Forecasting aortic aneurysm rupture: A systematic review of seasonal and atmospheric associations.

BACKGROUND: Abdominal aortic aneurysms (AAAs) represent a significant burden of disease worldwide, and their rupture, without treatment, has an invariably high mortality rate. Whereas some risk factors for ruptured AAAs (rAAAs) are well established, such as hypertension, smoking, and female sex, the impact of seasonal and meteorologic variables is less clear. We systematically reviewed the literature to determine whether these variables are associated with rAAA. METHODS: Review methods were according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We calculated pooled proportions and incidence rate ratios (IRRs) for the different months and seasons. Funnel plots were constructed to assess for publication bias. Given the poor methodologic quality of included studies, a sensitivity analysis was performed on better-quality studies, which scored 6 and above of 9 in the author-modified Newcastle-Ottawa Scale. RESULTS: The pooled proportion of rAAA was highest in the autumn season (incidence rate, 26.6%; 95% confidence interval [CI], 25.6%-27.7%; I2 = 15.4%), followed by winter (incidence rate, 26.2%; 95% CI, 24.1%-28.2%; I2 = 72.4%), and lowest in summer (incidence rate, 21.1%; 95% CI, 19.3%-23.0%; I2 = 70.4%). The IRRs of rAAA were -6.9% (95% CI, -9.8% to -3.9%), -19.5% (95% CI, -22% to -16.8%), +10.5% (95% CI, 7.2%-13.9%), and +18.1% (95% CI, 15%-22%) in spring, summer, autumn, and winter compared with the remaining seasons, respectively (all P < .0001), thus affirming existence of seasonal variation. The pooled proportion of rAAA was highest in December (incidence rate, 8.9%; 95% CI, 7.1%-10.9%; I2 = 54.5%) but lowest in July (incidence rate, 5.7%; 95% CI, 4.2%-7.3%; I2 = 54.5%). The IRR was significantly the highest in January (IRR, 1.14; 95% CI, 1.01-1.29; P = .031) but lowest in July (IRR, 0.75; 95% CI, 0.65-0.87; P < .0001). There is also some evidence for a possible association with atmospheric pressure. Associations with temperature and daylight hours, however, are at best speculative. CONCLUSIONS: Autumn and winter are significantly associated with a higher incidence of rAAAs, and autumn is associated with the highest rupture incidence of all the seasons. However, the inability to appropriately control for other confounding factors known to increase the risk of AAA rupture precludes any additional recommendations to alter current provision of vascular services on the basis of these data.

Forty hours with a traumatic carotid transection: A diagnostic caveat and review of the contemporary management of penetrating neck trauma.

Although penetrating neck trauma (PNT) is uncommon, it is associated with the significant morbidity and mortality. The management of PNT has changed significantly over the past 50 years. A radiological assessment now is a vital part of the management with a traditional surgical exploration. A 22 years old male was assaulted by a screwdriver and sustained multiple penetrating neck injuries. A contrast CT scan revealed a focal pseudoaneurysm in the left common carotid artery bulb. There was no active bleeding or any other vascular injuries and the patient remained haemodynamically stable. In view of these findings, he was initially managed conservatively without an open surgical exploration. However, the patient was noted to have an acute drop in his hemoglobin count overnight post injury and the catheter directed angiography showed active bleeding from the pseudoaneurysm. Surgical exploration 40 hours following the initial injury revealed a penetrating injury through both arterial walls of the left carotid bulb which was repaired with a great saphenous vein patch. A percutaneous drain was inserted in the carotid triangle and a course of intravenous antibiotics for five days was commenced. The patient recovered well with no complications and remained asymptomatic at five months followup.

Frailty and Geriatric Syndromes in Vascular Surgical Ward Patients.

