Project description:A 69-year-old woman with a history of graft replacement for abdominal aortic aneurysm developed a complicated type B aortic dissection that resulted in renal malperfusion after thoracic endovascular aortic repair (TEVAR). The primary entry tear was formed at the aortic arch and the false lumen (FL) continued to the abdominal aorta. The distal end of the FL formed a pouch-like blind alley above the suture line of the bifurcated abdominal graft. The true lumen (TL) was compressed and caused severe limb ischemia. The right renal artery (rRA) originated from the FL. The patient had initially undergone emergent axillofemoral bypass for limb malperfusion. Three weeks later, restenosis of the TL caused visceral malperfusion, and a huge thrombus formed in the FL pouch. TEVAR expanded the TL and restored visceral vascularization. However, the expanded TL compressed the thrombus in the blind alley to the rRA orifice and caused right renal malperfusion. The history of abdominal graft replacement may have increased the risk of a thrombotic event after TEVAR. Primary TEVAR may have helped prevent thrombus formation in the FL pouch. <Learning objective: This case report describes visceral arterial embolism induced by endovascular aortic repair (TEVAR) for type B aortic dissection in a patient with prior abdominal aortic grafting. A huge thrombus formed in the blind pouch of the false lumen (FL) above the graft suture line. TEVAR expanded the true lumen and the FL thrombus occluded a visceral artery with FL origin. Post-graft replacement has a risk of thrombus formation in the FL pouch and thrombus compression in visceral arteries.>.
Project description:BACKGROUND:Immediate open repair of acute type A aortic dissection is traditionally recommended to prevent death from aortic rupture. However, organ failure because of malperfusion syndrome (MPS) might be the most imminent life-threatening problem for a subset of patients. METHODS:From 1996 to 2017, among 597 patients with acute type A aortic dissection, 135 patients with MPS were treated with upfront endovascular reperfusion (fenestration/stenting) followed by delayed open repair (OR). We compared outcomes between the first and second decades and observed mortalities with those expected with an "upfront OR for every patient" approach, determined using prognostic models from the literature (Verona, Leipzig-Halifax, Stockholm, Penn, and GERAADA [German Registry for Acute Aortic Dissection Type A] models). RESULTS:Overall, in-hospital mortality improved between the 2 decades (21.0% versus 10.7%, P<0.001). In the second decade, for patients with MPS initially treated with fenestration/stenting, mortality from aortic rupture decreased from 16% to 4% ( P=0.05), the risk of dying from organ failure was 6.6 times higher than dying from aortic rupture (hazard ratio=6.63; 95% CI, 1.5-29; P=0.01), and 30-day mortality after OR for MPS patients was 3.7%. Compared to the expected mortalities with the upfront OR for every patient models, our observed 30-day and in-hospital mortalities (9% and 11%, respectively) of all patients with acute type A aortic dissection were significantly lower ( P?0.03). CONCLUSIONS:Immediate OR is the strategy to prevent death from aortic rupture for the majority of patients with acute type A aortic dissection. However, relatively stable (no rupture, no tamponade) patients with MPS benefit from a staged approach: upfront endovascular reperfusion followed by aortic OR at resolution of organ failure.
Project description:BackgroundPatients with acute type A aortic dissection with a previous cardiac surgery (PCS) and malperfusion syndrome (MPS) are extremely difficult to manage and have poor outcomes.MethodsFrom 1996 to 2018, 668 patients underwent emergent open aortic repair or endovascular fenestration/stenting for MPS for an acute type A aortic dissection, including those with PCS (PCS, n = 64) and those without PCS (No-PCS, n = 604). The groups were further divided into PCS+MPS, PCS+No-MPS, No-PCS+MPS, and No-PCS+No-MPS.ResultsCompared with the No-PCS group, the PCS group had significantly more coronary artery disease, acute renal failure, and mesenteric and renal MPS. Forty-two percent of patients with PCS underwent upfront endovascular fenestration/stenting for endovascular-amendable MPS. The in-hospital mortality was significantly higher in patients with PCS+MPS (40%) compared with PCS+No-MPS (5.9%), No-PCS+MPS (30%), and No-PCS+No-MPS (6.7%). Multivariable logistic regression showed cardiogenic shock (odds ratio, 7.3) and MPS (odds ratio, 6.6) were risk factors for in-hospital mortality (P < .001). After recovering from MPS the PCS group (n = 54) had similar rates of postoperative complications, including 30-day mortality (7.4% vs 6.3%, P = .77), compared with the No-PCS group (n = 557). The 5-year survival was significantly lower in the PCS group compared with the No-PCS group (60% vs 72%, P = .004) and was lowest in those with PCS+MPS (46%). PCS was not a significant risk factor for in-hospital (odds ratio, 1.2; P = .63) or late (hazard ratio, 1.3; P = .27) mortality.ConclusionsBecause of severe preoperative comorbidities and the complexity of open aortic repair, in acute type A aortic dissection patients with PCS and MPS, endovascular fenestration and stenting first with delayed redo sternotomy and central aortic repair was a valid approach.
