The incidence of elderly patients with acute type A aortic dissection is increasing. A recent analysis of the International Registry of Acute Aortic Dissection failed to show a mortality benefit with ...surgery compared with medical management in octogenarians. Therefore, we compared our institutional outcomes of emergency surgery for acute type A aortic dissection in octogenarians versus septuagenarians to understand the outcomes of surgical intervention in elderly patients.
From 2002 to 2017, 70 octogenarians (aged ≥80 years) and 165 septuagenarians (70-79 years) underwent surgery for acute type A aortic dissection (N = 235, total). Quality of life was assessed by the RAND Short Form-36 quality of life survey. Midterm clinical and functional data were obtained retrospectively.
At baseline, septuagenarians had a higher prevalence of diabetes (20.6% vs 5.7%, P = .01). The prevalence of cardiopulmonary resuscitation was 4.8% versus 10.0% (P = .24) in septuagenarians and octogenarians. The prevalence of cardiogenic shock was 18.2% versus 27.1% (P = .17). Thirty-day/in-hospital mortality was 21.2% versus 28.6% (P = .29). Multivariable logistic regression identified cardiogenic shock as an independent risk factor for in-hospital mortality (odds ratio, 10.07; 95% confidence interval, 2.30-44.03) in octogenarians. Survival at 5 years was 49.7% (42.1%-58.6%) versus 34.2% (23.9%-48.8%) in septuagenarians and octogenarians, respectively. Responses to the quality of life survey were no different between septuagenarians and octogenarians across all 8 quality of life categories.
Clinical outcomes after surgery for acute type A aortic dissection are similar in octogenarians and septuagenarians. For discharged survivors, quality of life remains favorable and does not differ between the 2 groups.
We review current knowledge regarding the natural transition of aortic dissection from acute to chronic stages. As this is not well understood, we also bring to bear new data from our institution. ...Type A dissection rarely transitions naturally into the chronic state; consequently, information is limited. Type B dissections are routinely treated medically and indeed undergo substantial changes during their temporal course. General patterns include: 1) the aorta dilates and, absent surgical intervention, aortic enlargement may cause mortality; 2) continued false lumen patency, particularly with an only partially thrombosed false lumen, increases aortic growth, whereas calcium-channel blockers affect aortic dilation favorably; 3) aortic dilation manifests a temporal dynamic, with early rapid growth and deceleration during transition; 4) the intimal flap dynamically changes over time via thickening, straightening, and loss of mobility; and 5) temporal remodeling, on the cellular level, initially shows a high grade of wall destruction; subsequently, significant fibrosis ensues.
Purpose: To present the early results of false lumen (FL) occlusion in chronic aortic dissection using the Candy-Plug generation II (CP II), which has a self-closing fabric channel that obviates the ...need for separate occlusion of its center. Materials and Methods: Fourteen consecutive patients (mean age 60±11 years; 10 men) with persistent FL backflow and aneurysm formation at the thoracic segment in chronic aortic dissection underwent thoracic endovascular aortic repair (TEVAR) with FL occlusion using the refined CP II. Primary endpoints were technical success (successful deployment) and clinical success (no FL backflow at the CP II level). Secondary endpoints included 30-day mortality and morbidity and aortic remodeling during follow-up. Results: Technical success was 100%. One patient required additional intraprocedural FL embolization at the CP II level due to persistent FL backflow on final angiography (clinical success 93%), though there was no flow through the CP II center. There were no intraprocedural complications. Immediate complete FL occlusion was achieved in 12 patients; the other 2 required reintervention. One had contrast enhancement in the distal FL proximal to the CP II and was treated with coil embolization. The other patient had persistent type I endoleak at the level of the left subclavian artery (LSA) and underwent left carotid–LSA bypass and proximal stent-graft extension. One patient died due to retrograde type A aortic dissection that was not related to CP II placement. Over a mean 8-month follow-up (range 3–12), 9 patients had computed tomography angiography; 8 patients had evidence of aortic remodeling, while 1 aneurysm sac was stable. Conclusion: The CP II reduces the number of procedural steps and offers good seal, with minimal morbidity and mortality and a high rate of aortic remodeling.