BACKGROUND: Preoperative frailty is an important predictor of poor outcomes but the relationship between frailty and geriatric syndromes is less clear. The aims of this study were to describe the prevalence of frailty and incidence of geriatric syndromes in a cohort of older vascular surgical ward patients, and investigate the association of frailty and other key risk factors with the occurrence of one or more geriatric syndromes (delirium, functional decline, falls, and/or pressure ulcers) and two hospital outcomes (acute length of stay and discharge destination). METHODS: This prospective cohort study was conducted in a vascular surgical ward in a tertiary teaching hospital in Brisbane, Australia. Consecutive patients aged ≥65 years, admitted for ≥72 hr, were eligible for inclusion. Frailty was defined as one or more of functional dependency, cognitive impairment, or nutritional impairment at admission. Delirium was identified using the Confusion Assessment Method and a validated chart extraction tool. Functional decline from admission to discharge was identified from daily nursing documentation of activities of daily living. Falls were identified according to documentation in the medical record cross-checked with the incident reporting system. Pressure ulcers, acute length of stay, and discharge destination were identified by documentation in the medical record. Risk factors associated with geriatric syndromes, acute length of stay, and discharge destination were assessed using multivariable logistic regression models. RESULTS: Of 110 participants, 43 (39%) patients were frail and geriatric syndromes occurred in 40 (36%). Functional decline occurred in 25% of participants, followed by delirium (20%), pressure ulcers (12%), and falls (4%). In multivariable logistic analysis, frailty [odds ratio (OR) 6.7, 95% confidence interval (CI) 2.0-22.1, P = 0.002], nonelective admission (OR 7.2, 95% CI 2.2-25.3, P = 0.002), higher physiological severity (OR 5.5, 95% CI 1.1-26.8, P = 0.03), and operative severity (OR 4.6, 95% CI 1.2-17.7, P = 0.03) increased the likelihood of any geriatric syndrome. Frailty was an important predictor of longer length of stay (OR 2.6, 95% CI 1.0-6.8, P = 0.06) and discharge destination (OR 4.2, 95% CI 1.2-13.8, P = 0.02). Nonelective admission significantly increased the likelihood of discharge to a higher level of care (OR 5.3, 95% CI 1.3-21.6, P = 0.02). CONCLUSIONS: Frailty and geriatric syndromes were common in elderly vascular surgical ward patients. Frail patients and nonelective admissions were more likely to develop geriatric syndromes, have a longer length of stay, and be discharged to a higher level of care.

Capillary ultrastructure and mitochondrial volume density in skeletal muscle in relation to reduced exercise capacity of patients with intermittent claudication.

Intermittent claudication (IC) is the most commonly reported symptom of peripheral arterial disease (PAD). Impaired limb blood flow is a major casual factor of lower exercise tolerance in PAD but cannot entirely explain it. We hypothesized that IC is associated with structural changes of the capillary-mitochondria interface that could contribute to the reduction of exercise tolerance in IC patients. Capillary and mitochondrial morphometry were performed after light and transmission electron microscopy using vastus lateralis muscle biopsies of 14 IC patients and 10 age-matched controls, and peak power output (PPO) was determined for all participants using an incremental single-leg knee-extension protocol. Capillary density was lower (411 ± 90 mm(-2) vs. 506 ± 95 mm(-2); P ≤ 0.05) in the biopsies of the IC patients than in those of the controls. The basement membrane (BM) around capillaries was thicker (543 ± 82 nm vs. 423 ± 97 nm; P ≤ 0.01) and the volume density of mitochondria was lower (3.51 ± 0.56% vs. 4.60 ± 0.74%; P ≤ 0.01) in the IC patients than the controls. In the IC patients, a higher proportion of capillaries appeared with collapsed slit-like lumen and/or swollen endothelium. PPO was lower (18.5 ± 9.9 W vs. 33.5 ± 9.4 W; P ≤ 0.01) in the IC patients than the controls. We suggest that several structural alterations in skeletal muscle, either collectively or separately, contribute to the reduction of exercise tolerance in IC patients.

Vasoactive enzymes and blood flow responses to passive and active exercise in peripheral arterial disease.

