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Presence of an endoleak can compromise aneurysm exclusion after endovascular abdominal aortic aneurysm repair (EVAR). Type II endoleaks (T2Es) are most common and may cause sac expansion. We report outcomes of translumbar embolization (TLE) of T2Es following EVAR.We conducted a retrospective chart review of patients with T2E after EVAR treated with TLE from 2011 to 2018 at a single academic institution. Treatment indications were the presence of persistent T2E and aneurysm growth ≥5 mm. Sac stabilization was defined as growth ≤5 mm throughout the follow-up period.Thirty consecutive patients were identified. The majority were men (n = 24), with a mean age of 74.3 years (95% confidence interval [CI], 70.9-77.6 years). The most common comorbidities were hypertension (83.3%) and coronary artery disease (54.0%). The mean maximal sac diameter at T2E discovery was 5.8 cm (95% CI, 5.4-6.2 cm). The mean time to intervention from endoleak discovery was 33.7 ± 28 months with a mean growth of 0.84 cm (95% CI, 0.48-1.2 cm) during that time period. The mean follow-up time after TLE was 19.1 months (95% CI, 11.1-27.2 months). Twenty-eight patients were treated with cyanoacrylate glue (CyG) alone, and two were treated with CyG plus coil embolization (CE). There was immediate complete endoleak resolution as assessed intraoperatively, and sac stabilization in 15 cases (50.0%). Eleven patients (36.7%) had evidence of persistent T2E on initial imaging after the embolization procedure; additional follow-up revealed eventual sac stabilization at a mean of 21.3 ± 7.2 months, and therefore, these patients did not require further intervention. In the remaining four cases (13.3%), there was persistent T2E after the initial TLE, requiring a second intervention. Repeat TLE stabilized growth in three of these four patients after a mean of 17.6 ± 12.9 months. One patient required open sacotomy and ligation of lumbar vessels due to continued persistence of the T2E and continued aneurysm growth. There were no ischemic complications related to the embolization procedures. Factors associated with persistent endoleak after initial embolization were larger aneurysm diameter at the time of initial endoleak identification (P .001) and the use of antiplatelet agents (P .02). The use of anticoagulation was not a significant risk factor for endoleak recurrence or aneurysm growth after TLE.TLE of T2E is a safe and effective treatment option for T2E with aneurysm growth following EVAR. Patients taking antiplatelet medication and those with larger aneurysms at the time of endoleak identification appear to be at increased risk for persistent endoleak and need for subsequent procedures following initial TLE. These patients may require more intensive monitoring and follow-up.

Beta-blockers (BBs) are first-line anti-impulse therapy for patients presenting with acute type B aortic dissection (TBAD). However, little is understood about their effects after aortic repair. The aim of the present study was to evaluate the role of postoperative BB use on the outcomes of thoracic endovascular aortic repair (TEVAR) in TBAD.The Vascular Quality Initiative database was queried for all patients who had undergone TEVAR for TBAD from 2012 to 2020. Aortic-related reintervention, all-cause mortality, and the effects of TEVAR on false lumen thrombosis of the treated aortic segment were assessed and compared between patients treated with and without BBs postoperatively. Cox proportional hazards models were used to estimate the effect of BB therapy on the outcomes.A total of 1114 patients who had undergone TEVAR for TBAD with a mean follow-up of 18 ± 12 months were identified. The mean age was 61.1 ± 11.9 years, and 791 (71%) were men. Of the 1114 patients, 935 (84%) continued BB therapy at discharge and follow-up. The patients taking BBs were more likely to have had an entry tear originating in zones 1 to 2 (22% vs 13%; P = .022). The prevalence of acute, elective, and symptomatic aortic dissection, prevalence of concurrent aneurysms, number of endografts used, distribution of proximal and distal zones of dissection, and operative times were comparable between the two cohorts. At 18 months, significantly more complete false lumen thrombosis (58% vs 47%; log-rank P = .018) was observed for patients taking BBs, and the rates of aortic-related reinterventions (13% vs 9%; log-rank P = .396) and mortality (0.2% vs 0.7%; log-rank P = .401) were similar for patients taking and not taking BBs, respectively. Even after adjusting for clinical and anatomic factors, postoperative BB use was associated with increased complete false lumen thrombosis (hazard ratio, 1.56; 95% confidence interval, 1.10-2.21; P = .012) but did not affect mortality or aortic-related reintervention. A secondary analysis of BB use for those with acute vs chronic TBAD showed a higher rate of complete false lumen thrombosis for patients with chronic TBAD and taking BBs (59% vs 38%; log-rank P = .038). In contrast, no difference was found in the rate of complete false lumen thrombosis for those with acute TBAD between the two cohorts (58% vs 51%; log-rank P = .158). When analyzed separately, postoperative angiotensin-converting enzyme inhibitor use did not affect the rates of complete false lumen thrombosis, mortality, and aortic-related reintervention.BB use was associated with promotion of complete false lumen thrombosis for patients who had undergone TEVAR for TBAD. In addition to its role in the acute setting, anti-impulse control with BBs appears to confer favorable aortic remodeling and might improve patient outcomes after TEVAR, especially for those with chronic TBAD.