Increasing evidence suggests that contractile dysfunction in smooth muscle cells (SMCs) plays a critical role in aortic biomechanical dysfunction and aortic aneurysm and dissection (AAD) development. ...However, the mechanisms underlying SMC contractile dysfunction in sporadic AAD are poorly understood. In this study, we examined the role of the NLRP3 (nucleotide oligomerization domain-like receptor family, pyrin domain containing 3)-caspase-1 inflammasome, a key inflammatory cascade, in SMC contractile dysfunction in AAD.
We observed significant SMC contractile protein degradation in aortas from patients with sporadic thoracic AAD. The contractile protein degradation was associated with activation of the NLRP3-caspase-1 inflammasome cascade. In SMCs, caspase-1 bound and directly cleaved and degraded contractile proteins, leading to contractile dysfunction. Furthermore,
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deficiency in mice significantly reduced angiotensin II-induced contractile protein degradation, biomechanical dysfunction, and AAD formation in both thoracic and abdominal aortas. Finally, blocking this cascade with the inflammasome inhibitor, glyburide (an antidiabetic medication), reduced angiotensin II-induced AAD formation.
Inflammasome-caspase-1-mediated degradation of SMC contractile proteins may contribute to aortic biomechanical dysfunction and AAD development. This cascade may be a therapeutic target in AAD formation. In addition, glyburide may have protective effects against AAD development.
Aberrant subclavian artery (aSCA) is a rare anatomic variant whose association with other aortic branch variations and aortic pathology has yet to be established. Knowledge of such an association ...could be relevant to recommendations for screening and awareness as associated variations are important for operative planning. We describe the incidence of aSCA variations, its association with aortic pathology, and a proposed classification system.
The thoracic cross-sectional imaging database at Keck Hospital of the University of Southern California from 2006 to 2018 was queried for presence of aSCA. Studies were evaluated for aSCA laterality, variant anatomy, and aortic and branch vessel disease. Medical records were reviewed for associated symptoms and diagnoses. The primary outcome was association of aSCA with aortic pathology (aneurysm or dissection). Secondary outcomes were comparison of right and left aSCA, comparison between the sexes, and creation of a proposed classification system.
Of 98,580 axial imaging studies, 810 studies (0.82%) were identified with aSCA in 312 unique patients. Right aSCA made up the majority of cases (90.1%). All aSCAs had a retroesophageal course. Kommerell’s diverticulum (KD) was present in 184 (59%) with an average diameter of 1.67 cm (range, 1.2-3.3 cm). KD was more frequent (84% vs 56%; P = .0003) and larger (2.05 cm vs 1.61 cm; P < .0001) in left aSCA patients. When present, KD was more often symptomatic in left aSCA compared with right aSCA (77.4% vs 49.1%; P = .005). Dysphagia, chest pain, reflux, and asthma were all more common in left aSCA patients. KD was also more common in men (73.3% vs 50%; P < .0001) and larger in men (1.81 cm vs 1.54 cm; P < .0001) but with no difference in symptoms between sexes. Our proposed classification system based on aortic arch branching is as follows: type 1, left arch with right aSCA (59.9%); type 2, left arch with common carotid trunk and right aSCA (30.1%); type 3, right arch with left aSCA (9.6%); and type 4, right arch with common carotid trunk and left aSCA (0.3%). Subtypes describe the right vertebral artery (RVA) and left vertebral artery (LVA) origin: subclavian (s, RVA 90.1%, LVA 96.8%), carotid (c, RVA 9.6%, LVA 0.3%), or arch (a, RVA 0.3%, LVA 2.9%). Overall, 9.9% (31/312) had associated aortic pathology, although the study was underpowered to detect a difference between right aSCA and left aSCA (9.3% vs 16.1%; P = .213). Type 3 and type 4 arches more often have associated aortic pathology, KD, and symptoms.
aSCAs are frequently symptomatic and commonly associated with aortic dissection and aneurysm. Our proposed classification scheme depicts all four aSCA arch variants and accounts for vertebral artery origin variation. These variants are common, and vertebral anatomy can differ greatly. Knowledge of these anatomic variations is critical to planning for endovascular and open repair of aortic arch pathology.
