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Objective This study investigated the diameter of internal iliac artery (IIA) aneurysms (IIAAs) at the time of rupture to evaluate whether the current threshold diameter for elective repair of 3 cm is reasonable. The prevalence of concomitant aneurysms and results of surgical treatment were also investigated. Methods This was a retrospective analysis of patients with ruptured IIAA from seven countries. The patients were collected from vascular registries and patient records of 28 vascular centers. Computed tomography images taken at the time of rupture were analyzed, and maximal diameters of the ruptured IIA and other aortoiliac arteries were measured. Data on the type of surgical treatment, mortality at 30 days, and follow-up were collected. Results Sixty-three patients (55 men and 8 women) were identified, operated on from 2002 to 2015. The patients were a mean age of 76.6 years (standard deviation, 9.0; range 48-93 years). A concomitant common iliac artery aneurysm was present in 65.0%, 41.7% had a concomitant abdominal aortic aneurysm, and 36.7% had both. IIAA was isolated in 30.0%. The mean maximal diameter of the ruptured artery was 68.4 mm (standard deviation, 20.5 mm; median, 67.0 mm; range, 25-116 mm). One rupture occurred at <3 cm and four at <4 cm (6.3% of all ruptures). All patients were treated, 73.0% by open repair and 27.0% by endovascular repair. The 30-day mortality was 12.7%. Median follow-up was 18.3 months (interquartile range, 2.0-48.3 months). The 1-year Kaplan-Meier estimate for survival was 74.5% (standard error, 5.7%). Conclusions IIAA is an uncommon condition and mostly coexists with other aortoiliac aneurysms. Follow-up until a diameter of 4 cm seems justified, at least in elderly men, although lack of surveillance data precludes firm conclusions. The mortality was low compared with previously published figures and lower than mortality in patients with ruptured abdominal aortic aneurysm. Abdominal aortic aneurysm (AAA) is the most common and studied aneurysm. Aneurysms of the iliac arteries are found considerably less often, and epidemiologic data on these do not exist. In many cases iliac artery aneurysms coexist with aortic aneurysms: ∼10% to 20% of patients with AAA also have a concomitant aneurysm in the iliac arteries. 1 The artery most often affected is the common iliac artery (CIA), followed by the internal iliac artery (IIA), also called the hypogastric artery. In the case of isolated aneurysms in the iliac arteries, without involvement of the aorta, the most common location is the IIA. 2 Aneurysms of the external iliac artery are extremely rare, possibly because these arteries originate later in development from a different cell population than the distal aorta and the CIA and IIA. Studies on IIA aneurysms (IIAAs) are scarce owing to the rarity of the condition. The existing literature consists primarily of case reports and small patient series. No prospective studies on IAAs exist. According to the literature, IAAs have a high rupture and mortality rate even in elective cases, possibly because of their deep location in the pelvis. 3 The etiology and risk factors of IAA seem to be the same as AAA. 4 Iliac aneurysms are mostly degenerative but can also be mycotic or caused by genetic disorders such as Marfan or Ehlers-Danlos syndromes. Traumatic aneurysms in the iliac arteries have also been described; for example, caused by iatrogenic trauma from hip, lumbar, or gynecologic operations. A mainly historical subpopulation of young women with IIAA caused by trauma from pregnancy and delivery has been described. 5 and 6 IAAs cause symptoms more often than AAA because of compression of pelvic structures such as ureters, bladder, veins, or lumbar nerves. Wilhelm et al 7 reported that 53% of published isolated IIAA cases were symptomatic, not including the ruptured ones (31%). The high proportion of symptomatic patients in these older reports may partly be explained, however, by the fact that most of these cases were from time before widespread use of modern imaging. IIAA are not easily discovered with clinical examination because of their location 8 but are detected increasingly often as a result of imaging and screening programs. Because the studies on IIAAs are scarce, the natural history is virtually unknown. A widely used threshold for elective repair is 3 cm, originally suggested by McCready et al 9 because their series did not include any ruptures under that diameter. However, only seven ruptures were included in that report. The reference list of this article illustrates that most of the papers on this subject were published when open repair was the only treatment option. Nowadays endovascular treatment is the first option in many centers. 10 The aim of this study was to investigate at what diameter IIAAs tend to rupture and whether the current operative threshold of 3 cm is rational. Secondary aims were to assess the prevalence of concomitant aortoiliac aneurysms, treatment patterns, and the results of treatment.