BACKGROUND: Peripheral arterial disease (PAD) is characterised by impaired leg blood flow, which contributes to claudication and reduced exercise capacity. This study investigated to what extent vasoactive enzymes might contribute to altered blood flow in PAD (Fontaine stage II). METHODS: We compared femoral artery blood flow during reactive hyperaemia, leg-extension exercise and passive leg movement, and determined the level of vasoactive enzymes in skeletal muscle samples from the vastus lateralis in PAD (n = 10, 68.5 ± 6.5 years) and healthy controls (CON, n = 9, 62.1 ± 12.3 years). Leg blood flow was measured with Doppler ultrasound and muscle protein levels of phosphorylated endothelial nitric oxide synthase, NADPH oxidase, cyclooxygenase 1 and 2, thromboxane synthase, and prostacyclin synthase were determined. RESULTS: Leg blood flow during the initial 90 s of passive leg movement (242 ± 33 vs 441 ± 75 ml min(-1), P = 0.03) and during reactive hyperaemia (423 ± 100 vs 1255 ± 175 ml min(-1), P = 0.002) was lower in PAD than CON, whereas no significant difference was observed for leg blood flow during exercise (1490 ± 250 vs 1887 ± 349 ml min(-1), P = 0.37). PAD had higher NADPH oxidase than CON (1.04 ± 0.19 vs 0.50 ± 0.06 AU, P = 0.02), with no differences for other enzymes. Leg blood flow during exercise was correlated with prostacyclin synthase (P = 0.001). CONCLUSION: Elevated NADPH oxidase indicates that oxidative stress may be a primary cause of low nitric oxide availability and impaired blood flow in PAD.

Non-aneurysmal abdominal aortic rupture in a patient with Marfan syndrome.

Aortic rupture in the presence of aneurysmal disease is well understood and extensively described in the literature. However, aortic rupture in a non-aneurysmal aorta is far less common. In the few reported cases, perforations are believed to result from a penetrating atheromatous ulcer of the aorta. We describe a rare case of non-aneurysmal aortic rupture in a 68-year-old man with Marfan syndrome and a history of proximal aortic surgery. The urgent need for hemorrhage control precluded any consideration of an endovascular repair.

Long-term outcomes and factors influencing late survival following elective abdominal aortic aneurysm repair: A 24-year experience.

BACKGROUND: Abdominal aortic aneurysms can be either treated by an open abdominal aortic aneurysm repair or an endovascular repair. Comparing clinical predictors of outcomes and those which influence survival rates in the long term is important in determining the choice of treatment offered and the decision-making process with patients. AIMS: To determine the influence of pre-existing clinical predictors and perioperative determinants on late survival of elective open abdominal aortic aneurysm repair and endovascular repair at a tertiary hospital. METHODS: Consecutive patients undergoing elective abdominal aortic aneurysm repair from 1990 to 2013 were included. Data were collected from a prospectively acquired database and death data were gathered from the Queensland state death registry. Pre-existing risks and perioperative factors were assessed independently. Kaplan-Meier and Cox regression modeling were performed. RESULTS: During the study period, 1340 abdominal aortic aneurysms were repaired electively, of which 982 were open abdominal aortic aneurysm repair. The average age was 72.4 years old and 81.7% were males. The cumulative percentage survival rates for open abdominal aortic aneurysms repair at 5, 10, 15 and 20 years were 79, 49, 31 and 22, respectively. The corresponding 5-, 10- and 15-year survival rates for endovascular repair were not significantly different at 75, 49 and 33%, respectively (P = 0.75). Predictors of reduced survival were advanced age, American Society of Anaesthesiology scores, chronic obstructive pulmonary disease, renal impairment, bifurcated grafts, peripheral vascular disease and congestive heart failure. CONCLUSIONS: Open repair offers a good long-term treatment option for patients with an abdominal aortic aneurysm and in our experience there is no significant difference in late survival between open abdominal aortic aneurysms repair and endovascular repair. Consideration of the factors identified in this study that predict reduced long-term survival for open abdominal aortic aneurysms repair and endovascular repair should be considered when deciding repair of abdominal aortic aneurysm.

