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Objective: The 2023 European Society for Vascular Surgery (ESVS) guidelines on radiation safety recommended establishment of national diagnostic reference levels (DRLs) for endovascular procedures, which indicate an expected radiation dose for any given procedure for the average sized patient. The aim of this study was to propose a national DRL for Sweden for standard endovascular aortic repair (EVAR).

Methods: This was a national registry based study where all EVARs performed in Sweden over a two year period (2021 – 2022) were identified in the Swedish vascular registry, Swedvasc. Patient demographics were extracted from Swedvasc and radiation related parameters were collected at centre level. Multivariable analyses were performed to assess which factors affected fluoroscopy time, total dose area product (DAP), and cumulative air kerma (CAK). The national DRL was defined as the third quartile of all centre specific median values for DAP total.

Results: Nine hundred and thirty-three procedures at 23 centres were included; 831 (89.1%) intact abdominal aortic aneurysms (AAAs) and 102 (10.9%) ruptured AAAs. The median (interquartile range [IQR]) DAP for EVAR at centre level varied from 28.3 Gy·cm2 (IQR 14.1, 76.1) to 212.7 Gy·cm2 (IQR 196.8, 275.0). Overall, the third quartile of the DAP radiation dose for EVAR in Sweden was 152.6 Gy·cm2. The DAP was a median 81.1  Gy·cm2 and 116.5 Gy·cm2 for intact and ruptured EVARs, respectively (p < .001). The DRL was 147.7 Gy·cm2 and 213.8 Gy·cm2 for intact and ruptured EVARs, respectively. In a multivariable linear regression analysis, rupture, iliac branched repair, access complication, obesity, low centre volume and larger aneurysm were predictors for higher DAP during EVAR.

Conclusion: The current report proposes a DRL for DAP of 152.6 Gy·cm2 for EVAR procedures in Sweden, with specific benchmark DAP values proposed for subgroups of patients. There is a considerable difference in radiation dose between different centres, suggesting a potential for implementation of improved radiation routines in some centres based on benchmarking.

Objective: Previous studies suggest partly different risk factor profiles of thoracic aortic aneurysms (TAAs) and abdominal aortic aneurysms (AAAs), but prospective data are scarce. The purpose of this prospective population-based case-control study was to investigate differences in risk factor profile between TAAs and AAAs.

Methods: Participants in two prospective population-based studies, the Västerbotten Intervention Project (VIP) and the Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) study, between 1986 and 2010, underwent cardiovascular risk assessments, including blood samples, oral glucose tolerance test, blood pressure readings, and a self-reported health questionnaire. All individuals who were later diagnosed with TAAs or AAAs were identified. Age, sex, and time-matched controls were selected from the same cohorts, aiming at four controls/case. Adjusted odds ratios (aORs) for potential risk factors for later diagnosis of TAAs and AAAs, respectively, were estimated by multivariate conditional logistic regression analyses.

Results: From a total of 96,196 individuals with prospectively collected data in the VIP/MONICA cohort, a total of 236 individuals with AAAs (181 men and 55 women) and 935 matched controls, and 168 individuals with TAAs (115 men and 53 women) and 662 controls were included. The average age at baseline examination was 57.0 ± 5.7 years for AAA cases and controls, and 52.1 ± 8.8 years for TAA cases and controls. Mean time between baseline examination and diagnosis of AAAs/TAAs was 12.1 and 11.7 years, respectively. There was a clear difference in risk factor profile between AAAs and TAAs. Smoking, hypertension, and coronary artery disease were significantly associated with later diagnosis of AAAs, with highest aORs for a history of smoking (aOR, 10.3; 95% confidence interval [CI], 6.3-16.8). For TAAs, hypertension was the only positive risk factor (aOR, 1.7; 95% CI, 1.1-2.7), whereas smoking was not associated. Diabetes was not associated with either AAAs or TAAs; neither was self-reported physical activity.

Conclusions: In this prospective, population-based, case-control study, risk factor profile differed between AAAs and TAAs. This suggests a partially different etiology for TAAs and AAAs.

