Baseline Abdominal Aortic Aneurysm Research Articles

MR Elastography of Abdominal Aortic Aneurysms: Relationship to Aneurysm Events.

Background Abdominal aortic aneurysm (AAA) diameter remains the standard clinical parameter to predict growth and rupture. Studies suggest that using solely AAA diameter for risk stratification is insufficient. Purpose To evaluate the use of aortic MR elastography (MRE)-derived AAA stiffness and stiffness ratio at baseline to identify the potential for future aneurysm rupture or need for surgical repair. Materials and Methods Between August 2013 and March 2019, 72 participants with AAA and 56 healthy participants were enrolled in this prospective study. MRE examinations were performed to estimate AAA stiffness and the stiffness ratio between AAA and its adjacent remote normal aorta. Two Cox proportional hazards models were used to assess AAA stiffness and stiffness ratio for predicting aneurysmal events (subsequent repair, rupture, or diameter >5.0 cm). Log-rank tests were performed to determine a critical stiffness ratio suggesting high-risk AAAs. Baseline AAA stiffness and stiffness ratio were studied using Wilcoxon rank-sum tests between participants with and without aneurysmal events. Spearman correlation was used to investigate the relationship between stiffness and other potential imaging markers. Results Seventy-two participants with AAA (mean age, 71 years ± 9 [SD]; 56 men and 16 women) and 56 healthy participants (mean age, 42 years ± 16; 27 men and 29 women) were evaluated. In healthy participants, aortic stiffness positively correlated with age (ρ = 0.44; P < .001). AAA stiffness (event group [n = 21], 50.3 kPa ± 26.5 [SD]; no-event group [n = 21], 86.9 kPa ± 52.6; P = .01) and the stiffness ratio (event group, 0.7 ± 0.4; no-event group, 2.0 ± 1.4; P < .001) were lower in the event group than the no-event group at a mean follow-up of 449 days. AAA stiffness did not correlate with diameter in the event group (ρ = -0.06; P = .68) or the no-event group (ρ = -0.13; P = .32). AAA stiffness was inversely correlated with intraluminal thrombus area (ρ = -0.50; P = .01). Conclusion Lower abdominal aortic aneurysm stiffness and stiffness ratio measured with use of MR elastography was associated with aneurysmal events at a 15-month follow-up. © RSNA, 2022 See also the editorial by Sakuma in this issue.

One Year Full Volume Follow Up of Abdominal Aortic Aneurysms with Transducer Navigation System Assisted Three Dimensional Ultrasound

Introduction: Surveillance of abdominal aortic aneurysms (AAAs) is based on the assessment of maximum diameter growth to infer risk of rupture. Diameter growth is an incomplete measure of aneurysmal activity, as one year volume growth has been found in approximately 40% of “diameter stable” AAAs. In a study that assessed the three dimensional geometry of AAAs, based on computed tomography, it has been shown that baseline AAA volume predicts volume growth, while baseline AAA diameter does not predict diameter growth.

Optimal Timing of Surveillance Ultrasounds in Small Aortic Aneurysms

Small abdominal aortic aneurysms (AAA) surveillance intervals remain controversial and difficult to standardize. Current Society for Vascular Surgery guidelines lack quality evidence. The objective of this study is to examine patients followed in a high volume non-invasive vascular laboratory, determine if the current guidelines are fitting in clinical practice, and attempt to further identify risk factors for accelerated aneurysm growth. A retrospective analysis of patients who underwent at least two ultrasounds for AAA in the vascular laboratory during 2008 -2018 with baseline diameter less than 5.0 cm was conducted. Patient demographics were collected. Groups were then created for comparison using the size criteria according to SVS guidelines. In addition, we compared overall growth rates specifically evaluating rapid growth (rate of at least 1.0 cm/year and size change of at least 0.5 cm from previous imaging), expected growth (any growth below 1.0 cm/year and of at least 0.5 cm from baseline) and no growth. A total of 1581 patients (1232 male and 349 female) were identified with a total of 5945 ultrasound studies. The median age was 73 years and mean follow-up was 27.8 months. Baseline AAA size was 3.0 -3.9 cm in 986 patients and 4.0 -4.9 cm in 595 patients. The average maximum growth rate was 0.18 cm/year for AAAs 3.0 -3.9 cm and 0.36 cm/year for AAAs 4.0 -4.9 cm (P <0.001). Patients with AAA 4.0 -4.9 cm at baseline were more likely to be white, male, hypertensive and have chronic kidney disease (P <0.05). 1078 patients (68.2%) demonstrated no growth over the observed time period with 342 patients (21.6%) demonstrating expected growth and 161 (10.2%) rapid growth. Male gender and baseline AAA size of 4.0 -4.9 cm were more likely to demonstrate rapid growth (P=0.002) and eventual repair (P <0.001). Metformin use was more common in the AAA group with no growth (P <0.05). Freedom from rapid growth and repair indication at 2 years was significantly lower in those patients with baseline aneurysms 3.0 -3.9 cm (P <0.001). The overall low rate of events in small AAAs supports continued surveillance every 3 years for AAAs 3.0-3.9 cm and yearly for male patients with AAAs 4.0 -4.9 cm as recommended by the SVS Guidelines. Female gender may have less rapid growth than previously reported but likely merit more rigorous surveillance particularly as the AAAs approach 5.0 cm. Metformin use continues to demonstrate it may abrogate aneurysmal growth. Lastly, there is a subset of patients that exhibit more rapid growth of their small AAAs, and further study will be required to classify these patients.

