Increasing Use of Prophylactic Open Abdomen Therapy With Vacuum Assisted Wound Closure and Mesh Mediated Fascial Traction After Repair of Ruptured Abdominal Aortic Aneurysm.

OBJECTIVE: Open abdomen therapy (OAT) is commonly used to prevent or treat abdominal compartment syndrome (ACS) in patients with ruptured abdominal aortic aneurysms (rAAAs). This study aimed to evaluate the incidence, treatment, and outcomes of OAT after rAAA from 2006 to 2021. Investigating data on resuscitation fluid, weight gain, and cumulative fluid balance could provide a more systematic approach to determining the timing of safe abdominal closure. METHODS: This was a single centre observational cohort study. The study included all patients treated for rAAA followed by OAT from October 2006 to December 2021. RESULTS: Seventy-two of the 244 patients who underwent surgery for rAAA received OAT. The mean age was 72 ± 7.85 years, and most were male (n = 61, 85%). The most frequent comorbidities were cardiac disease (n = 31, 43%) and hypertension (n = 31, 43%). Fifty-two patients (72%) received prophylactic OAT, and 20 received OAT for ACS (28%). There was a 25% mortality rate in the prophylactic OAT group compared with the 50% mortality in those who received OAT for ACS (p = .042). The 58 (81%) patients who survived until closure had a median of 12 (interquartile range [IQR] 9, 16.5) days of OAT and 5 (IQR 4, 7) dressing changes. There was one case of colocutaneous fistula and two cases of graft infection. All 58 patients underwent successful abdominal closure, with 55 (95%) undergoing delayed primary closure. In hospital survival was 85%. Treatment trends over time showed the increased use of prophylactic OAT (p ≤ .001) and fewer ACS cases (p = .03) assessed by Fisher's exact test. In multivariable regression analysis fluid overload and weight reduction predicted 26% of variability in time to closure. CONCLUSION: Prophylactic OAT after rAAA can be performed safely, with a high rate of delayed primary closure even after long term treatment.

Women with large intact abdominal aortic aneurysms remain untreated.

OBJECTIVE: A lower elective repair rate among women with abdominal aortic aneurysms (AAAs) has been a consistent finding. Reasons behind this gender gap have not been thoroughly outlined. METHODS: This was a retrospective multicenter cohort study (ClinicalTrials.gov: NCT05346289) at three European vascular centers in Sweden, Austria and Norway. Patients in surveillance with AAAs were consecutively identified starting from January 1, 2014, until reaching a total sample size of 200 women and 200 men. All individuals were followed for 7 years through medical records. Final treatment distributions and the proportion of "truly untreated" (surgically untreated despite reaching guideline-directed thresholds: 50 mm for women and 55 mm for men) were determined. In a complementary analysis, a universal 55-mm threshold was used. Gender-specific primary reasons behind untreated statuses were clarified. Eligibility for endovascular repair among the truly untreated was assessed in a structured computed tomography analysis. RESULTS: Women and men had similar median diameters at inclusion (46 mm; P = .54) and at treatment decisions (55 mm; P = .36). After 7 years, the repair rate was lower among women (47% vs 57%). More women were truly untreated (26% vs 8%; P < .001) despite similar mean ages as for male counterparts (79.3 years; P = .16). With the 55-mm threshold, 16% women still classified as truly untreated. Similar reasons for nonintervention were captured for women and men (50% due to comorbidities alone, 36% morphology and comorbidity). The endovascular repair imaging analysis revealed no gender differences. Among truly untreated women, ruptures were common (18%), and mortality was high (86%). CONCLUSIONS: Surgical AAA management differed between women and men. Women could be underserved in terms of elective repairs: one in every four women was untreated with over-the-threshold AAAs. The lack of obvious gender differences in eligibility analyses could imply unmeasured discrepancies (eg, in disease extent or patient frailty).

Genetic Architecture of Abdominal Aortic Aneurysm in the Million Veteran Program.

BACKGROUND: Abdominal aortic aneurysm (AAA) is an important cause of cardiovascular mortality; however, its genetic determinants remain incompletely defined. In total, 10 previously identified risk loci explain a small fraction of AAA heritability. METHODS: We performed a genome-wide association study in the Million Veteran Program testing ≈18 million DNA sequence variants with AAA (7642 cases and 172 172 controls) in veterans of European ancestry with independent replication in up to 4972 cases and 99 858 controls. We then used mendelian randomization to examine the causal effects of blood pressure on AAA. We examined the association of AAA risk variants with aneurysms in the lower extremity, cerebral, and iliac arterial beds, and derived a genome-wide polygenic risk score (PRS) to identify a subset of the population at greater risk for disease. RESULTS: Through a genome-wide association study, we identified 14 novel loci, bringing the total number of known significant AAA loci to 24. In our mendelian randomization analysis, we demonstrate that a genetic increase of 10 mm Hg in diastolic blood pressure (odds ratio, 1.43 [95% CI, 1.24-1.66]; P=1.6×10-6), as opposed to systolic blood pressure (odds ratio, 1.06 [95% CI, 0.97-1.15]; P=0.2), likely has a causal relationship with AAA development. We observed that 19 of 24 AAA risk variants associate with aneurysms in at least 1 other vascular territory. A 29-variant PRS was strongly associated with AAA (odds ratioPRS, 1.26 [95% CI, 1.18-1.36]; PPRS=2.7×10-11 per SD increase in PRS), independent of family history and smoking risk factors (odds ratioPRS+family history+smoking, 1.24 [95% CI, 1.14-1.35]; PPRS=1.27×10-6). Using this PRS, we identified a subset of the population with AAA prevalence greater than that observed in screening trials informing current guidelines. CONCLUSIONS: We identify novel AAA genetic associations with therapeutic implications and identify a subset of the population at significantly increased genetic risk of AAA independent of family history. Our data suggest that extending current screening guidelines to include testing to identify those with high polygenic AAA risk, once the cost of genotyping becomes comparable with that of screening ultrasound, would significantly increase the yield of current screening at reasonable cost.