As of April 7, 2020, approximately 1,300,000 cases and 80,000 deaths related to coronavirus disease 2019 (COVID-19) have been reported in more than 180 countries/territories. Health care ...infrastructures and resources, particularly as it relates to the care of the most critically ill patients, are currently being strained globally. In this context, however, there has been little clinical guidance or information regarding life-threatening conditions requiring emergency operation that cannot be delayed. We present a case of acute type A aortic dissection in a patient with COVID-19 to highlight the clinical implications of a true emergent procedure during the COVID-19 outbreak.
Thoracic aortic aneurysms (TAAs) are common, but experimental TAA models are limited and the role of interleukin-1β (IL-1β) is undetermined.
IL-1β protein was measured in human TAAs and control ...aortas, and IL-1β protein was increased ≈20-fold in human TAAs. To develop an experimental model of TAAs, 8- to 10-week-old male C57Bl/6 mice (wild type WT) underwent thoracotomy with application of periadventitial elastase (WT TAA) or saline (WT control; n=30 per group). Elastase treatment to thoracic aortas resulted in progressive dilation until day 14 with maximal dilation of 99.6±24.7% compared with 14.4±8.2% for WT saline control (P<0.0001). WT TAAs demonstrated elastin fragmentation, smooth muscle cell loss, macrophage infiltration, and increased IL-1β expression. Next, TAAs were induced in mice deficient of IL-1β (IL-1β knockout) or IL-1 receptor (IL-1R knockout; n=10 each). Genetic deletion of IL-1β and IL-1R significantly decreased thoracic aortic dilation (IL-1β knockout=54.2±16.8% and IL-1R knockout=62.6±17.2% versus WT TAA=104.7±23.8%; P<0.001for both). IL-1β knockout and IL-1R knockout aortas demonstrated preserved elastin and smooth muscle cells with fewer inflammatory cells. Correspondingly, IL-1β and IL-1R knockout aortas had decreased inflammatory cytokine and matrix metalloproteinase 9 expression. Separately, WT mice pretreated with either IL-1R antagonist anakinra (100 mg/kg per day) or vehicle alone (control) underwent elastase treatment. Pretreatment of WT mice with anakinra attenuated TAA formation (control: 99.2±15.5% versus anakinra: 68.3±19.2%; P<0.005). Finally, to investigate treatment of small TAAs, WT mice were treated with anakinra 3 days after TAA induction. Anakinra treatment in WT mice with small TAAs reduced aortic dilation on day 14 (control treatment: 89.1±18.6% versus anakinra treatment: 59.7±25.7%; P=0.01).
Periadventitial application of elastase to murine thoracic aortas reproducibly produced aneurysms with molecular and histological features consistent with TAA disease. Genetic and pharmacological inhibition of IL-1β decreased TAA formation and progression, indicating that IL-1β may be a potential target for TAA treatment.
Stroke is an increasingly recognised complication following thoracic endovascular aortic repair (TEVAR). The aim of this study was to systematically synthesise the published data on perioperative ...stroke incidence during TEVAR for patients with descending thoracic aneurysmal disease and to assess the impact of left subclavian artery (LSA) coverage on stroke incidence.
A systematic review of English and German articles on perioperative (in-hospital or 30 day) stroke incidence following TEVAR for descending aortic aneurysm was performed, including studies with ≥50 cases, using MEDLINE and EMBASE (2005–2015). The pooled prevalence of perioperative stroke with 95% CI was estimated using random effect analysis. Heterogeneity was examined using I2 statistic.