Clinical Significance of Increased Computed Tomography Attenuation of Periaortic Adipose Tissue in Patients With Abdominal Aortic Aneurysms.

Recent imaging studies reported an association between vascular inflammation and progression of abdominal aortic aneurysm (AAA). This study investigated the clinical significance of periaortic adipose tissue inflammation derived from multidetector computed tomography angiography (MDCTA).Methods and Results:Patients with asymptomatic AAA (n=77) who underwent an index and >6 months follow-up MDCTA examinations were retrospectively investigated. MDCTA analysis included AAA diameter and the periaortic adipose tissue attenuation index (PAAI). The PAAI was defined as the mean CT attenuation value within a predefined range from -190 to -30 Hounsfield units of adipose tissue surrounding the AAA. The growth rate of the AAA was calculated as the change in diameter. AAA progression (AP) was defined as an AAA growth rate ≥5 mm/year. Univariate and multivariate logistic regression analysis were performed to determine the predictors of AP. AP was observed in 19 patients (24.7%), the median baseline AAA diameter was 38.9 mm (interquartile range [IQR] 32.7-42.9 mm), and the median growth rate was 3.1 mm/year (IQR 1.5-4.9 mm/year). Baseline AAA diameter (odds ratio [OR] 1.16; 95% confidence interval [CI] 1.05-1.28; P=0.001) and PAAI (OR 1.12; 95% CI 1.05-1.20; P=0.004) were independent predictors of AP. PAAI was an independent and significant predictor of AP, supporting the notion that local adipose tissue inflammation may contribute to aortic remodeling.

Role of volume in small abdominal aortic aneurysm surveillance

ObjectiveCurrent management of small abdominal aortic aneurysms (AAAs) primarily involves serial imaging surveillance of maximum transverse diameter (MTD) to estimate rupture risk. Other measurements, such as volume and tortuosity, are less well-studied and may help characterize and predict AAA progression. This study evaluated predictors of AAA volume growth and discusses the role of volume in clinical practice. MethodsSubjects from the Non-invasive Treatment of Abdominal Aortic Aneurysm Clinical Trial (baseline AAA MTD, 3.5-5.0 cm) with ≥2 computed tomography scans were included in this study (n = 250). Computed tomography scans were conducted approximately every 6 months over 2 years. MTD, volume, and tortuosity were used to model growth. Univariable and multivariable backwards elimination least squares regressions assessed associations with volume growth. ResultsBaseline MTD accounted for 43% of baseline volume variance (P < .0001). Mean volume growth rate was 10.4 cm3/year (standard deviation, 8.8 cm3/year) (mean volume change +10.4%). Baseline volume accounted for 30% of volume growth variance; MTD accounted for 13% of volume growth variance. More tortuous aneurysms at baseline had significantly larger volume growth rates (difference, 32.8 cm3/year; P < .0001). Univariable analysis identified angiotensin II receptor blocker use (difference, −3.4 cm3/year; P = .02) and history of diabetes mellitus (difference, −2.8 cm3/year; P = .04) to be associated with lower rates of volume growth. Baseline volume, tortuosity index, current tobacco use, and absence of diabetes mellitus remained significantly associated with volume growth in multivariable analysis. AAAs that reached the MTD threshold for repair had a wide range of volumes: 102 cm3 to 142 cm3 in female patients (n = 5) and 105 cm3 to 229 cm3 in male patients (n = 20). ConclusionsBaseline AAA volume and MTD were found to be moderately correlated. On average, AAA volume grows about 10% annually. Baseline volume, tortuosity, MTD, current tobacco use, angiotensin II receptor blocker use, and history of diabetes mellitus were predictive of volume growth over time.

Abstract P101: Suppression Of Serum Amyloid A Limits Progression Of Obesity Associated Abdominal Aortic Aneurysms