Near-occlusion (NO) with and without full collapse seems to cause low blood flow in symptomatic carotid stenosis. If the stroke mechanism is hypoperfusion in NO, the stump pressure should be low. The aim was to compare and describe stump pressure and blood flow in conventional ≥ 50% stenosis, NO without full collapse, and NO with full collapse. In this prospective single-center study, consecutive patients with symptomatic ≥ 50% carotid stenosis (NASCET grading), undergoing carotid endarterectomy (CEA) were recruited. NO was diagnosed by three blinded observers who reviewed computed tomography angiographies (CTA). Intraoperative measurements of ICA flow before and after CEA and stump pressure were recorded. One hundred and eighty-one patients were included; 116 (64%) had conventional ≥ 50% stenosis, and 66 (36%) had NO. Before CEA, the median ICA flow was significantly lower in NO (90 ml/min) compared to conventional ≥ 50% stenosis (170 mL/min, p < 0.001). In contrast, no difference was observed after CEA (NO 170 mL/min, conventional ≥ 50% stenosis 180 mL/min, p = 0.48). The ICA flow change was significantly higher in NO compared to conventional stenosis (p < 0.001). There was a significant correlation between the distal ICA diameter on CTA and the ICA flow before CEA (r = 0.579, p < 0.001). There were no differences in stump pressure between NO and conventional ≥ 50% stenoses (median 53 (range 41–66) mmHg and median 54 (range 40–67) mmHg, respectively, p = 0.93), nor any correlation between the stump pressure and the distal ICA diameter (r = 0.063, p = 0.41). NO causes low ICA flow, and to our knowledge, this is the first time this causal link between ICA flow and NO is clearly established. Since patients with NO did not have low stump pressure, the mechanism of stroke in NO does not seem to be hypoperfusion.

Objective: The aim of this study was to determine how many pre-operative ischaemic events occurring within a specific timeframe before carotid endarterectomy (CEA) are needed to increase the peri-operative 30 day risk of stroke or death.

Methods: This was a secondary exploratory analysis based on pooled data from three observational studies sourced from a single centre. Patients with recently symptomatic conventional ≥ 50% carotid stenosis were included. The principal analysis was limited to patients presenting with stroke or transient ischaemic attack (TIA). The primary outcome was 30 day risk of peri-operative stroke or death. Whether one, two, three, or four or more ipsilateral pre-operative ischaemic events within three, seven, 14, or 30 days before CEA were associated with the primary outcome was assessed.

Results: The study included 382 patients who underwent CEA with symptomatic conventional ≥ 50% carotid stenosis with stroke or TIA as the presenting event. Mean patient age ± standard deviation was 72 ± 7 years, 117 (30.6%) were female, and 5% were treated with dual antiplatelet therapy. The primary outcome occurred in 21 patients (5.5%). Two or more events within 7 days before CEA was the most discriminative definition of repeated events, with a 14.3% (8/56) risk of the primary outcome. Those who fell outside this definition of two or more events within seven days before CEA had a 4.0% (13/326; p = .006) risk of experiencing the primary outcome (adjusted odds ratio 4.1, 95% confidence interval 1.6 – 10.5). Several alternative definitions were assessed, but patients with two or more events within seven days before CEA and negative for these alternatives still had a > 10% risk of the primary outcome.

Conclusion: Two or more ipsilateral ischaemic events within seven days before CEA is associated with an increased risk of peri-operative stroke or death in cases with symptomatic conventional ≥ 50% carotid stenosis and TIA or stroke as the presenting event. Studies assessing whether delayed or immediate CEA is preferable for this patient group are warranted.

Objective: Mycotic aortic aneurysms are rare, life threatening, and complex. This nationwide study aimed to assess outcome after repair of mycotic thoracic aortic aneurysms (MTAAs).

Methods: Patients treated in Sweden for MTAAs between 2000 and 2016 were identified in the Swedish vascular registry (2010–16) and local patient registries (2000–09). Primary outcome was survival, and secondary outcomes included surgical strategy, rate of infection related complications (IRC), and re-operations.

Results: Fifty-two patients (median age 71 ± 8.1 years; 28 [54%] men, 13 [25%] ruptured) were identified (3.6% of all thoracic aortic aneurysm repairs in Sweden). Aneurysm location was aortic arch (n = 6; 11%), descending aorta (n = 42; 81%), and multiple locations (n = 4; 8%). Twenty-nine (56%) patients had positive cultures; the most prevalent agent was Staphylococcus aureus (n = 16; 31%). Operative techniques included thoracic endovascular aortic repair (TEVAR; n = 35 [67%]), fenestrated/branched TEVAR (n = 8; 15%), hybrid repair (n = 7; 14%), and open patch repair (n = 2; 4%). Survival was 92% (95% confidence interval [CI] 88–96) at 30 days, 88% (95% CI 84–93) at three months, 78% (73–84) at one year, and 71% (64–77) at five years. The mean follow up among survivors (> 90 days) was 45 months (range 4–216 months). Antibiotics were administered for a median of 15 weeks (range 0–220 weeks). IRCs occurred in nine patients (17%): sepsis (n = 3), graft infection (n = 3), recurrent mycotic aneurysm (n = 1), aorto-oesophageal/bronchial fistula (n = 2). Six (67%) IRCs were fatal; 80% occurred within the first year. Re-operations were performed in nine patients (17%).

