogens or their by-products contribute to systemic and local innate immunity likely to be associated with AAA physiopathology. Periodontitis seems to play a role in the development and progression of AAA. The present systematic review suggests that the presence of periodontal bacteria in the bloodstream or in situ in the vascular lesion is a risk associated with aneurysmal disease progression. ispartof: ANGIOLOGY vol:70 issue:6 pages:479-491 ispartof: location:United States status: published

Background Abdominal aortic aneurysm (AAA) is a degenerative disease that causes mortality in people aged > 65 years. Increased reactive oxygen species (ROS) and oxidative stress seem to play a pivotal role in AAA pathogenesis. Several sources of ROS have been identified in aortic tissues using experimental models: inflammation, increased activity of NAD(P)H or NOX, over-expression of inducible nitric oxide synthase (iNOS), uncoupled endothelial nitric oxide synthase (eNOS), platelets activation and iron release from hemoglobin. Objectives Human studies confirmed that oxidative stress and endothelial dysfunction, an important source of ROS production, were well associated with AAA development. Reducing oxidative stress by antioxidants can therefore be a good strategy for limiting AAA development. The objective of the present study is to review literature data favoring or not such a hypothesis. There is currently no evidence showing that strategies using classical low molecular weight antioxidants (vitamins C and E, β- carotene) as target for ROS is effective to reduce human AAA progression. However, recent epidemiological data have highlighted the positive role of a diet enriched in fruits which contain high amounts of antioxidant polyphenols. By their ability to restore endothelial function and also their capacity to stimulate enzymatic antioxidants through activation of the Keap1/Nrf2/ARE pathway, polyphenols can represent a promising treatment target for reducing human AAA progression. Conclusion Clinical studies are therefore urgently necessary to confirm the potential beneficial effect of polyphenols in preventing or limiting AAA.

Environmental and genetic risk factors contribute to the etiology of abdominal aortic aneurysms (AAAs). Matrix metalloproteinases (MMPs) have been associated with the pathophysiology of AAAs. A prospective, nonrandomized case–control study was undertaken to investigate the risk factors for large AAAs (≥5.5 cm) among 175 male Greek AAA patients and to compare the results with a cohort of 166 male controls free from any aortic dilatation, as confirmed by ultrasonography from an existing AAA screening program in the same region. We also assessed the potential association between 2 functional single nucleotide polymorphisms in the genes MMP9 (−1561C/T; rs3918242) and MMP13 (−77A/G; rs2252070), and the presence of large AAAs. Multiple logistic regression analysis revealed AAA family history ( P = .028), hypercholesterolemia ( P < .001), and current smoking ( P < .001) as AAA risk factors. Statistical difference was reached in genotype ( P = .047) and allele ( P = .037) frequencies for rs2252070, but the results did not remain significant after correction for multiple testing. No significant differences in genotype or allele frequencies for rs3918242 were detected. In summary, AAA family history, hypercholesterolemia, and current smoking were found to be risk factors for large AAAs.

Heterozygous mutations in the SMAD3 gene were recently described as the cause of a form of non-syndromic familial aortic thoracic aneurysm and dissection (FTAAD) transmitted as an autosomal dominant disorder and often associated with early-onset osteoarthritis. This new clinical entity, called aneurysms-osteoarthritis syndrome (AOS) or Loeys-Dietz syndrome 3 (LDS3), is characterized by aggressive arterial damages such as aneurysms, dissections and tortuosity throughout the arterial tree. We report, here, the case of a 45 year-old man presenting multiple visceral arteries and abdominal aortic aneurysms but without dissection of the thoracic aorta and without any sign of osteoarthritis. Exome-sequencing revealed a new frameshift heterozygous c.455delC (p.Pro152Hisfs*34) mutation in the SMAD3 gene. This deletion is located in the exon 3 coding for the linker region of the protein and causes a premature stop codon at positions 556–558 in the exon 4. The same mutation was found in the proband's mother and sister who had open surgery for abdominal aortic aneurysm and in one of his children who was 5 year-old and did not present aneurysm yet.