Neovascular Glaucoma Post Carotid Endarterectomy: A Case Report and Review of the Literature.

Carotid endarterectomy is a standard vascular surgical procedure performed worldwide and encompasses multiple risks including cerebral hyperperfusion syndrome, stroke, carotid dissection and aneurysmal formation, all of which are well documented in the literature. However, neovascular glaucoma manifesting post carotid endarterectomy, is extremely rare and can have disastrous consequences if left undiagnosed. In this article, we present one such case of neovascular glaucoma manifesting post carotid endarterectomy and review the available literature on this uncommon entity.

TElmisartan in the management of abDominal aortic aneurYsm (TEDY): The study protocol for a randomized controlled trial.

BACKGROUND: Experimental studies suggest that angiotensin II plays a central role in the pathogenesis of abdominal aortic aneurysm. This trial aims to evaluate the efficacy of the angiotensin receptor blocker telmisartan in limiting the progression of abdominal aortic aneurysm. METHODS/DESIGN: Telmisartan in the management of abdominal aortic aneurysm (TEDY) is a multicentre, parallel-design, randomised, double-blind, placebo-controlled trial with an intention-to-treat analysis. We aim to randomly assign 300 participants with small abdominal aortic aneurysm to either 40 mg of telmisartan or identical placebo and follow patients over 2 years. The primary endpoint will be abdominal aortic aneurysm growth as measured by 1) maximum infra-renal aortic volume on computed tomographic angiography, 2) maximum orthogonal diameter on computed tomographic angiography, and 3) maximum diameter on ultrasound. Secondary endpoints include change in resting brachial blood pressure, abdominal aortic aneurysm biomarker profile and health-related quality of life. TEDY is an international collaboration conducted from major vascular centres in Australia, the United States and the Netherlands. DISCUSSION: Currently, no medication has been convincingly demonstrated to limit abdominal aortic aneurysm progression. TEDY will examine the potential of a promising treatment strategy for patients with small abdominal aortic aneurysms. TRIAL REGISTRATION: Australian and Leiden study centres: Australian New Zealand Clinical Trials Registry ACTRN12611000931976 , registered on 30 August 2011; Stanford study centre: clinicaltrials.gov NCT01683084 , registered on 5 September 2012.

Differential gene expression in human abdominal aortic aneurysm and aortic occlusive disease.

Abdominal aortic aneurysm (AAA) and aortic occlusive disease (AOD) represent common causes of morbidity and mortality in elderly populations which were previously believed to have common aetiologies. The aim of this study was to assess the gene expression in human AAA and AOD. We performed microarrays using aortic specimen obtained from 20 patients with small AAAs (≤ 55mm), 29 patients with large AAAs (> 55mm), 9 AOD patients, and 10 control aortic specimens obtained from organ donors. Some differentially expressed genes were validated by quantitative-PCR (qRT-PCR)/immunohistochemistry. We identified 840 and 1,014 differentially expressed genes in small and large AAAs, respectively. Immune-related pathways including cytokine-cytokine receptor interaction and T-cell-receptor signalling were upregulated in both small and large AAAs. Examples of validated genes included CTLA4 (2.01-fold upregulated in small AAA, P = 0.002), NKTR (2.37-and 2.66-fold upregulated in small and large AAA with P = 0.041 and P = 0.015, respectively), and CD8A (2.57-fold upregulated in large AAA, P = 0.004). 1,765 differentially expressed genes were identified in AOD. Pathways upregulated in AOD included metabolic and oxidative phosphorylation categories. The UCP2 gene was downregulated in AOD (3.73-fold downregulated, validated P = 0.017). In conclusion, the AAA and AOD transcriptomes were very different suggesting that AAA and AOD have distinct pathogenic mechanisms.