Ischemic complications (including in the lower extremity, visceral, spinal, and pelvic territories) following standard endovascular aortic repair (EVAR) are well recognized but fortunately uncommon. The incidence of such complications following fenestrated and branched aortic repair (F/BEVAR) has not been well defined in the literature. The objective of this study was to compare the incidence of ischemic complications between EVAR and F/BEVAR and to elucidate potential risk factors for these complications.We identified all patients who underwent EVAR from 2003 to 2017 or F/BEVAR from 2012 to 2017 in the national Vascular Quality Initiative database. We assessed differences in perioperative ischemic outcomes with methods including logistic regression and inverse probability of treatment propensity score weighting, using a composite end point of lower extremity ischemia, intestinal ischemia, stroke, or new dialysis as the primary end point.The data comprised 35,379 EVAR patients and 3374 F/BEVAR patients. F/BEVAR patients were more likely to be female, have had previous aneurysm repairs, and be deemed unfit for open aneurysm repair; they were less likely to have ruptured aneurysms; and they had higher estimated blood losses, contrast volumes, and fluoroscopy and procedure times. The incidence of any ischemic event (7.7% vs 2.2%) as well as the incidences of the component end points of lower extremity ischemia (2.3% vs 1.0%), intestinal ischemia (2.7% vs 0.7%), stroke (1.5% vs 0.3%), and new hemodialysis (3.1% vs 0.4%) were all significantly increased (all P .001) in F/BEVAR compared with standard EVAR. After propensity adjustment, F/BEVAR conferred increased odds of any ischemic complication (1.8), intestinal ischemia (2.0), lower extremity ischemia (1.3), new hemodialysis (10.2), and stroke (2.3).Rates of lower extremity ischemia, intestinal ischemia, new dialysis, and stroke each range from 0% to 1% for standard EVAR and 1% to 3% for F/BEVAR. The incidence of perioperative ischemic complications following F/BEVAR is significantly increased compared to EVAR. The real-world data in this study should help guide decision-making for surgeons and patients as well as serve as one metric for progress in device and technique development. Improvements in ischemic complications may come from continued technology development such as smaller sheaths, improved imaging to decrease procedure time and contrast volume, embolic protection, and increased operator skill with wire and catheter manipulation.