Background: Some studies focusing on the endovascular repair of abdominal aortic aneurysms (AAA) have demonstrated that cancer is often found in such patients. Retrospective investigations have also indicated that AAA patients have an increased risk of cancer. However, the incidence rate of cancer and survival rate in patients with AAA compared to the population remains unknown. Methods: We conducted a prospective, single center, non-randomized, comparative cohort study including 223 AAA patients and 1000 Coronary artery disease (CAD) patients enrolled in our department between 01/01/2008 and 31/12/2011 with annual follow-up until 31/12/2018. Based on statistics from the Belgian cancer registry Belgium, the incidence rate of cancer was calculated for both men and women in the general population. The primary endpoint was the cumulative incidence rate of cancer in all three groups and the secondary endpoint was overall survival. Results: After nine years of follow-up, the cancer incidence was 30·1% (95%CI: 21·6-39·3%) in AAA patients and 23·5% (95%CI: 20·0-27·1%) in CAD subjects, markedly higher than the Walloon population (17·4%). Moreover, the development of metastases among patients with AAA was higher compared to CAD patients (38·7% vs.18·6%, P=0·03). In terms of overall survival, the proportion of cancer deaths in AAA patients was twice as high as in CAD patients. Conclusions: This study confirms an increased incidence of cancers and decreased survival in AAA patients compared to the general population. Funding Statement: This work was supported by the European Program FP7 “Fighting aneurysmal diseases” (no. 200647). Audrey Courtois and Jacobine Munten were funded by the Aneurysmal Pathology Foundation. Declaration of Interests: The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article. Ethics Approval Statement: The study was designed and conducted within the framework of the European program “Fighting Aneurysmal Disease (FAD; B70720095774 and B70720095773 9)” approved by the ethics committee (n°200647). All the participants were instructed on the study objectives and provided informed consent. The study was approved by the ethics board of the University hospital of Liege.

Thoracic aortic aneurysm (TAA) can lead to fatal complications such as aortic dissection. Since aneurysm dimension poorly predicts dissection risk, microRNAs (miRNAs) may be useful to diagnose or risk stratify TAA patients. We aim to identify miRNAs associated with TAA pathogenesis and that are possibly able to improve TAA diagnosis. MiRNA microarray experiments of aortic media tissue samples from 19 TAA patients and 19 controls allowed identifying 232 differentially expressed miRNAs. Using interaction networks between these miRNAs and 690 genes associated with TAA, we identified miR-574-5p as a potential contributor of TAA pathogenesis. Interestingly, miR-574-5p was significantly down-regulated in the TAA tissue compared to the controls, but was up-regulated in serum samples from a separate group of 28 TAA patients compared to 20 controls (p &lt, 0.001). MiR-574-5p serum levels discriminated TAA patients from controls with an area under the receiver operating characteristic curve of 0.87. In the Fbn1C1041G/+ mouse model, miR-574-5p was down-regulated in aortic tissue compared to wild-type (p &lt, 0.05), and up-regulated in plasma extracellular vesicles from Fbn1C1041G/+ mice compared to wild-type mice (p &lt, 0.05). Furthermore, in vascular smooth muscle cells, angiotensin II appears to induce miR-574-5p secretion in extracellular vesicles. In conclusion, miR-574-5p is associated with TAA pathogenesis and may help in diagnosing this disease.

BACKGROUND: There is evident benefit in terms of reduced aneurysm-related mortality from screening programs of abdominal aortic aneurysm (AAA) in men aged 65 years and more. Recent studies in the United Kingdom and Sweden have shown a decline of the prevalence of AAA in the general population. Current screening policies (e.g., men aged 65-74 years), however, do not account for aging and increased life expectancy of Western populations. This study investigated AAA detection by extending the target population to older age groups (75-85 years).METHODS: AAA screening was conducted in the County of Chaudfontaine (Liège, Belgium) on the population of elderly (n = 3,054). The participation rate was 36%. The 1,101 participants (722 men aged 65-85 years and 379 women aged 74-85 years) were examined by ultrasound scan. AAA was defined as an infrarenal aortic outer-outer diameter of at least 3 cm. Demographics, clinical parameters, and risk factors were also recorded. AAA prevalence was estimated, and patients with and without AAA were compared by logistic regression.RESULTS: The overall AAA prevalence was 3.6% (n = 40). In female participants, AAA prevalence was low (1.3%). In men, it amounted 2.7% in the 65-74 age group but rose to 7.3% in the age-extended group (75-85 years). Further in addition to age, height, current smoking, history of coronary artery disease, hypercholesterolemia, peripheral artery disease of the lower limbs, and varicose veins were significantly associated with the presence of AAA.CONCLUSIONS: These preliminary findings, based on a representative sample of the elderly population of the Liège region, support the idea that current AAA screening policies should be updated to cover an increasingly aging population. The presence of varicose veins as a potential risk factor for AAA should also be considered during screening.