Obesity increases the risk for abdominal aortic aneurysms (AAA) in humans, and enhances angiotensin II (AngII)-induced AAA formation in C57BL/6 mice. Obesity is also associated with increases in serum amyloid A (SAA). We previously reported that deficiency of SAA significantly reduces AngII-induced inflammation and AAA in apoE-deficient mice. In this study we investigated whether SAA plays a role in progression of an established AAA in obese C57BL/6 mice. Approach and Results: Male C57BL/6 mice were fed a high fat diet (60% kcal as fat) throughout the study. After 4 months of diet the mice were infused with angiotensin II (AngII) at 1000ng/kg/min until the end of the study. Ultrasound (US) was performed in all mice before and after 28 days of AngII infusion, and mice that had at least a 25% increase in the luminal diameter of the abdominal aorta were stratified by luminal diameter into 3 groups. Group 1 was killed to establish baseline AAA. Groups 2 and 3 continued to receive AngII for a further 8 weeks along with an antisense oligonucleotide (ASO) that suppresses all 3 acute phase SAA isoforms (SAA-ASO), or a control ASO (5 mg/kg/wk). US was repeated at study end to assess AAA progression. Plasma SAA at the end of the experiment was 89.2±83.2 mg/L in the control ASO group, and 18.6±0.7 mg/L in the SAA-ASO group (mean±SD , p=0.008). There was no impact of SAA suppression on body weight, body fat, or blood pressure. After the first 4 weeks of AngII infusion, the average luminal diameter in all mice was 1.81±0.40 mm (mean±SD). Mice that received the control ASO had continued aortic dilation (average luminal aortic diameter 2.06±0.42 mm), whereas the mice that received the SAA-ASO had a significant reduction in progression of aortic dilation (average luminal diameter 1.64±0.43 mm, p=0.0015 for interaction between time and group). Conclusions: We demonstrate for the first time that suppression of SAA protects obese C57BL/6 mice from progression of AngII-induced AAA. Suppression of SAA may be a therapeutic approach to limit AAA progression.

Anatomic eligibility for endovascular aneurysm repair preserved over 2 years of surveillance

ObjectiveEndovascular aneurysm repair (EVAR) is a widely used option for patients with suitable vascular anatomy who have a large infrarenal abdominal aortic aneurysm (AAA). Patients with small AAAs are managed with careful surveillance and it is a common concern that their anatomy may change with AAA growth, and their option for EVAR may become limited. Device innovation has resulted in expanded ranges of anatomy that may be eligible for EVAR. This study sought to identify changes in anatomic eligibility for repair with contemporary endovascular devices in AAA patients, monitored by computed tomography scan over the course of 2 years. MethodsPatients from the Non-Invasive Treatment of Abdominal Aortic Aneurysm Clinical Trial (N-TA3CT, NCT01756833) were included in this analysis. Females had baseline AAA maximum transverse diameter between 3.5 and 4.5 cm, and males had baseline maximum transverse diameter between 3.5 and 5.0 cm. Patients were included in this analysis if they completed pre-enrollment and 2-year follow-up computed tomography imaging. Pertinent anatomic measurements were performed on a postprocessing workstation in a centralized imaging core laboratory. EVAR candidacy was determined by measuring proximal aortic neck diameter, AAA length, and infrarenal neck angulation. Patients were considered to be eligible for EVAR if they qualified for at least one of the seven studied devicesʼ instructions for use at baseline and at 2 years. A paired t test analysis was used to detect differences in aortic measurements over 2 years, and the McNemar test was used to compare eligibility over 2 years. ResultsWe included 192 patients in this analysis—168 male and 24 female. Of these patients, 85% were eligible for EVAR at baseline and 85% after 2 years of follow-up (P = 1.00; 95% confidence interval –0.034 to 0.034). Of the 164 EVAR candidates at baseline, 160 (98%) remained eligible over 2 years of surveillance. Insufficient neck length was the most common reason for both ineligibility at baseline (18 of 28 patients) as well as loss of candidacy over 2 years (3 of 4 patients). ConclusionsThe majority of patients eligible for EVAR when entering a surveillance program for small AAA remain eligible after 2 years. Substantial changes in AAA neck anatomy resulting in loss of EVAR treatment options are infrequent. Patients with anatomic AAA progression beyond EVAR eligibility remain candidates for complex EVAR and open repair.

Evaluating Growth Patterns of Abdominal Aortic Aneurysm Diameter With Serial Computed Tomography Surveillance