Changes in temperature affect the risk of abdominal aortic aneurysm rupture.

BACKGROUND: There is a well-established link between exposure to hot and cold temperatures and an increased risk of cardiovascular hospitalization or death. There is also contrasting evidence of a seasonal increase in aortic ruptures related to atmospheric pressure, but an association with environmental temperature has never been formally modelled. METHODS: Using a prospective database, we identified 295 patients who were operated in a single centre for ruptured abdominal aortic aneurysm in south-east Queensland between 1990 and 2010. We matched patients to their nearest weather station to estimate their exposure to temperature and air pressure in the days leading up to their rupture. We used the case-crossover method to estimate the risks of temperature, which we allowed to be non-linear (increased risks at high and low temperatures) and delayed by up to 25 days. RESULTS: There was an immediate increase in risk after exposure to cold, and a delayed risk after exposure to heat. An increased risk after exposure to high pressures disappeared after adjusting for temperature. At a mean temperature of 19°C (66°F), the odds ratio for rupture was 1.73 (95% confidence interval: 1.09, 2.76) compared with the reference temperature of 24°C. CONCLUSION: This is the first study to demonstrate an association between temperature and risk of aortic aneurysm rupture in the Southern Hemisphere. The physiological changes caused by thermoregulation may be a trigger for those people with a fragile aneurysm.

Visceral adiposity is not associated with abdominal aortic aneurysm presence and growth.

Previous studies in rodent models and patients suggest that visceral adipose could play a direct role in the development and progression of abdominal aortic aneurysm (AAA). This study aimed to assess the association of visceral adiposity with AAA presence and growth. This study was a case-control investigation of patients that did (n=196) and did not (n=181) have an AAA who presented to The Townsville Hospital vascular clinic between 2003 and 2012. Cases were patients with AAA (infra-renal aortic diameter >30 mm) and controls were patients with intermittent claudication but no AAA (infra-renal aortic diameter <30 mm). All patients underwent computed tomography angiography (CTA). The visceral to total abdominal adipose volume ratio was estimated from CTAs by assessing total and visceral adipose deposits using an imaging software program. Measurements were assessed for reproducibility by repeat assessments on 15 patients. AAA risk factors were recorded at entry. Forty-five cases underwent two CTAs more than 6 months apart to assess AAA expansion. The association of visceral adiposity with AAA presence and growth was examined using logistic regression. Visceral adipose assessment by CTA was highly reproducible (mean coefficient of variation 1.0%). AAA was positively associated with older age and negatively associated with diabetes. The visceral to total abdominal adipose volume ratio was not significantly associated with AAA after adjustment for other risk factors. Patients with a visceral to total abdominal adipose volume ratio in quartile four had a 1.63-fold increased risk of AAA but with wide confidence intervals (95% CI 0.71-3.70; p=0.248). Visceral adiposity was not associated with AAA growth. In conclusion, this study suggests that visceral adiposity is not specifically associated with AAA presence or growth although larger studies are required to confirm these findings.

Geriatric syndromes in individuals admitted to vascular and urology surgical units.