Abdominal aortic aneurysm (AAA) rupture is a significant cause of mortality in developed countries. The growth rate and the rupture of AAA may be unpredictable. This chapter places a special emphasis on evaluating patient-specific approaches to the risk of rupture of AAA, using imaging. Specifically, we describe two pathways of assessing this risk: one being the use of morphologic imaging data to compute wall stress (and wall stress-related parameters) via finite element simulation (FES) and the other, the use of 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) to assess biological processes in the aortic wall components. Both methods are described, along with the limits preventing their widespread use. Nevertheless, the current diameter-based clinical scenarios could be yet impacted by the reported value of FES and FDG PET to predict the risk of AAA rupture. Lastly, the relationship between wall stress and the biological activities as described by FDG PET points at least partially to genetic or acquired alterations of the arterial wall response to wall stress, which can be found in familial aneurysms or in smokers, for example. An integrated patient-specific risk assessment strategy that would include imaging parameters along with personal and heritable risk factors is becoming increasingly suitable.

An abdominal aortic aneurysm (AAA) is a localized dilatation of the infrarenal aorta. AAA is a multifactorial disease, and genetic and environmental factors play a part; smoking, male sex and a positive family history are the most important risk factors, and AAA is most common in men65 years of age. AAA results from changes in the aortic wall structure, including thinning of the media and adventitia due to the loss of vascular smooth muscle cells and degradation of the extracellular matrix. If the mechanical stress of the blood pressure acting on the wall exceeds the wall strength, the AAA ruptures, causing life-threatening intra-abdominal haemorrhage - the mortality for patients with ruptured AAA is 65-85%. Although AAAs of any size can rupture, the risk of rupture increases with diameter. Intact AAAs are typically asymptomatic, and in settings where screening programmes with ultrasonography are not implemented, most cases are diagnosed incidentally. Modern functional imaging techniques (PET, CT and MRI) may help to assess rupture risk. Elective repair of AAA with open surgery or endovascular aortic repair (EVAR) should be considered to prevent AAA rupture, although the morbidity and mortality associated with both techniques remain non-negligible.

An abdominal aortic aneurysm (AAA) is a localized dilatation of the infrarenal aorta. AAA is a multifactorial disease, and genetic and environmental factors play a part; smoking, male sex and a positive family history are the most important risk factors, and AAA is most common in men >65 years of age. AAA results from changes in the aortic wall structure, including thinning of the media and adventitia due to the loss of vascular smooth muscle cells and degradation of the extracellular matrix. If the mechanical stress of the blood pressure acting on the wall exceeds the wall strength, the AAA ruptures, causing life-threatening intra-abdominal haemorrhage — the mortality for patients with ruptured AAA is 65–85%. Although AAAs of any size can rupture, the risk of rupture increases with diameter. Intact AAAs are typically asymptomatic, and in settings where screening programmes with ultrasonography are not implemented, most cases are diagnosed incidentally. Modern functional imaging techniques (PET, CT and MRI) may help to assess rupture risk. Elective repair of AAA with open surgery or endovascular aortic repair (EVAR) should be considered to prevent AAA rupture, although the morbidity and mortality associated with both techniques remain non-negligible. An abdominal aortic aneurysm (AAA) is an enlargement of the abdominal aorta. As the AAA grows, the aortic wall becomes progressively thin, and the risk of rupture increases; AAA rupture causes severe intra-abdominal haemorrhage and has a very high mortality.