Small abdominal aortic aneurysms (AAAs) are common in the elderly population. Their growth rates and patterns, which drive clinical surveillance, are widely disputed. To assess the growth patterns and rates of AAAs as documented on serial computed tomography (CT) scans. Cohort study and secondary analysis of the Non-Invasive Treatment of Abdominal Aortic Aneurysm Clinical Trial (N-TA3CT), a randomized, double-blind placebo-controlled clinical trial conducted from 2013 to 2018, with CT imaging every 6 months for 2 years. The trial was a multicenter, observational secondary analysis, not related to treatment hypotheses of data collected in the N-TA3CT. Participants included 254 patients with baseline AAA diameter between 3.5 and 5.0 cm. Patients received serial CT scan measurements, analyzed for maximum transverse diameter, at 6-month intervals. The primary study outcome was AAA annual growth rate. Secondary analyses included characterizing AAA growth patterns, assessing likelihood of AAA diameter to exceed sex-specific intervention thresholds over 2 years. A total of 254 patients, 35 women with baseline AAA diameter 3.5 to 4.5 cm and 219 men with baseline diameter 3.5 to 5.0 cm, were included. Yearly growth rates of AAA diameters were a median of 0.17 cm/y (interquartile range [IQR], 0.16) and a mean (SD), 0.19 (0.14) cm/y. Ten percent of AAAs displayed minimal to no growth (<0.05 cm/y), 62% displayed low growth (0.05-0.25 cm/y), and 28% displayed high growth (>0.25 cm/y). Baseline AAA diameter accounted for 5.4% of variance of growth rate (P < .001; R2, 0.054). Most AAAs displayed linear growth (70%); large variations in interval growth rates occurred infrequently (3% staccato growth and 4% exponential growth); and some patients' growth patterns were not clearly classifiable (23% indeterminate). No patients with a maximum transverse diameter less than 4.25 cm exceeded sex-specific repair thresholds at 2 years (men, 0 of 92; 95% CI, 0.00-0.055; women, 0 of 25 ; 95% CI, 0.00-0.247). Twenty-six percent of patients with a maximum transverse diameter of at least 4.25 cm exceeded sex-specific repair thresholds at 2 years (n = 12 of 83 men with diameter ranging from 4.25 to <4.75 cm; 95% CI, 0.091-0.264; n = 21 of 44 men with diameter ranging from 4.75-5.0 cm; 95% CI, 0.362-0.669; n = 3 of 10 women with diameter ≥4.25 cm; 95% CI, 0.093-0.726). Most small AAAs showed linear growth; large intrapatient variations in interval growth rates were infrequently observed over 2 years. Linear growth modeling of AAAs in individual patients suggests smaller AAAs (<4.25 cm) can be followed up with a CT scan in at least 2 years with little chance of exceeding interventional thresholds. ClinicalTrials.gov Identifier: NCT01756833.

Comparison of Outcomes Following EVAR Based on Aneurysm Diameter and Volume and Their Postoperative Variations

to evaluate the impact of bi- and 3-dimensional preoperative aortic morphological features and their immediate postoperative variations on the outcome of abdominal aortic aneurysms (AAA) treated by endovascular exclusion with standard devices (EVAR). Double centre retrospective analysis of prospectively collected registry data of EVAR patients. For all patients, preoperative and 30-day computed tomographic angiography images (CTA) were reviewed. Preoperative maximum AAA diameter >59 mm and volume >159 cm3, and any 30-day postoperative increasing at CTA, were considered as potentially influencing the outcome. The outcome measures were: primary technical success; 30-day, 1-year, and mean follow-up reintervention, all-cause and AAA-related mortality rates, and also endoleak-related reinterventions. Three hundred and thrity-three patients were enrolled. Mean preoperative and 30-day AAA diameter and volume were 50.4 mm ± 11.8 vs. 49.1 mm ± 12.1, and 112.9 cm3 ± 79.5 vs. 112.1 cm3 ± 80.5, respectively. Primary technical success was achieved in all cases. At 34.9 months follow-up, cumulative reintervention rate was 12.0%, mortality rates 7.2%, without AAA-related deaths. Endoleak-related reintervention rate was 7.5%. At uni- and multi-variate analysis, preoperative AAA diameter >59 mm, and AAA volume >159 cm3 were significantly associated to reintervention (P = 0.012; P = 0.002), and reintervention and death (P = 0.002; P = 0.001) during follow-up. Additionally, any increase in postoperative AAA diameter or volume was significantly associated with reintervention (P = 0.001, P = 0.001) and reintervention and death (P = 0.006, P = 0.001). Endoleak-related reintervention were also significantly associated with all of the analysed morphological parameters (P = 0.019, P = 0.005, P = 0.005, and P = 0.002, respectively). Patients with larger baseline AAA size and volume as well as unfavourable early remodelling of the sac are associated to worse long-term EVAR outcome.

Abstract 13513: Serial CT Surveillance of Abdominal Aortic Aneurysm Diameter Demonstrates Predominantly Linear Growth (N-TA 3 CT)

Objective: Small abdominal aortic aneurysms (AAAs) have a low risk of rupture. Intervention is indicated when diameters exceed established thresholds. This study assessed the growth rates and patterns of AAAs over 2 years as documented on serial CT scans from the Non-Invasive Treatment of AAA Clinical Trial. Methods: 254 patients, 35 females with baseline AAA maximum transverse diameter (MTD) between 3.5-4.5 cm and 219 males with baseline MTD 3.5-5.0 cm, were included in this study. Linear regressions and segmental growth rates were used to model growth rates and patterns. Results: The yearly growth rates of AAA MTDs had a median of 0.17 cm/yr and mean of 0.19 cm/yr ± 0.14 (Figure 1). 10% of AAA displayed minimal to no growth (&lt; 0.05 cm/yr), 62% low growth (0.05-0.25 cm/yr), 28% high growth (&gt; 0.25 cm/yr). Baseline AAA diameter accounted for only 5.4% of growth rate variance (P&lt;0.001, R 2 0.05). Most AAAs displayed linear growth (70%); large variations in interval growth rates occurred infrequently (3% staccato growth, 4% exponential growth); a minority of subjects’ growth patterns were not clearly classifiable (11% indeterminate-not growing, 12% indeterminate-growing) (Figure 2). No patients with baseline MTD &lt; 4.25 cm exceeded sex-specific repair thresholds (males 0 / 92, [95% CI, 0.00-0.06]; females 0 / 25 [95% CI, 0.00-0.25]) in the course of follow-up for as long as two years. Conclusions: The majority of small AAAs exhibit linear growth; large intra-patient growth rate variations were infrequently observed over 2 years. AAA &lt; 4.25 cm can be followed with a CT scan in 2 years with little chance of exceeding interventional MTD thresholds of 5.5 cm for men.