The decision of whether to treat incidental intracranial saccular aneurysms is complicated by limitations in current knowledge of their natural history. We combined individual patient data from prospective cohort studies to determine predictors of aneurysm rupture and to construct a risk prediction chart to estimate 5-year aneurysm rupture risk by risk factor status. We did a systematic review and pooled analysis of individual patient data from 8382 participants in six prospective cohort studies with subarachnoid haemorrhage as outcome. We analysed cumulative rupture rates with Kaplan-Meier curves and assessed predictors with Cox proportional-hazard regression analysis. Rupture occurred in 230 patients during 29 166 person-years of follow-up. The mean observed 1-year risk of aneurysm rupture was 1·4% (95% CI 1·1–1·6) and the 5-year risk was 3·4% (2·9–4·0). Predictors were age, hypertension, history of subarachnoid haemorrhage, aneurysm size, aneurysm location, and geographical region. In study populations from North America and European countries other than Finland, the estimated 5-year absolute risk of aneurysm rupture ranged from 0·25% in individuals younger than 70 years without vascular risk factors with a small-sized (<7 mm) internal carotid artery aneurysm, to more than 15% in patients aged 70 years or older with hypertension, a history of subarachnoid haemorrhage, and a giant-sized (>20 mm) posterior circulation aneurysm. By comparison with populations from North America and European countries other than Finland, Finnish people had a 3·6-times increased risk of aneurysm rupture and Japanese people a 2·8-times increased risk. The PHASES score is an easily applicable aid for prediction of the risk of rupture of incidental intracranial aneurysms. Netherlands Organisation for Health Research and Development.

Background Although an association between elevated blood pressure and risk of aortic aneurysm is established, few studies have investigated the association with aortic aneurysm subtypes. We investigated the association between systolic and diastolic blood pressure and hypertension status with the risk of aortic aneurysm in the UK Biobank. Methods The analysis included 495,542 men and women aged 37–73 years at recruitment between 2006 and 2010. Aortic aneurysm cases were identified by linkage to hospitalization and mortality records. Multivariable Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between blood pressure and hypertension and risk of aortic aneurysm overall and for subtypes. Results During a mean follow-up of 12.3 years, 3,346 incident aortic aneurysm cases were identified. Hypertension vs. no hypertension was associated with increased risk (HR, 95% CI) of aortic aneurysm (1.17, 1.08–1.27), and for thoracic (1.23, 1.04–1.46), abdominal (1.16, 1.04–1.30), and non-ruptured (1.18, 1.08–1.28) aortic aneurysm, and suggestively with unspecified site aortic aneurysm (1.18, 0.96–1.46) and aortic aneurysm mortality (1.26, 0.87–1.82), but not ruptured aortic aneurysm (1.02, 0.67–1.58). Systolic blood pressure was not associated with risk of aortic aneurysm overall or for any subtype. Diastolic blood pressure was positively associated with aortic aneurysm (1.74, 1.26–2.41, p trend <0.0001) for ≥ 110 vs. <80 mmHg, abdominal aortic aneurysm (1.95, 1.28–2.96, p trend <0.0001), unspecified site aortic aneurysm (2.02, 0.94–4.33, p trend =0.005), non-ruptured aortic aneurysm (1.79, 1.29–2.47), and aortic aneurysm mortality (2.32, 0.56–9.58, p trend <0.0001), and with ruptured aortic aneurysm (2.48, 1.22–5.03, p trend <0.0001 for 100–109 vs. <80 mmHg), while the association with thoracic aortic aneurysm was less clear (1.30, 0.64–2.63). These associations were strengthened and positive associations emerged for systolic blood pressure and abdominal and non-ruptured aortic aneurysm in sensitivity analyses when excluding participants with prevalent ischemic heart disease, stroke, those using hypertension medications and the first 3 years of follow-up. Conclusion We found that hypertension status and higher diastolic blood pressure were associated with increased risk of aortic aneurysm overall and most aortic aneurysm subtypes. No association was observed for systolic blood pressure. Although further studies are needed on aortic aneurysm subtypes, these findings provide strong support that controlling blood pressure is important for reducing the risk of aortic aneurysm.