OBJECTIVES: To document the incidence of geriatric syndromes (delirium, functional decline, falls, and pressure ulcers) in two surgical units and to determine the association between the occurrence of geriatric syndromes and admission type (elective vs nonelective), severity of surgery, and surgical subspecialty unit. DESIGN: Retrospective cohort study. SETTING: One vascular surgical unit and one urology surgical unit in an Australian tertiary teaching hospital. PARTICIPANTS: Individuals aged 65 and older admitted to a study unit for 3 days or more (N = 112). MEASUREMENTS: Delirium was identified using a validated chart extraction tool. Functional decline from admission to discharge was identified from nursing documentation. Falls were identified according to documentation in the medical record cross-checked with the hospital incident reporting system. Pressure ulcers were identified according to documentation in the medical record. RESULTS: Geriatric syndromes were present in 32% of participants. Delirium was identified in 21%, functional decline in 14%, falls in 8%, and pressure ulcers in 5%. Individuals admitted directly from the emergency or outpatient department and interhospital transfers (nonelective) were significantly more likely to develop any geriatric syndrome than those on an elective surgery list before admission to the hospital (41% vs 18%, P = .01). In multivariable analysis, nonelective admission (odds ratio (OR) = 3.3, 95% confidence interval (CI) = 1.6-4.7, P = .005), major surgery (OR = 3.1, 95% CI = 1.7-3.7, P = .004) and preexisting impairment in activities of daily living (OR 2.9, 95% CI 1.5-3.6, P = .007) increased the likelihood of geriatric syndromes. CONCLUSION: Geriatric syndromes are common in older adults undergoing surgery, and nonelective admission and major surgery increase the likelihood of geriatric syndromes occurring during hospitalization. Baseline dependency in ADLs is an important risk factor for the occurrence of these conditions.

Abdominal aortic aneurysm calcification and thrombus volume are not associated with outcome following endovascular abdominal aortic aneurysm repair.

OBJECTIVES: Aortic calcification and thrombus have been postulated to worsen outcome following endovascular abdominal aortic aneurysm repair (EVAR). The purpose of this study was to assess the association of abdominal aortic aneurysm (AAA) calcification and thrombus volume with outcome following EVAR using a reproducible, quantifiable computed tomography (CT) assessment protocol. METHODS: Patients with elective EVAR performed between January 2002 and 2012 at the Townsville Hospital, Mater Private Hospital (Townsville) and Royal Brisbane and Women's Hospital (RBWH) were included if preoperative CTAs were available for analysis. AAA calcification and thrombus volume were measured using a semiautomated workstation protocol. Outcomes were assessed in terms of clinical failure, endoleak (type I, type II) and reintervention. Univariate and multivariate analyses were performed. Median follow-up was 1.7 years and the interquartile range 1.0-3.8 years. RESULTS: One hundred thirty-four patients undergoing elective EVAR were included in the study. Rates of primary clinical success and freedom from reintervention were 82.8% and 88.9% at the 24-month follow-up. AAA calcification and thrombus volume were not associated with clinical failure, type I endoleak, type II endoleak or reintervention. CONCLUSIONS: AAA calcification and thrombus volume were not associated with poorer outcome after EVAR in this study. KEY POINTS: • The association of calcification and thrombus volumes with EVAR outcome is unclear • Quantifiable methods for assessing calcification and thrombus were not used previously • This study used reproducible methods for assessing AAA calcification and thrombus volumes.

A deletion in chromosome 6q is associated with human abdominal aortic aneurysm.

Current efforts to identify the genetic contribution to abdominal aortic aneurysm (AAA) have mainly focused on the assessment of germ-line variants such as single-nucleotide polymorphisms. The aim of the present study was to assess the presence of acquired chromosomal aberrations in human AAA. Microarray data of ten biopsies obtained from the site of main AAA dilatation (AAA body) and three control biopsies obtained from the macroscopically non-dilated neck of the AAA (AAA neck) were initially compared with identified chromosomal aneuploidies using the Chromosomal Aberration Region Miner (ChARM) software. A commonly deleted segment of chromosome bands 6 (q22.1-23.2) was predicted within AAA biopsies. This finding was confirmed by quantitative real-time PCR (qPCR)-based DNA copy number assessments of an independent set of six AAA body and neck biopsies which identified a fold copy number change (∆KCt) of -1±0.35, suggesting the loss of one copy of the long interspersed nucleotide element type 1 (LINE-1) mapped to chromosome 6 (q22.1-23.2). The median relative genomic content of LINE-1 DNA was also reduced in AAA body compared with AAA neck biopsies (1.540 compared with 3.159; P=0.031). A gene important for vascular homoeostasis mapped to 6q23.1, connective tissue growth factor (CTGF), was assessed and found to be significantly down-regulated within AAA bodies compared with AAA necks (0.261 compared with 0.627; P=0.031), as determined by reverse transcription qPCR using total RNA as a template. Histology demonstrated marked staining for macrophages within AAA body biopsies. We found in vitro that the median relative genomic content of LINE-1 DNA in aortic vascular smooth muscle cells (AoSMCs) exposed to pro-inflammatory medium was ~1.5 times greater than that measured in control AoSMCs exposed to non-conditioned medium (3.044 compared with 2.040; P=0.015). Our findings suggest that acquired chromosomal aberrations associated with retrotransposon propagation may predispose to sporadic AAA.