Plasma Desmosine and Abdominal Aortic Aneurysm Disease.

BackgroundIt is recognized that factors beyond aortic size are important in predicting outcome in abdominal aortic aneurysm (AAA) disease. AAA is characterized by the breakdown of elastin within the aortic tunica media, leading to aortic dilatation and rupture. The aim of this study was to investigate the association of plasma desmosine (pDES), an elastin‐specific degradation product, with disease severity and clinical outcome in patients with AAA.Methods and ResultsWe measured pDES and serum biomarker concentrations in 507 patients with AAAs (94% men; mean age, 72.4±6.1 years; mean AAA diameter, 48±8 mm) and 162 control subjects (100% men; mean age, 71.5±4.4 years) from 2 observational cohort studies. In the longitudinal cohort study (n=239), we explored the incremental prognostic value of pDES on AAA events. pDES was higher in patients with AAA compared with control subjects (mean±SD: 0.46±0.22 versus 0.33±0.16 ng/mL; P<0.001) and had the strongest correlation with AAA diameter (r=0.39; P<0.0001) of any serum biomarker. After adjustment for baseline AAA diameter, pDES was associated with an AAA event (hazard ratio, 2.03 per SD increase [95% CI, 1.02–4.02]; P=0.044). In addition to AAA diameter, pDES provided incremental improvement in risk stratification (continuous net reclassification improvement, 34.4% [95% CI, −10.8% to 57.5%; P=0.09]; integrated discrimination improvement, 0.04 [95% CI, 0.00–0.15; P=0.050]).ConclusionspDES concentrations predict disease severity and clinical outcomes in patients with AAA.Clinical Trial Registrationhttp://www.isrctn.com. Unique identifier: ISRCTN76413758.

Abstract MP24: Women Experience Higher Rates of Surgical Repair and Mortality for Abdominal Aortic Aneurysm

Background: It is unknown how gender disparities in the clinical presentation of abdominal aortic aneurysm (AAA) affects AAA repair type and long-term survival. We assessed the hypothesis that compared to men, women face a higher risk of death after AAA repair due to differences in demographics, disease severity, and repair type. Methods: We analyzed all endovascular (EVAR) and open surgical (OPEN) AAA repairs from 2003-2015 in the Vascular Quality Initiative-Medicare linked registry. Using inverse probability weighting, we balanced patient demographics, comorbidities, and disease severity among men and women. Then, we evaluated the effect of gender on AAA treatment and subsequent survival using Poisson and Cox regression, respectively. Results: In this cohort (n=16,085), patients undergoing EVAR (79%) or OPEN (21%) had up to 12 years of follow-up. Women comprised 22% of the cohort and were older (mean age 77 ±6.6 vs. 75 ±6.5 years, p&lt;0.001), less likely to smoke (28% vs. 33%, p&lt;0.001), and had smaller aneurysms (58.7 ±18.5 mm vs 56.5 ±12 mm) than men (Figure). After balancing key risk factors, women were 1.6 times more likely to receive OPEN vs. EVAR (RR: 1.59, 95% CI: 1.46-1.72). The 12-year mortality rate after AAA repair was 74% in men vs 84% in women. After adjustment, women faced a 12% increased risk of death (HR: 1.12, 95% CI: 1.04-1.21). Sub-analysis by repair type revealed a gender discrepancy among EVAR patients, where women experienced poorer survival (HR: 1.18, 95% CI: 1.09-1.29), while men and women faced an equal risk of death after OPEN (HR: 1.00, 95% CI: 0.90-1.12). Conclusion: In conclusion, women were 1.6 times more likely to undergo OPEN repair than men, despite balancing key baseline AAA risk factors associated between men and women. After EVAR, women were 12% more likely to die than men, though no gender-based morality difference exists following OPEN repair. The differential treatment benefit of EVAR in women is concerning given the trend toward an endovascular-first treatment approach to AAA.