Objectives Arterial calcification is thought to protect against rupture of intracranial aneurysms, but studies in a representative population of intracranial aneurysm patients have not yet been performed. The aim was to compare the prevalence of aneurysm wall calcification and intracranial carotid artery calcification (ICAC) between patients with an unruptured intracranial aneurysm (UIA) and a ruptured intracranial aneurysm (RIA). Materials and methods We matched 150 consecutive UIA patients to 150 RIA patients on age and sex. Aneurysm wall calcification and ICAC were quantified on non-contrast enhanced computed tomography images with the modified Agatston score. We compared the prevalence of aneurysm wall calcification, ICAC, and severe ICAC (defined as a modified Agatston score in the fourth quartile) between UIA and RIA patients using univariate and multivariate conditional logistic regression models adjusted for aneurysm characteristics and cardiovascular risk factors. Results Aneurysm wall calcification was more prevalent in UIA compared to RIA patients (OR 5.2, 95% CI: 2.0–13.8), which persisted after adjustment (OR 5.9, 95% CI: 1.7–20.2). ICAC prevalence did not differ between the two groups (crude OR 0.9, 95% CI: 0.5–1.8). Severe ICAC was more prevalent in UIA patients (OR 2.0, 95% CI: 1.1–3.6), but not after adjustment (OR 1.0, 95% CI: 0.5–2.3). Conclusions Aneurysm wall calcification but not ICAC was more prevalent in UIAs than in RIAs, which corresponds to the hypothesis that calcification may protect against aneurysmal rupture. Aneurysm wall calcification should be further assessed as a predictor of aneurysm stability in prospective cohort studies. Clinical relevance statement Calcification of the intracranial aneurysm wall was more prevalent in unruptured than ruptured intracranial aneurysms after adjustment for cardiovascular risk factors. Calcification may therefore protect the aneurysm against rupture, and aneurysm wall calcification is a candidate predictor of aneurysm stability. Key Points Aneurysm wall calcification was more prevalent in patients with unruptured than ruptured aneurysms, while internal carotid artery calcification was similar . Aneurysm wall calcification but not internal carotid artery calcification is a candidate predictor of aneurysm stability . Cohort studies are needed to assess the predictive value of aneurysm wall calcification for aneurysm stability . Graphical Abstract

Abstract BACKGROUND Maximal size and other morphological parameters of intracranial aneurysms (IAs) are used when deciding if an IA should be treated prophylactically. These parameters are derived from postrupture morphology. As time and rupture may alter the aneurysm geometry, possible morphological predictors of a rupture should be established in prerupture aneurysms. OBJECTIVE To identify morphological parameters of unruptured IAs associated with later rupture. METHODS Nationwide matched case-control study. Twelve IAs that later ruptured were matched 1:2 with 24 control IAs that remained unruptured during a median follow-up time of 4.5 (interquartile range, 3.7-8.2) yr. Morphological parameters were automatically measured on 3-dimensional models constructed from angiograms obtained at time of diagnosis. Cases and controls were matched by aneurysm location and size, patient age and sex, and the PHASES (population, hypertension, age, size of aneurysm, earlier subarachnoid hemorrhage from another aneurysm, and site of aneurysm) score did not differ between the 2 groups. RESULTS Only inflow angle was significantly different in cases vs controls in univariate analysis (P = .045), and remained significant in multivariable analysis. Maximal size correlated with size ratio in both cases and controls (P = .015 and <.001, respectively). However, maximal size and inflow angle were correlated in cases but not in controls (P = .004. and .87, respectively). CONCLUSION A straighter inflow angle may predispose an aneurysm to changes that further increase risk of rupture. Traditional parameters of aneurysm morphology may be of limited value in predicting IA rupture.

Finnish saccular intracranial aneurysm (sIA) disease associates to 2q33, 8q11, and 9p21 loci and links to 19q13, Xp22, and kallikrein cluster in sIA families. Detailed phenotyping of familial and sporadic sIA disease is required for fine mapping of the Finnish sIA disease. Eastern Finland, which is particularly isolated genetically, is served by Kuopio University Hospital's Department of Neurosurgery. We studied the site and size distribution of unruptured and ruptured sIAs in correlation to age and sex in 316 familial and 1454 sporadic sIA patients on first admission from 1993 to 2007. The familial and sporadic aneurysmic subarachnoid hemorrhage patients had slightly different median ages (46 vs 51 years in men; 50 vs 57 years in women), different proportion of males (50% vs 42%), equal median diameter of ruptured sIAs (7 mm vs 7 mm) with no correlation to age, and equally unruptured sIAs (30% vs 28%). The unruptured sIAs were most frequent at the middle cerebral artery (MCA) bifurcation (44% vs 39%) and the anterior communicating artery (12% vs 13%), in contrast to the ruptured sIAs at the anterior communicating artery (37% vs 29%) and MCA bifurcation (29% vs 29%). The size of unruptured sIAs increased by age in the sporadic group. The MCA bifurcation was most prone to develop unruptured sIAs, suggesting that MCA branching during the embryonic period might be involved. The different site distribution of ruptured and unruptured sIAs suggests different etiologies for sIA formation and rupture. The lack of correlation of size and age at rupture (exposure to risk factors) suggests that the size at rupture is more dependent on hemodynamic stress.