Aortic dissection is where the medial layer of the arterial wall is separated by a tear leading to intramural bleeding. The blood forms an alternate channel of flow known as the false lumen. Thrombosis of the false lumen (FL) is common in cases of dissection as flow conditions are typically more stagnant than in the true lumen (TL). Central to the process of thrombosis is the activation and aggregation of platelets in the blood. Therefore, the aim of this work is to simulate the transport of platelets in a case of Type-B aortic dissection in a clinically-relevant timeframe.

Aortitis is a generic term defined as an inflammatory condition involving the aortic wall, of infectious or noninfectious origin. This inflammatory process may deteriorate the aortic wall, resulting in potentially life-threatening vascular complications. Therefore, it is important to establish a diagnosis as early as possible.During a 4-year period, 428 consecutive patients referred to our department for aortic diseases underwent FDG PET/CT examinations. Among these, 18 patients (4.2%) were suspected to have aortitis. All of them had an initial positive FDG PET/CT uptake occurring in the aorta and major branches as evaluated by visual analysis of images and assessed with the final diagnosis of aortitis. During follow-up, after surgery and/or upon immunosuppressive treatment, each of these patients underwent a second PET/CT that was compared with the initial evaluation. In all cases, normalization of FDG uptake was correlated with clinical improvement.Our study aimed to illustrate the potential clinical value of functional monitoring with PET/CT in the management of aortitis. FDG PET/CT constitutes a valuable imaging modality to establish an early diagnosis, monitor disease progression and treatment, and evaluate vascular complication and relapse. We highlight the importance of an early detection of inflammatory large-vessel pathology, which may represent a major threat.

Supplemental Material, Appendix_I_II_III_IV for Can Periodontitis Influence the Progression of Abdominal Aortic Aneurysm? A Systematic Review by Leila Salhi, Eric Rompen, Natzi Sakalihasan, Isabelle Laleman, Wim Teughels, Jean-Baptiste Michel, and France Lambert in Angiology

Aims Despite adequate medical management, dissection of the descending aorta (type B) may develop complications, including aneurysmal progression and eventually rupture. Partial false lumen thrombosis has been identified as a marker of adverse evolution in chronic dissection. The aim of this study was to test the ability of complementary information, provided by 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography/computed tomography (PET/CT) and peripheral biomarkers, to add pathophysiological significance and a prognostic value to morphological data. Methods and results We explored serial aortic 18F-FDG uptake by PET/CT imaging and plasma biomarkers in a series of 23 patients with type B dissection to predict complications from initial data and to investigate potential associations with aneurysmal expansion during follow-up. Complications occurred in 17 patients. Acute initial characteristics associated with complications were male gender ( P = 0.021), arterial hypertension ( P = 0.040), aortic dissection diameter ( P = 0.0086), partial thrombosis of the false channel ( P = 0.0046), and enhanced focal 18F-FDG uptake ( P = 0.045). During follow-up (mean 16.7 ± 8.0 months), aneurysmal expansion was associated with false lumen morphology ( P

Background Abdominal aortic aneurysm (AAA) is one of the leading causes of death in western countries. Surgery is still, at the present time, the sole treatment that has however a significant mortality and cost rate. Many pharmacological agents are under investigation aiming to reduce growth and prevent AAA rupture. These drugs target different pathological pathways and, notably, the excessive production of prostanoids by cyclooxygenases (COX). Intra-aneurysmal thrombus plays an adverse key role in the progression of AAA, platelets being a primary source of prostanoids as thromboxane A2. Objective In this review, we summarize studies targeting prostanoids production and down-stream pathways in cardiovascular diseases, and more specifically in AAA. Results and conclusion Various inhibitors of COX or antagonists of prostanoids receptors have been investigated in AAA animal models with conflicting results. In human AAA, only a few number of studies focused on anti-platelet therapy mostly using acetylsalicylic acid (aspirin, ASA), a COX1 inhibitor. Finally, we report preliminary promising results of a model of AAA in rats receiving a thromboxane A2 inhibitor, BM-573 that induced a reduction of aneurysmal growth.