Metformin prescription status and abdominal aortic aneurysm disease progression in the U.S. veteran population

BackgroundIdentification of a safe and effective medical therapy for abdominal aortic aneurysm (AAA) disease remains a significant unmet medical need. Recent small cohort studies indicate that metformin, the world's most commonly prescribed oral hypoglycemic agent, may limit AAA enlargement. We sought to validate these preliminary observations in a larger cohort. MethodsAll patients with asymptomatic AAA disease managed in the Veterans Affairs Health Care System between 2003 and 2013 were identified by International Classification of Diseases, Ninth Revision codes. Those with a concomitant diagnosis of diabetes mellitus who also received two or more abdominal imaging studies (computed tomography, magnetic resonance imaging, or ultrasound) documenting the presence and size of an AAA, separated by at least 1 year, were included for review. Maximal AAA diameters were determined from radiologic reports. Further data acquisition was censored after surgical AAA repair, when performed. Comorbidities, active smoking status, and outpatient medication records (within 6 months of AAA diagnosis) were also queried. Yearly AAA enlargement rates, as a function of metformin treatment status, were compared using two statistical models expressed in millimeters per year: a multivariate linear regression (model 1) and a multivariate mixed-effects model with random intercept and random slope (model 2). ResultsA total of 13,834 patients with 58,833 radiographic records were included in the analysis, with radiology imaging follow-up of 4.2 ± 2.6 years (mean ± standard deviation). The average age of the patients at AAA diagnosis was 69.8 ± 7.8 years, and 39.7% had a metformin prescription within ±6 months of AAA. The mean growth rate for AAAs in the entire cohort was 1.4 ± 2.0 mm/y by model 1 analysis and 1.3 ± 1.6 mm/y by model 2 analysis. The unadjusted mean rate of AAA growth was 1.2 ± 1.9 mm/y for patients prescribed metformin compared with 1.5 ± 2.2 mm/y for those without (P < .001), a 20% decrease. This effect remained significant when adjusted for variables relevant on AAA progression: metformin prescription was associated with a reduction in yearly AAA growth rate of −0.23 mm (95% confidence interval, −0.35 to −0.16; P < .001) by model 1 analysis and 0.20 mm/y (95% confidence interval, −0.26 to −0.14; P < .001) by model 2 analysis. A subset analysis of 7462 patients with baseline AAA size of 35 to 49 mm showed a similar inhibitory effect (1.4 ± 2.0 mm/y to 1.7 ± 2.2 mm/y; P < .001). Patients' factors associated with an increased yearly AAA growth rate were baseline AAA size, metastatic solid tumors, active smoking, chronic obstructive pulmonary disease, and chronic renal disease. Factors associated with decreased yearly AAA growth rates included prescriptions for angiotensin II type 1 receptor blockers or sulfonylureas and the presence of diabetes-related complications. ConclusionsIn a nationwide analysis of diabetic Veterans Affairs patients, prescription for metformin was associated with decreased AAA enlargement. These findings provide further support for the conduct of prospective clinical trials to test the ability of metformin to limit progression of early AAA disease.

Influencia de la actividad inflamatoria del trombo mural en los pacientes con aneurisma de aorta abdominal con reparación endoluminal

IntroductionThe pathophysiological mechanisms that are involved in the growth of abdominal aortic aneurysms (AAA) are multifactorial, and include inflammatory changes, as well as haemostatic and endothelial dysfunctions and, the classic atherosclerotic risk factors. The persistence of a biologically active mural thrombus and the aneurysmal sac, as well as the possible development of type 2 endoleaks, can be the origin of the activation of inflammatory mediators, the consequences of which are unknown. The aim of this study is to define a predictive model of complications after endoluminal repair of abdominal aortic aneurysm in the short and medium-term using clinical, serological, and anatomical variables. Material and methodsA total of 50 hospital patients with asymptomatic atherosclerotic AAA were included in the study between January 2016 and November 2016, in the Angiology and Vascular Surgery Department of the Hospital Clínico Universitario de Valladolid. Clinical data were collected (age, gender, cardiovascular risk factors, comorbidity, medication), baseline AAA diameter, aortic growth at 6 months, as well as baseline C-reactive protein levels, interleukin-2 (IL2), IL6 and homocysteine, preoperatively, 7 days postoperatively, and 6 months later. The patients had an angioCT scan in the immediate postoperative period, and at 6 months. ResultsA mean growth in diameter of 6.18mm was observed in the AAA with a leak, while the correctly pressurised AAA showed a decrease of 4.69mm in their mean diameter, with this difference being statistically significant (P=.001). As regards the changes in the thrombus of the aneurysmal sac, in patients with AAA with a leak the thrombus increased by a mean of 7.74mm, while patients with AAA correctly sealed and without leakage only increased by 3.08mm, with this difference being statistically significant (P=.027). A statistically significant relationship was observed between the change in the size of the post-EVAR aneurysm and the plasma levels of CRP and homocysteine at 7 days, and of the change in the size of the intra-aortic thrombus and the plasma levels of IL2 at 7 days and at 6 months. ConclusionsThe biomarker patterns studied in the short and medium term after EVAR should be considered as indicators of an active inflammation process that exerts its influence on aortic remodelling.