Quantitative data on the impact of smoking on genesis of intracranial aneurysms (IA) is sparse. We aimed to analyze the association between lifetime and current smoking exposure and IA characteristics. In this prospective observational cohort study (07/2016–01/2023, n = 918), all patients or next of kin filled out the questionnaire for assessment of smoking habits including the status (no/former/current) and consumption level (heavy vs light current smoker [≥/<10 cigarettes/day], and lifetime exposure in pack-years). The study endpoints were the ruptured status, size, and presence of multiple IA. The distribution of non-, former, light, and heavy smokers was 23.2 %, 25.6 %, 11.2 % and 40 % respectively. The median lifetime smoking exposure was 20 pack-years. Current smokers were at higher risk of presenting with ruptured (adjusted odds ratio [aOR]=1.71, 95 % confidence interval [CI]=1.29–2.26, p < 0.0001), large (≥7 mm, aOR=1.41, 95 % CI=1.05–1.89, p = 0.022) and multiple IA (aOR=1.34, 95 % CI=1.01–1.77, p = 0.045). In the subgroup analysis among ever smokers, heavy smoking additionally increased the risk of IA rupture (aOR=1.83, 95 % CI=1.33–2.50, p < 0.0001) and larger size (aOR=1.65, 95 % CI=1.19–2.30, p = 0.003). Finally, longer history of smoking (>20 pack-years) was related to higher probability of multiple (aOR=1.61, 95 % CI=1.21–2.13, p = 0.001) and large IA (aOR=1.40, 95 % CI=1.04–1.87, p = 0.025). Our data underline the role of smoking in IA genesis, and the importance of smoking cessation for rupture prevention. Current and particularly heavy smoking increases the risk of IA rupture, whereas the chronic exposure over years more likely results in the development of multiple and large IA. •Our manuscript analyses the impact of smoking exposure on the rupture status, size, and number of intracranial aneurysms.•Current smokers were at higher risk of presenting with ruptured, large and multiple IA.•In the subgroup analysis among ever smokers, heavy smoking additionally increased the risk of IA rupture and larger size.•Longer history of smoking (>20 pack-years) was related to higher probability of multiple and large IA.•Our data underline the role of smoking in IA genesis, and the importance of smoking cessation for rupture prevention.

Purpose Determine whether mirror intracranial aneurysms (MIAs) confer risk beyond aneurysm multiplicity and describe their distribution and longitudinal change. Methods Retrospective two-centre UK cohort of unruptured intracranial aneurysms (UIAs) diagnosed 2006–2020; outcomes to 2022. Endpoints: first rupture, SAH-specific/all-cause mortality, time to treatment, and lesion-level growth/morphology change. Rates used Poisson models with person-time offsets; lesion-level risks used GEE (modified Poisson). Rupture-free survival used inverse-probability-weighted Kaplan–Meier. Models adjusted for baseline aneurysm count. Results 1,985 UIAs were identified; 289 (14.6%) were MIAs. MIAs clustered at the MCA bifurcation (57.8%) and ICA terminus (34.6%). First-rupture incidence was higher in MIAs (1.74/100 person-years (PY)) than aMIAs (0.76/100 PY) or SIAs (0.39/100 PY); MIA > SIA IRR 4.46 ( q  = 0.0003), MIA > aMIA IRR 2.29 ( q  = 0.0044). SAH-specific mortality incidence was higher in MIAs (1.21/100 PY) than SIAs (0.36/100 PY; IRR 3.36, q  = 0.0057) and aMIAs (0.19/100 PY; IRR 6.37, q  = 0.0002). IPW survival was poorer for MIAs vs aMIAs (weighted log-rank χ 2  = 9.95, p  = 0.0016) and vs SIAs (χ 2  = 18.09, p  = 2.11 × 10⁻ 5 ). Lesion-level GEE showed no symmetry-specific increase in rupture risk (omnibus p  = 0.72). Lesion-level growth ≥ 1 mm (RR 1.67, q  = 0.0380) and morphology change (RR 2.10, q  = 0.0121) were higher in MIAs. With aneurysm count adjustment, effects attenuated with wide CIs, consistent with limited power. Conclusion MIAs were associated with higher patient-time rupture and SAH-specific mortality and greater lesion-level instability, but not with an independent per-aneurysm rupture hazard. The excess patient-level risk is largely explained by exposure (multiplicity); a symmetry-related effect remains plausible but unconfirmed. Larger, prospectively harmonised datasets are needed.