Differential gene expression in the proximal neck of human abdominal aortic aneurysm.

OBJECTIVE: Abdominal aortic aneurysm (AAA) represents a common cause of morbidity and mortality in elderly populations but the mechanisms involved in AAA formation remain incompletely understood. Previous human studies have focused on biopsies obtained from the center of the AAA however it is likely that pathological changes also occur in relatively normal appearing aorta away from the site of main dilatation. The aim of this study was to assess the gene expression profile of biopsies obtained from the neck of human AAAs. METHODS: We performed a microarray study of aortic neck specimens obtained from 14 patients with AAA and 8 control aortic specimens obtained from organ donors. Two-fold differentially expressed genes were identified with correction for multiple testing. Mechanisms represented by differentially expressed genes were identified using Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. Some of the differentially expressed genes were validated by quantitative real-time PCR (qPCR) and immunohistochemistry. RESULTS: We identified 1047 differentially expressed genes in AAA necks. The KEGG analysis revealed marked upregulation of genes related to immunity. These pathways included cytokine-cytokine receptor interaction (P = 8.67*10(-12)), chemokine signaling pathway (P = 5.76*10(-07)), and antigen processing and presentation (P = 4.00*10(-04)). Examples of differentially expressed genes validated by qPCR included the T-cells marker CD44 (2.16-fold upregulated, P = 0.008) and the B-cells marker CD19 (3.14-fold upregulated, P = 0.029). The presence of B-cells in AAA necks was confirmed by immunohistochemistry. CONCLUSIONS: The role of immunity in AAA is controversial. This study suggests that immune pathways are also upregulated within the undilated aorta proximal to an AAA.

Thrombus volume is similar in patients with ruptured and intact abdominal aortic aneurysms.

OBJECTIVE: Most abdominal aortic aneurysms (AAAs) contain intraluminal thrombus (ILT), which has been demonstrated to contain proteolytic enzymes and proinflammatory cytokines implicated in AAA progression and rupture. In animal models, anticoagulants have been shown to limit AAA progression. Whether ILT plays a role in AAA rupture is unknown. The aim of this study was to compare the volume of ILT in patients with ruptured and intact AAAs. METHODS: We matched by maximum axial diameter alone, on a 1:2 basis, 28 patients with ruptured AAAs and 56 patients with intact AAAs. Total infrarenal aortic volume and ILT volume were measured from computed tomography angiograms using a previously validated and reproducible semiautomated workstation protocol. Clinical risk factors were also recorded. The Mann-Whitney U test was used to compare ILT volumes between patients with ruptured and intact AAAs. RESULTS: Median (interquartile range [IQR]) maximum AAA diameter (84.0 [77.5-93.9] mm vs 82.6 [77.1-93.3] mm; P = .769) and median (IQR) total AAA volume (372.8 [277.4-486.1] cm(3) vs 358.4 [289.1-563.4] cm(3); P = .977) were similar in patients with ruptured and intact AAAs. Median (IQR) AAA ILT volume was similar in patients with ruptured (152.7 [84.8-252.4] cm(3)) and intact (180.1 [89.9-254.8] cm(3); P = .414) AAAs. CONCLUSIONS: This study suggests that ILT volume is not different in ruptured and intact AAAs.