Project description:ObjectiveTo assess outcomes of endovascular reperfusion followed by delayed open aortic repair for stable patients with acute type A aortic dissection and mesenteric malperfusion syndrome (mesMPS).MethodsAmong 602 patients with acute type A aortic dissection who presented to our center from 1996 to 2017, all 82 (14%) with mesMPS underwent upfront endovascular fenestration/stenting. Primary outcomes were in-hospital mortality and long-term survival. Patients with acute type A aortic dissection with no malperfusion syndrome of any organ (n = 419) served as controls.ResultsIn-hospital mortality of all comers with mesMPS was 39%. After endovascular fenestration/stenting, 20 mesMPS patients (24%) died from organ failure and 11 patients (13%) died from aortic rupture before open aortic repair, 47 patients (58%) underwent aortic repair, and 4 patients (5%) survived without open repair. No patients died from aortic rupture during the second decade (2008-2017). The significant risk factors for death from organ failure after endovascular reperfusion were acute stroke (odds ratio, 23; 95% confidence interval, 4-144; P = .0008), gross bowel necrosis at laparotomy (odds ratio, 7; 95% confidence interval, 1.4-34; P = .016), and serum lactate ≥6 mmol/L (odds ratio, 13.5; 95% confidence interval, 2-97; P = .0097). There was no significant difference in operative mortality (2.1% vs 7.5%; P = .50) or long-term survival between patients with mesMPS who underwent open aortic repair after recovering from mesMPS and patients with no malperfusion syndrome.ConclusionsIn patients with acute type A aortic dissection with mesMPS, endovascular fenestration/stenting, and delayed open aortic repair achieved favorable short- and long-term outcomes. Surgeons should consider correcting mesenteric malperfusion before undertaking open aortic repair in patients with mesMPS, especially those with acute stroke, gross bowel necrosis at laparotomy, or serum lactate ≥6 mmol/L.
Project description:ObjectiveThe study objective was to evaluate the progression of dissected distal aorta in patients with acute type A aortic dissection with malperfusion syndrome treated with endovascular fenestration/stenting and delayed open aortic repair.MethodsFrom 1996 to 2021, 927 patients presented with acute type A aortic dissection. Of these, 534 had DeBakey I dissection with no malperfusion syndrome and underwent emergency open aortic repair (no malperfusion syndrome group), whereas 97 patients with malperfusion syndrome underwent fenestration/stenting and delayed open aortic repair (malperfusion syndrome group). Sixty-three patients with malperfusion syndrome treated with fenestration/stenting were excluded due to no open aortic repair, including death from organ failure (n = 31), death from aortic rupture (n = 16), and discharged alive (n = 16).ResultsCompared with the no malperfusion syndrome group, the malperfusion syndrome group had more patients with acute renal failure (60% vs 4.3%, P < .001). Both groups had similar aortic root and arch procedures. Postoperatively, the malperfusion syndrome group had similar operative mortality (5.2% vs 7.9%, P = .35) and permanent dialysis (4.7% vs 2.9%, P = .50), but more new-onset dialysis (22% vs 7.7%, P < .001) and prolonged ventilation (72% vs 49%, P < .001). The growth rate of the aortic arch (0.38 vs 0.35 mm/year, P = .81) was similar between the malperfusion syndrome and no malperfusion syndrome groups. The descending thoracic aorta growth rate (1.03 vs 0.68 mm/year, P = .001) and abdominal aorta growth rate (0.76 vs 0.59 mm/year, P = .02) were significantly higher in the malperfusion syndrome group. The cumulative incidence of reoperation over 10 years (18% vs 18%, P = .81) and 15-year survival outcome (50% vs 48%, P = .43) were similar between the malperfusion syndrome and no malperfusion syndrome groups.ConclusionsEndovascular fenestration/stenting followed by delayed open aortic repair was a valid approach for patients with malperfusion syndrome.