Rupture of abdominal aortic aneurysm (AAA) is associated with high mortality rates. Risk of rupture is multi-factorial involving AAA geometric configuration, vessel tortuosity, and the presence of intraluminal pathology. Fluid structure interaction (FSI) simulations were conducted in patient based computed tomography scans reconstructed geometries in order to monitor aneurysmal disease progression from normal aortas to non-ruptured and contained ruptured AAA (rAAA), and the AAA risk of rupture was assessed. Three groups of 8 subjects each were studied: 8 normal and 16 pathological (8 non-ruptured and 8 rAAA). The AAA anatomical structures segmented included the blood lumen, intraluminal thrombus (ILT), vessel wall, and embedded calcifications. The vessel wall was described with anisotropic material model that was matched to experimental measurements of AAA tissue specimens. A statistical model for estimating the local wall strength distribution was employed to generate a map of a rupture potential index (RPI), representing the ratio between the local stress and local strength distribution. The FSI simulations followed a clear trend of increasing wall stresses from normal to pathological cases. The maximal stresses were observed in the areas where the ILT was not present, indicating a potential protective effect of the ILT. Statistically significant differences were observed between the peak systolic stress and the peak stress at the mean arterial pressure between the three groups. For the ruptured aneurysms, where the geometry of intact aneurysm was reconstructed, results of the FSI simulations clearly depicted maximum wall stress at the a priori known location of rupture. The RPI mapping indicated several distinct regions of high RPI coinciding with the actual location of rupture. The FSI methodology demonstrates that the aneurysmal disease can be described by numerical simulations, as indicated by a clear trend of increasing aortic wall stresses in the studied groups, (normal aortas, AAAs and rAAAs). Ultimately, the results demonstrate that FSI wall stress mapping and RPI can be used as a tool for predicting the potential rupture of an AAA by predicting the actual rupture location, complementing current clinical practice by offering a predictive diagnostic tool for deciding whether to intervene surgically or spare the patient from an unnecessary risky operation.

Abdominal aortic aneurysm (AAA) is a complex multifactorial disease with genetic and environmental components. AAA is more common in men, whereas women have a greater risk of rupture and more frequently have concomitant thoracic aortic aneurysms. Moreover, women are diagnosed with AAA about 10 years later and seem to be protected by female sex hormones. In this MEDLINE-based review of literature, we examined human and animal in vivo and in vitro studies to further deepen our understanding of the sexual dimorphism of AAA. We focus on the role of sex hormones during the formation and growth of AAA. Endogenous estrogens and exogenous 17β-estradiol were found to exert favorable actions protecting from AAA in animal models, whereas exogenous hormone replacement therapy in humans had inconclusive results. Androgens, known to have detrimental effects in the vasculature, in sufficient levels maintain the integrity of the aortic wall through their anabolic actions and act differentially in men and women, whereas lower levels of testosterone have been associated with AAA in humans. In conclusion, sex differences remain an important area of AAA research, but further studies especially in humans are needed. Furthermore, differential molecular mechanisms of sex hormones constitute a potential therapeutic target for AAA.

ObjectivesCurrently, the prevalence of abdominal aortic aneurysm (AAA) in patients with coronary artery disease (CAD) and the correlation between CAD severity and AAA prevalence are not clearly known. We conducted a prospective study to determine the prevalence of AAA in patients undergoing coronary angiography and to determine the risk factors and a coronary profile associated with AAA.MethodsOver an 18-month period, abdominal aortic ultrasound was performed on 1,000 patients undergoing coronary angiography for suspected or known CAD, or prior to valve surgery. Clinical characteristics and coronary profile were collected from the patients.ResultsThe overall number of previously repaired, already diagnosed, and new cases of AAA in the study population was 42, yielding a prevalence of 4.2%. Among the patients with newly detected AAAs, only two had an AAA diameter of >54 mm and were therefore treated surgically. In men aged ≥65 years, the prevalence reached 8.6%, while in men with three-vessel CAD it was 14.4%. Multivariate analysis showed that age ≥65 years (p = .003), male gender (p = .003), family history of AAA (p = .01), current smoking (p = .002), and three-vessel CAD (p