Of 215 studies identified, 10 were considered suitable for inclusion. The included studies enrolled a total of 2594 persons (61% male) between 1997 and 2014 with a mean weighted age of 71.8 (95% CI 71.1–73.6) years. The pooled prevalence for stroke was 4.1% (95% CI 2.9–5.5) with moderate heterogeneity between studies (I2 = 49.8%, p = .04). Five studies reported stroke incidences stratified by the management of the LSA, that is uncovered versus covered and revascularised versus covered and not-revascularised. In cases where the LSA remained uncovered, the pooled stroke incidence was 3.2% (95% CI 1.0–6.5). There was, however, an indication that stroke incidence increased following LSA coverage, to 5.3% (95% CI 2.6–8.6) in those with a revascularisation and 8.0% (95% CI 4.1–12.9) in those without revascularisation.
Stroke incidence is an important morbidity after TEVAR, and probably increases if the LSA is covered during the procedure, particularly in those without revascularisation.
Thoracic aortic aneurysms leading to type A dissections (TAAD) can be inherited in isolation or in association with genetic syndromes, such as Marfan syndrome and Loeys-Dietz syndrome. When TAAD ...occurs in the absence of syndromic features, it is inherited in an autosomal dominant manner with decreased penetrance and variable expression, the disease is referred to as familial TAAD. Familial TAAD exhibits significant clinical and genetic heterogeneity. The first genes identified to cause TAAD were FBN1, TGFBR2, and TGFBR1. The identification and characterization of these genes suggested that increased TGF-beta signaling plays a role in pathogenesis. The recent discovery that mutations in the vascular smooth muscle cell (SMC)-specific beta-myosin (MYH11) and alpha-actin (ACTA2) can also cause this disorder has focused attention on the importance of the maintenance of SMC contractile function in preserving aortic structure and preventing TAAD.
We have reported the short-term outcomes regarding the safety of the off-the-shelf Zenith t-Branch multibranched thoracoabdominal stent-graft (William Cook Europe ApS, Bjaeverskov, Denmark) in a ...postmarket, multicenter study.
Patients who had been treated with the t-Branch device from September 2012 to November 2017 at three European centers were either prospectively or retrospectively enrolled in the present study. Device implantation and postprocedural follow-up were performed according to the standard of care at each center. The primary objectives of the present study were to assess the procedure-related mortality and morbidity at 30 days and 1 year and to assess the presence of endoleaks, device integrity, and stent-graft and branch vessel patency.
A total of 80 patients were included in the present study (mean age, 71.0 ± 7.4 years; 70.0% male). Most (n = 77) had been treated for thoracoabdominal aortic aneurysms (TAAAs) and the rest for dissection (n = 3). Most TAAAs were stable (72.7%; 56 of 77). The remaining TAAAs were symptomatic (7.8%; 6 of 77) or had a contained rupture (19.5%; 15 of 77). The t-Branch device was successfully deployed in 79 patients. In one patient, the delivery system of the device could not be advanced through the iliac artery. Within 30 days, one patient had died (1.3%). At 1 year, seven patients had died (8.8%), and no aortic rupture or conversion to open surgery had been reported. The 30-day neurologic events included stroke in three patients (3.8%), paraplegia in one (1.3%), and paraparesis in six patients (7.5%). Secondary interventions were required in nine patients (11.3%) during follow-up. Postoperative endoleaks were observed in 37 of 72 patients (51.4%), including type II endoleak in 30, type Ia in 4, and type III endoleak in 6 patients. At 1 year, endoleaks had been reported in 20 patients (16 with type II and 4 with type III). The t-Branch main body graft patency was 100% throughout the 1-year follow-up period. At 30 days after the procedure, all celiac and superior mesenteric artery branches were patent and one left renal and one right renal branch were occluded. At 1 year, occlusion had developed in three bridging stent-grafts for the celiac artery, one for the left renal artery, and two for the right renal artery.
The t-Branch device appears safe, with good 30-day and 1-year mortality and morbidity in the present study, including both stable and symptomatic cases.
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