Project description:ObjectiveThe study objective was to evaluate the management of malperfusion in acute type B aortic dissection with endovascular fenestration/stenting.MethodsFrom 1996 to 2018, 182 patients with an acute type B aortic dissection underwent fenestration/stenting for suspected malperfusion based on imaging, clinical manifestations, and laboratory findings. Data were obtained from medical record review and the National Death Index database.ResultsThe median age of patients was 55 years. Signs of malperfusion included abdominal pain (61%), lower-extremity weakness (27%), nonpalpable lower-extremity pulses (24%), and abnormal lactate, creatinine, liver enzymes, and creatine kinase levels. Confirmed hemodynamically significant malperfusion affected the spinal cord (2.7%), celiac (24%), superior mesenteric (40%), renal (51%), and iliofemoral (43%) arterial distributions. Of the 182 patients, 99 (54%) underwent aortic fenestration/stenting, 108 (59%) had 1 or multi-branch vessel fenestration/stenting, 5 (2.7%) had concomitant thoracic endovascular aortic repair, 17 (9.3%) had additional thrombolysis or thromboembolectomy, and 48 (26%) received no intervention. After fenestration/stenting, 24 patients (13%) required additional procedures for necrotic bowel or limb and 9 patients (4.9%) had subsequent aortic repair (thoracic endovascular aortic repair, open repair) before discharge. The new-onset paraplegia was 0%. The in-hospital mortality was 7.7% over 20+ years and 0% in the last 8 years. The 5- and 10-year survivals were 72% and 49%, respectively. The significant risk factors for late mortality were age and acute paralysis (hazard ratio, 3.5; both P < .0001). Given death as a competing factor, the 5- and 10-year cumulative incidence of reintervention was 21% and 31% for distal aortic pathology, respectively.ConclusionsPatients with acute type B aortic dissection with malperfusion can be managed with endovascular fenestration/stenting with excellent short- and long-term outcomes. This approach is particularly helpful to patients with static malperfusion of aortic branch vessels.
Project description:ObjectiveThe study objective was to evaluate the surgical results in patients with acute type A aortic dissection and cerebral malperfusion.MethodsFrom 2000 to 2019, 234 patients with type A aortic dissection and cerebral malperfusion were stratified into 3 groups: 50 (21%) with syncope (group 1), 152 (65%) with persistent loss of focal neurological function (group 2), and 32 (14%) with coma (group 3). Results were evaluated and compared by univariable and multivariable analyses.ResultsMedian age was higher in group 1, and incidence of cardiogenic shock was higher in group 3. The femoral artery was the most common cannulation site, whereas the axillary artery was used in 18% of group 1, 30% of group 2, and 25% of group 3 patients (P = .337). Antegrade cerebral perfusion was performed in more than 80% of patients, and ascending aorta/arch replacement was performed in 40% of group 1, 27% of group 2, and 31% of group 3 (P = .21). In-hospital mortality was 18% in group 1, 27% in group 2, and 56% in group 3 (P = .001). Survival at 5 years is 57.0% in group 1, 57.7% in group 2, and 38.7% in group 3 (P = .0005). On multivariable analysis, age, cardiopulmonary bypass time, and group 3 versus group 2 were independent risk factors for mortality, whereas axillary cannulation was a protective factor.ConclusionsPatients with aortic dissection and cerebral malperfusion without preoperative coma showed acceptable mortality, and those with coma had a high in-hospital mortality regardless of the type of brain protection. Overall axillary artery cannulation appeared to be a protective factor.
Project description:ObjectivesThe management of acute type A aortic dissection with malperfusion syndrome remains challenging. To evaluate preoperative condition, symptoms might be subjective and objective evaluation of cerebral artery has not yet been established. For quantitative evaluation, this study focused on brain computed tomography perfusion (CTP), which has been recommended by several guidelines of acute ischaemic stroke.MethodsIn the last 2 years, 147 patients hospitalized due to acute type A aortic dissection were retrospectively reviewed. Among the 23 (16%) patients with cerebral malperfusion, 14 who underwent brain CTP (6 preoperative and 8 postoperative) were enrolled. CTP parameters, including regional blood flow and time to maximum, were automatically computed using RApid processing of Perfusion and Diffusion software. The median duration from the onset to hospital arrival was 129 (31-659) min.ResultsAmong the 6 patients who underwent preoperative CTP, 4 with salvageable ischaemic lesion (penumbra: 8-735 ml) without massive irreversible ischaemic lesion (ischaemic core: 0-31 ml) achieved acceptable neurological outcomes after emergency aortic replacement regardless of preoperative neurological severity. In contrast, 2 patients with an ischaemic core of >50 ml (73, 51 ml) fell into a vegetative state or neurological death due to intracranial haemorrhage. CTP parameters guided postoperative blood pressure augmentation without additional supra-aortic vessel intervention in the 8 patients who underwent postoperative CTP, among whom 6 achieved normal neurological function regardless of common carotid true lumen stenosis severity.ConclusionsCTP was able to detect irreversible ischaemic core, guide critical decisions in preoperative patients and aid in determining the blood pressure augmentation for postoperative management focusing on residual brain ischaemia.