Background Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder associated with high incidences of intracranial aneurysms. We performed a systematic review with the purpose of clarifying the prevalence, risk of rupture, and appropriate management of intracranial aneurysms in the ADPKD population. Method PRISMA guidelines were followed. We conducted a comprehensive literature search of three databases (PubMed, Ovid MEDLINE, and Ovid EMBASE) on all series reporting ADPKD patients with intracranial aneurysms. Results Our systematic review included 16 articles with a total of 563 patients with ADPKD and intracranial aneurysms. The prevalence of unruptured aneurysms was 11.5% (95% CI = 10.1–13%), whereas 1.9% (95% CI = 1.3–2.6%) of aneurysms were ruptured. Hypertension was present in 79.3% of patients with ADPKD and renal impairment in 65%. The mean size of ruptured aneurysms was slightly higher than unruptured (6 mm vs. 4.4 mm). The most common locations of unruptured and ruptured aneurysms were the ICA (40.5%) and MCA (45%), respectively. Asymptomatic patients studied with four-vessel angiography experienced 25% transient complications. Overall, 74% unruptured aneurysms were surgically treated with lower complication rates compared to endovascular treatment (11% vs. 27.7%). Among conservatively treated aneurysms, 2.9% ruptured at follow-up (rupture rate 0.4%/patient-year). Finally, the growth rate was 0.4% per patient-year, and the incidence of de novo aneurysm formation was 1.4% per patient-year. Conclusions The prevalence of unruptured intracranial aneurysms in the ADPKD population is approximately 11%. Given the non-negligible rate of procedural complications, the management of these patients must be cautious and individualised. The rupture rate appears comparable to that of the general population. On the other hand, the 1.4% rate per patient-year of de novo aneurysms is non-negligible. These findings should be considered when counselling ADPKD patients regarding the appropriate management of intracranial aneurysms.

•64 pediatric patients with intracranial aneurysms (IAs) were analyzed.•Extremely high risk of seizure was observed.•Several unique risk factors of seizures in pediatric IAs were reported.•Surgical and endovascular treatments were compared on the control of seizures. Seizures are common complications following intracranial aneurysms and present a greater risk to pediatric patients than adults. Though the risk factors of seizures in adults with intracranial aneurysms have been well documented, the risk factors in pediatric patients remain unknown. The aim of this study was to evaluate the risk factors for preoperative seizures and the effect of the treatment approach on postoperative seizures in pediatric patients with intracranial aneurysms. The data of 64 pediatric patients (mean age 11.4 ± 5.7 years; 68.8 % of males) with intracranial aneurysms were retrospectively analyzed from January 2012 to April 2017. Comparisons were made between patients with preoperative seizures (case group) and those without (control group). Twenty-four patients (37.5 %) had preoperative seizures, and 15 patients (23.4 %) had postoperative seizures. Multiple logistic regression analysis revealed that younger age (0–5 years), head trauma history, ruptured aneurysms, lobe hematomas, modified Fisher grade 3–4, giant aneurysms, pseudoaneurysms and distal arterial aneurysms were independently associated with the increased risk of preoperative seizures. Patients in the surgical and endovascular groups did not differ significantly in the rates of preoperative seizures or early postoperative seizures (within 1 month) (P > 0.05). However, a significantly lower incidence of late postoperative seizures (1–3 months and 3–6 months) was observed in the surgical group compared with the endovascular group (P < 0.05). Pediatric patients with intracranial aneurysms are at high risk for seizures. Risk factors for preoperative seizures included younger age (0–5 years), head trauma history, lobe hematomas, modified Fisher grade 3–4, giant aneurysms, pseudoaneurysms and distal arterial aneurysms. Compared with the endovascular treatment, surgical intervention provided more benefits with regard to reducing the risk of late postoperative seizures.