Applied Machine Learning for the Prediction of Growth of Abdominal Aortic Aneurysm in Humans

ObjectiveAccurate prediction of abdominal aortic aneurysm (AAA) growth in an individual can allow personalised stratification of surveillance intervals and better inform the timing for surgery. The authors recently described the novel significant association between flow mediated dilatation (FMD) and future AAA growth. The feasibility of predicting future AAA growth was explored in individual patients using a set of benchmark machine learning techniques.MethodsThe Oxford Abdominal Aortic Aneurysm Study (OxAAA) prospectively recruited AAA patients undergoing the routine NHS management pathway. In addition to the AAA diameter, FMD was systemically measured in these patients. A benchmark machine learning technique (non-linear Kernel support vector regression) was applied to predict future AAA growth in individual patients, using their baseline FMD and AAA diameter as input variables.ResultsProspective growth data were recorded at 12 months (360 ± 49 days) in 94 patients. Of these, growth data were further recorded at 24 months (718 ± 81 days) in 79 patients. The average growth in AAA diameter was 3.4% at 12 months, and 2.8% per year at 24 months. The algorithm predicted the individual's AAA diameter to within 2 mm error in 85% and 71% of patients at 12 and 24 months.ConclusionsThe data highlight the utility of FMD as a biomarker for AAA and the value of machine learning techniques for AAA research in the new era of precision medicine.

Low baseline and subsequent higher aortic abdominal aneurysm FDG uptake are associated with poor sac shrinkage post endovascular repair.

The growth phases of medically treated abdominal aortic aneurysms (AAA) are frequently associated with an 18F-fluorodesoxyglucose positron emission tomography (FDG-PET) pattern involving low baseline and subsequent higher FDG uptake. However, the FDG-PET patterns associated with the endovascular aneurysm repair (EVAR) of larger AAA are presently unknown. This study aimed to investigate the relationship between serial AAA FDG uptake measurements, obtained before EVAR and 1 and 6months post-intervention and subsequent sac shrinkage at 6months, a well-recognized indicator of successful repair. Thirty-three AAA patients referred for EVAR (maximal diameter: 55.4 ± 6.0mm, total volume: 205.7 ± 63.0mL) underwent FDG-PET/computed tomography (CT) before EVAR and at 1 and 6months thereafter, with the monitoring of AAA volume and of a maximal standardized FDG uptake [SUVmax] averaged between the axial slices encompassing the AAA. Sac shrinkage was highly variable and could be stratified into three terciles: a first tercile in which shrinkage was absent or very limited (0-29mL) and a third tercile with pronounced shrinkage (56-165mL). SUVmax values were relatively low at baseline in the 1st tercile (SUVmax: 1.69 ± 0.33), but markedly increased at 6months (2.42 ± 0.69, p = 0.02 vs. baseline). These SUV max values were by contrast much higher at baseline in the 3rd tercile (SUVmax: 2.53 ± 0.83 p = 0.009 vs. 1st tercile) and stable at 6months (2.49 ± 0.80), while intermediate results were documented in the 2nd tercile. Lastly, the amount of sac shrinkage, expressed in absolute values or in percentages of baseline AAA volumes, was positively correlated with baseline SUVmax (p = 0.001 for both). A low pre-EVAR FDG uptake and increased AAA FDG uptake at 6months are associated with reduced sac shrinkage. This sequential FDG-PET pattern is similar to that already shown to accompany growth phases of medically treated AAA.

A DAB2IP genotype: sex interaction is associated with abdominal aortic aneurysm expansion

A faster expansion rate of abdominal aortic aneurysm (AAA) increases the risk of rupture. Women are at higher risk of rupture than men, but the mechanisms underlying this increased risk...

Effect of antiplatelet therapy on aneurysmal sac expansion associated with type II endoleaks after endovascular aneurysm repair

ObjectiveEndovascular aneurysm repair (EVAR) of abdominal aortic aneurysms (AAAs) has gained widespread use through a solid reputation of safety and effectiveness. However, some issues, such as endoleaks and sac growth over time, still arise as important concerns. Antiplatelet therapy, mandatory as secondary prevention of cardiovascular disease, may play a role in both phenomena by interfering with blood clotting properties and the inflammatory process associated with AAA. We analyzed whether different antiplatelet therapies were independent risk factors for type II endoleak (T2E) persistence and midterm sac growth after EVAR. MethodsAll patients with T2E detected in the first post-EVAR control were included, except those without at least 1 year of complete follow-up. Data for demographics, clinical comorbidities, EVAR devices, and antiplatelet therapies were recorded. All patients underwent routine follow-up with contrast-enhanced tomography at 1 month, 6 months, 12 months, and annually thereafter. A three-dimensional rendering of each endoleak was performed for detailed volumetry. Main outcomes were endoleak persistence at 6 months and sac growth >5 mm at end of follow-up. ResultsDuring a 9-year period, 87 patients with initial T2E were monitored for a mean of 41.5 months. On discharge, salicylates were prescribed to 50, clopidogrel to 16, and multiagent therapy or anticoagulation to 9; no therapy was given to 12. No significant differences in comorbidities or baseline AAA characteristics were found between groups. At 6 months thereafter, 59% (n = 51) of the initial T2Es persisted. At end of follow-up, 32 patients had sac growth >5 mm (37%). Sac growth was significantly less frequent in the group treated with salicylates (26% vs 60%; P = .004). Cox proportional hazards model reinforced the role of salicylates as protectors for sac growth over time (hazard ratio, 0.34; 95% confidence interval, 0.13-0.87; P = .024), whereas T2E nidus volume and endoleak complexity behaved like independent risk factors. ConclusionsAntiplatelet therapy with salicylates appears to be linked to a decreased risk of sac growth >5 mm over time in patients with T2Es detected right after EVAR. Population-based cohort studies are mandatory to confirm this finding and to guide a potential recommendation.