Conclusions: TEVAR was often used as treatment for MTAAs, with acceptable short- and long-term survival when compared with open cohorts in the literature. IRCs are of concern and warrant follow up and long-term antibiotic treatment.

An abdominal aortic aneurysm (AAA) is a degenerative disease, characterized by advanced inflammation and extracellular matrix (ECM) remodelling. Enhanced protease activity mediated by cytokines results in the degradation of ECM proteins, leading to the generation of different bioactive fragments. Some of these generated fragments are released from the vascular basement membrane (VBM), a highly specialized ECM. VBM provides mechanical and structural stability and regulates many important cellular functions of the vascular system. Type IV and XVIII collagens are two structural proteins in VBM, with crucial roles in maintaining of the VBM integrity and vascular architecture. Circulating levels of type IV and XVIII collagen fragments are found physiologically, but have also been associated with many diseases. Remodelling of VBM and expression of its components has not been as well studied in AAA as that of the interstitial ECM.

Here we investigate these VBM collagens, their expression and possible association with aortic diameter and expansion rate in individuals with an AAA in comparison with different control groups. Further we study whether there is a link between the circulating VBM collagen fragments and several inflammatory markers, all highly involved in AAA pathogenesis. Lastly, we study the impact of surgical intervention on plasma levels of VBM collagens in patients treated by either open surgical repair (OSR) or endovascular aortic aneurysm repair (EVAR).

Methods: Circulating levels of type IV and XVIII collagen fragments were analysed in individuals with an AAA and compared with healthy controls and patients with peripheral artery disease (paper I). A possible association between VBM collagen fragments and the aortic diameter and expansion was studied in a large population-based cohort of 615 men stratified into three aortic diameter groups based on initial maximum aortic diameter (paper II). Furthermore, 159 individuals were followed up over time with repeated measurements of aortic diameter and blood samples. The follow up cohort were divided into two subgroups based on expansion rate of AAA. Moreover, the location of VBM collagens in tissue from aortic wall in individuals with an AAA was characterized and the expression pattern was compared with normal aorta (paper II). In paper III, the association between the plasma levels of VBM collagens and inflammatory markers; IL-1 (IL-1α and IL-1β), IL-6, IL-8, TNF-α INF-γ and hs-CRP were studied in same cohort as paper II. Finally, the effect of surgical intervention on circulating levels of VBM collagen fragments was investigated in AAA patients who had undegone either OSR or EVAR by comparison of plasma levels before and after AAA repair.

Ultrasound technique was used for measurements of aortic diameter (paper I, II, III and IV). Analysis of circulating VBM collagens and inflammatory markers were performed by ELISA-assay (Paper I, II, III and IV) and Multiplex-assays, respectively (paper III). Aortic wall tissues were analysed by haematoxylin and eosin (H&E) and immunofluorescence staining (Paper II).

Results: There were significantly increased plasma levels of VBM collagen fragments in individuals with an AAA, compared with healthy controls and individulas with a peripheral artery disease (PAD), (Paper I). The levels of type IV collagen in AAA patients did not differ from the group with PAD, and there were no significant differences between the control groups regarding plasma levels of both VBM collagen fragments (Paper I). The increased levels of VBM collagen fragments were significantly associated with aortic diameter with highest levels in the group with an AAA (Paper II). Altered expression of the VBM collagens and fragmentation of elastic fibres were observed in tissue from AAA patients (Paper II). A significant association between the levels of pro-inflammatory cytokines IL-6 and IL-8, and VBM collagens was found. Additionally, there were a significant association between the plasma levels of IL-8, TNF-α and hs-CRP and an AAA (Paper III). Aneurysms with faster expansion rate had significantly higher levels of IL-6, IL-1β, and type XVIII/endostatin collagen. Additionally, IL-6, type XVIII/endostatin collagen and baseline-aortic diameter were significantly associated with expansion rate (Paper III). AAA repair was associated with changes in plasma levels of VBM collagens (Paper IV).

Conclusion: Circulating levels of VBM collagens were increased in patients with an AAA, and significantly associated with aortic diameter and expansion rate. The expression of VBM collagens was altered in AAA tissue compared with normal aorta. In addition, plasma levels of several inflammatory markers were associated as with VBM collagens, aortic diameter and expansion rate. The levels of both VBM collagens were altered at short and long time after AAA repair.