Background— The relationship between biomechanical properties and biological activities in aortic aneurysms was investigated with finite element simulations and 18 F-fluoro-deoxy-glucose ( 18 F-FDG) positron emission tomography. Methods and Results— The study included 53 patients (45 men) with aortic aneurysms, 47 infrarenal (abdominal aortic) and 6 thoracic (thoracic aortic), who had ≥1 18 F-FDG positron emission tomography/computed tomography. During a 30-month period, more clinical events occurred in patients with increased 18 F-FDG uptake on their last examination than in those without (5 of 18 [28%] versus 2 of 35 [6%]; P =0.03). Wall stress and stress/strength index computed by finite element simulations and 18 F-FDG uptake were evaluated in a total of 68 examinations. Twenty-five (38%) examinations demonstrated ≥1 aneurysm wall area of increased 18 F-FDG uptake. The mean number of these areas per examination was 1.6 (18 of 11) in thoracic aortic aneurysms versus 0.25 (14 of 57) in abdominal aortic aneurysms, whereas the mean number of increased uptake areas colocalizing with highest wall stress and stress/strength index areas was 0.55 (6 of 11) and 0.02 (1 of 57), respectively. Quantitatively, 18 F-FDG positron emission tomographic uptake correlated positively with both wall stress and stress/strength index ( P 18 F-FDG uptake was particularly high in subjects with personal history of angina pectoris and familial aneurysm. Conclusions— Increased 18 F-FDG positron emission tomographic uptake in aortic aneurysms is strongly related to aneurysm location, wall stress as derived by finite element simulations, and patient risk factors such as acquired and inherited susceptibilities.

Rupture of abdominal aortic aneurysms (AAAs) leads to a significant morbidity and mortality in aging populations, and its prediction would be most beneficial to public health. Spots positive for uptake of 18F-FDG detected by PET are found in 12% of AAA patients (PET+), who are most often symptomatic and at high rupture risk. Comparing the 18F-FDG–positive site with a negative site from the same aneurysm and with samples collected from AAA patients with no 18F-FDG uptake should allow the discrimination of biologic alterations that would help in identifying markers predictive of rupture. Methods: Biopsies of the AAA wall were obtained from patients with no 18F-FDG uptake (PET0, n = 10) and from PET+ patients (n = 8), both at the site positive for uptake and at a distant negative site of the aneurysmal wall. Samples were analyzed by immunohistochemistry, quantitative real-time polymerase chain reaction, and zymography. Results: The sites of the aneurysmal wall with a positive 18F-FDG uptake were characterized by a strikingly increased number of adventitial inflammatory cells, highly proliferative, and by a drastic reduction of smooth muscle cells (SMCs) in the media as compared with their negative counterpart and with the PET0 wall. The expression of a series of genes involved in the maintenance and remodeling of the wall was significantly modified in the negative sites of PET+, compared with the PET0 wall, suggesting a systemic alteration of the aneurysmal wall. Furthermore, a striking increase of several matrix metalloproteinases (MMPs), notably the MMP1 and MMP13 collagenases, was observed in the positive sites, mainly in the adventitia. Moreover, PET+ patients were characterized by a higher circulating C-reactive protein. Conclusion: Positive 18F-FDG uptake in the aneurysmal wall is associated with an active inflammatory process characterized by a dense infiltrate of proliferating leukocytes in the adventitia and an increased circulating C-reactive protein. Moreover, a loss of SMC in the media and alterations of the expression of genes involved in the remodeling of adventitia and collagen degradation potentially participate in the weakening of the aneurysmal wall preceding rupture.