Late Survival in Nonoperated Patients with Infrarenal Abdominal Aortic Aneurysm

Historical studies report high rupture rates in patients with nonoperated abdominal aortic aneurysms (AAAs) of > 5.5cm diameter, although a recent audit has questioned this. This was a retrospective review of 138/764 (18%) patients with AAAs evaluated in a preassessment anaesthetic clinic (PAC) between 2006 and 2012, who either did not undergo elective AAA repair or who underwent deferred repair. The remaining 626 underwent repair. Patients with severe comorbidities (dementia, advanced malignancy, life-expectancy<1 year) and not referred to PAC were excluded. At a median of 27 months, 71 (52%) died, 36 (51%) following rupture. Cumulative survival, free from rupture or surgery for acute symptoms, was 96% at 1 year, 84% at 3 years, and 64% at 5 years, where baseline AAA diameters were 5.5-6.9cm. For diameters ≥ 7cm, survival, free from rupture, was 65% at 1 year, 29% at 3 years, and 0% at 5 years. Median interval to rupture was 47 months (AAA diameter 5.5-6.9cm) and 21 months where baseline diameters were ≥ 7cm. Rupture accounted for 32% of late deaths in patients with AAAs of 5.5-5.9cm diameter, 46% in those with AAAs measuring 6.0-6.9cm in diameter, and 71% in patients with AAA measuring ≥ 7cm in diameter. Approximately half of all late deaths in this nonoperated cohort were not AAA related, suggesting that even had repair been undertaken, it would not have prolonged patient survival. The incidence of rupture in "high-risk" patients with an AAA < 7cm diameter was < 5% at 1 year, thereby giving ample time to optimise risk factors and improve pre-existing medical conditions prior to undertaking a deferred intervention. Even if these patients did not undergo surgical repair, the risk of late rupture was relatively low. By contrast, nonoperated patients with AAAs ≥ 7cm in diameter face a very high risk of rupture and will probably benefit from elective surgery, with the caveat that a higher procedural risk might have to be incurred.

Abstract 37: A Multi-locus Genetic Risk Score for Abdominal Aortic Aneurysm

Background: Genome-wide association studies (GWAS) have identified several common variants associated with abdominal aortic aneurysm (AAA). We investigated whether a multi-locus genetic risk score (GRS) for AAA was associated with presence and progression of AAA in a case-control study. Methods: The study comprised of 1098 patients with AAA (74±8 years, 83% men) and 6538 controls (67±10 years, 58% men) enrolled in the Mayo Vascular Disease Biorepository. AAA was defined as a transverse diameter of abdominal aorta ≥ 3.0 cm or history of AAA repair. Controls were participants without known AAA. We found five single nucleotide polymorphisms (SNPs) previously shown to be associated with AAA at GWAS significance (P≤10^-8) in NHGRI GWAS catalog and PubMed. A GRS for AAA for each individual was calculated from four SNPs (rs2383107, rs7025486, rs599839, rs1466535) that were replicated in our cohort, by summing the number of risk alleles for each SNP weighted by their estimated effect sizes in GWAS catalog or published largest meta-analysis. Results: GRS was associated with presence of AAA: odds ratio (OR) (95% confidence interval): 1.06 (1.03-1.08). The association remained significant after adjustment for age, sex, cardiovascular risk factors, and atherosclerotic cardiovascular diseases: adjusted OR: 1.05 (1.03-1.08). Further adjustment for each SNP did not attenuate association of GRS with presence of AAA (All P&lt;0.001). GRS was not associated with family history of aortic aneurysm (P=0.4). Adding GRS to conventional risk factors improved net reclassification index by 16% (P&lt;0.001).In a subset of patients with AAA who had sequential imaging studies (n=628), GRS was associated with AAA growth rate ≥ 1.75 mm/year (median of the cohort) after adjustment for baseline AAA size: adjusted OR: 1.07 (1.00-1.14). No conventional risk factors were associated with AAA growth. Patients with GRS &gt; 5.24 (median of the cohort) had 1.31 times higher odds of having AAA and 1.64 times higher odds of having AAA growth rate ≥1.75 mm/year compared to those with GRS ≤ 5.24 (both P≤0.005). Conclusions: A multi-locus GRS was associated with presence of AAA and aneurysm growth, suggesting genetic predisposition to disease initiation and progression.