The carotid artery plaque burden, indirectly measured by the degree of stenosis, quantifies a patient's future embolic risk. In natural history studies, patients with moderate degrees of stenosis have had a lower stroke risk than those with severe stenosis. However, patients with symptomatic carotid stenosis who have experienced transient ischemic attack (TIA) or stroke were found to have both moderate and severe degrees of stenosis. We examined the association of carotid artery stenosis severity with the outcomes for symptomatic patients who had undergone carotid intervention, including carotid endarterectomy (CEA), transfemoral carotid artery stenting (TFCAS), and transcervical carotid artery revascularization (TCAR).The Society for Vascular Surgery Vascular Quality Initiative database was queried for all patients who had undergone TFCAS, CEA, or TCAR between 2003 and 2020. The patients were stratified into two groups according to stenosis severity-nonsevere (0%-69%) and severe (≥70%). The primary end point was periprocedural neurologic events (stroke and TIA). The secondary end points were periprocedural death, myocardial infarction (MI), and the composite outcomes of stroke/death and stroke/death/MI in accordance with the reporting standards for carotid intervention.Of the 29,614 included symptomatic patients, 5296 (17.9%) had undergone TCAR, 7844 (26.5%) TFCAS, and 16,474 (55.6%) CEA for symptomatic carotid artery stenosis. In the CEA cohort, the neurologic event rate was significantly lower for the patients with severe stenosis than for those with nonsevere stenosis (2.6% vs 3.2%; P = .024). In the TCAR cohort, the periprocedural neurologic even rate was lower for those with severe stenosis than for those with nonsevere stenosis (3% vs 4.3%; P = .033). No similar difference was noted for the TFCAS cohort, with a periprocedural neurologic event rate of 3.8% in the severe group vs 3.5% in the nonsevere group (P = .518). On multivariable analysis, severe stenosis was associated with significantly decreased odds of postprocedural neurologic events after CEA (odds ratio, 0.75; 95% confidence interval, 0.6-0.92; P = .007) and TCAR (odds ratio, 0.83; 95% confidence interval, 0.69-0.99; P = .039) but not after TFCAS.Severe carotid stenosis, in contrast to more moderate stenosis degrees, was associated with decreased rates of periprocedural stroke and TIA in symptomatic patients undergoing TCAR and CEA but not TFCAS. The finding of increased rates of periprocedural neurologic events in symptomatic patients with lesser degrees of stenosis undergoing TCAR and CEA warrants further evaluation with a particular focus on plaque morphology and brain physiology and their inherent risks with carotid revascularization procedures.

There is a lack of evidence regarding the effect of anticoagulation and antiplatelet medications on aortic remodeling for aortic dissection after endovascular repair. We investigated whether anticoagulation and antiplatelet medications affect aortic remodeling after thoracic endovascular aortic repair (TEVAR) for type B aortic dissection (TBAD).Records of the Vascular Quality Initiative TEVAR registry (2012-2020) were reviewed. Procedures performed for TBAD were included. Aortic reintervention, false lumen thrombosis of the treated aorta, and all-cause mortality at follow-up were compared between patients treated with and without anticoagulation medications. A secondary analysis was performed to assess the effect of antiplatelet therapy in patients not on anticoagulation. Cox proportional hazards models were used to estimate the effect of anticoagulation and antiplatelet therapies on outcomes.A total of 1210 patients (mean age, 60.7 ± 12.2 years; 825 males [68%]) were identified with a mean follow-up of 21.2 ± 15.7 months (range, 1-94 months). One hundred sixty-six patients (14%) were on anticoagulation medications at discharge and at follow-up. Patients on anticoagulation were more likely to be older (mean age, 65.5 vs 60 years; P .001) and Caucasian (69% vs 55%; P = .003), with higher proportions of coronary artery disease (10% vs 3%; P .001), congestive heart failure (10% vs 2%; P .001), and chronic obstructive pulmonary disease (15% vs 9%; P = .017). There were no differences in the mean preoperative thoracic aortic diameter or the number of endografts used. At 18 months, the rates of aortic reinterventions (8% vs 9%; log-rank P = .873), complete false lumen thrombosis (52% vs 45%; P = .175), and mortality (2.5% vs 2.7%; P = .209) were similar in patients with and without anticoagulation, respectively. Controlling for covariates with the Cox regression method, anticoagulation use was not independently associated with a decreased rates of complete false lumen thrombosis (hazard ratio [HR], 0.74; 95% confidence interval [CI], 0.5-1.1; P = .132), increased need for aortic reinterventions (HR, 1.02; 95% CI, 0.62-1.68; P = .934), and mortality (HR, 1.25; 95% CI, 0.64-2.47; P = .514). On a secondary analysis, antiplatelet medications did not affect the rates of aortic reintervention, complete false lumen thrombosis, and mortality.Anticoagulation and antiplatelet medications do not appear to negatively influence the midterm endpoints of aortic reintervention or death in patients undergoing TEVAR for TBAD. Moreover, it did not impair complete false lumen thrombosis. Anticoagulation and antiplatelet medications do not adversely affect aortic remodeling and survival in this population at midterm.