Background: To evaluate the feasibility and the safety of performing urgent (within 24 hours) carotid endarterectomy in patients with carotid stenosis presenting with repetitive transient ischemic attacks or progressing stroke. Methods: Thirty consecutive patients underwent urgent carotid endarterectomy for repetitive transient ischemic attacks (N = 12) or progressing stroke (N = 18) according to the following criteria: two or more transient ischemic attacks or a fluctuating neurological deficit over a period of less than 24 hours (progressing stroke), no impairment of consciousness, no cerebral infarct larger than 1.5 cm in diameter on computed tomography and a carotid artery stenosis of 70% or more on the appropriate side, diagnosed by echodoppler ultrasonography and/or arteriography. Patients with cerebral hemorrhage were excluded. All patients were examined pre- and postoperatively by the same neurologist and surgery was performed by the same vascular surgeon. All the patients underwent a cerebral CT scan within 5 days after surgery. Results: There were 19 men and 11 women. The mean age was 71 ± 7.6 years. The time delay of surgery after the onset of transient ischemic attacks or progressing stroke averaged 19.4 ± 11.5 hours. For patients suffering progressive stroke, one developed a fatal ischemic stroke 24 hours after surgery, five showed no improvement of their neurological status after surgery, but none worsened. Twelve patients experienced significant improvement of their neurological status with an European Stroke Scale of 77.9 ± 25.2 at admission and 95.8 ± 4.6 at discharge, and all but one of those patients had a Barthel's index value over 85/100 at discharge. The 12 patients with repetitive transient ischemic attacks had an uneventful postoperative outcome. The mean duration of follow-up was 3.4 ± 1.2 years. No patient developed another transient ischemic attack or ischemic stroke during the follow-up period. Conclusions: The results of our series documented the feasibility and the safety of performing urgent (within 24 hours) carotid endarterectomy in patients presenting with repetitive transient ischemic attacks or progressing stroke. This procedure seems to us to be justified by the fact that waiting for surgery may lead to the development of a more profound deficit or another stroke in these neurologically unstable patients whose only chance for neurological recovery is in the early phase.

The current state of research and treatment on aortic diseases was discussed in the "3rd International Meeting on Aortic Diseases" (IMAD3) held on October 4-6, 2012, in Liege, Belgium. The 3-day meeting covered a wide range of topics related to thoracic aortic aneurysms and dissections, abdominal aortic aneurysms, and valvular diseases. It brought together clinicians and basic scientists and provided an excellent opportunity to discuss future collaborative research projects for genetic, genomics, and biomarker studies, as well as clinical trials. Although great progress has been made in the past few years, there are still a large number of unsolved questions about aortic diseases. Obtaining answers to the key questions will require innovative, interdisciplinary approaches that integrate information from epidemiological, genetic, molecular biology, and bioengineering studies on humans and animal models. It is more evident than ever that multicenter collaborations are needed to accomplish these goals.

Objective Thoracic endovascular aortic repair (TEVAR) has demonstrated encouraging results and is gaining increasing acceptance as a treatment option for aortic aneurysms and dissections. Yet, its role in managing proximal aortic pathologies is unknown—this is important because in proximal (Stanford type A) aortic dissections, 10% to 30% are not accepted for surgery and 30% to 50% are technically amenable for TEVAR. We describe our case series of type A aortic dissections treated by using TEVAR. Methods Between year 2009 and 2016, 12 patients with acute, subacute, or chronic type A aortic dissection with the proximal entry tear located between the coronaries and brachiocephalic artery were treated with TEVAR at 3 centers. Various stent-graft configurations were used to seal the proximal entry tear in the ascending aorta under rapid pacing. Results A total of 12 patients (9 male, 3 female), mean age 81 ± 7 years, EuroSCORE II 9.1 ± 4.5, underwent TEVAR for the treatment of type A aortic dissection. Procedural success was achieved in 11 of 12 patients (91.7%). There was 1 minor stroke and 1 intraprocedural death. No additional deaths were reported at 30 days. At 36 months, there were 4 further deaths (all from nonaortic causes). The mean survival of these 4 deceased was 23 months (range 15-36 months). Follow-up computed tomography demonstrated favorable aortic remodeling. Conclusions TEVAR is feasible and reveals promising early results in selected patients with type A aortic dissection who are poor candidates for surgical repair. The current iteration of stent-graft technology, however, needs to be adapted to features specific to the ascending aorta.

Nature Reviews Disease Primers 2, 16053 (2016) In the version of the article originally published, Michael P. Jenkins was incorrectly stated as Michael T. Jenkins. The article has now been corrected.