Are telocytes related to maintenance of vascular homeostasis in normal and pathological aorta?

The telocyte (TC) is a new interstitial cell type described in a wide variety of organs and loose connective tissues around small vessels, but its presence in large arteries remains unexplored. TCs have small cell bodies and remarkably thin, long, moniliform processes called telopods (Tps). Using transmission electron microscopy and immunofluorescence, we identified TCs in normal human thoracic aortas and in those with aneurysm or acute dissection (TAAD). In normal aortas the TCs were distributed throughout the connective tissue of the adventitial layer, in its innermost portion and at the zone of transition with the medial layer, with their long axes oriented parallel to the external elastic lamellae, forming a three-dimensional network, without prevalence in the media layer. In contrast, TAAD TCs were present in the medial layer and in regions of neovascularization. The most important feature of the adventitia of diseased aortas was the presence of numerous contacts between TCs and stem cells, including vascular progenitor cells. Although the biologically functional correlations need to be elucidated, the morphological observations presented here provide strong evidence of the involvement of TCs in maintaining vascular homeostasis in pathological situations of tissue injury.

Effect of False Lumen Occlusion Treatment With AFX VELATM, Candy-Plug Technique for Chronic Aortic Dissection.

INTRODUCTION: We sought to examine midterm results and remodeling effect of false-lumen occlusion treatment using AFX VELA in case of chronic dissection repair. MATERIAL AND METHODS: From June 2019 to May 2022, we performed false lumen occlusion treatment using a modified Candy-Plug technique with AFX VELA on 8 chronic aortic dissection patients with a patent false lumen. We collected operative data, short-term clinical outcomes, mid-term clinical outcomes and imaging test results. We conducted follow-up examinations at postoperative, 6-month and 1-, 2- and 3-year intervals, including contrast-enhanced computed tomography to evaluate the diameter, false lumen thrombosis and any events. RESULTS: The average time from the symptom onset to the thoracic endovascular repair was 81.5 (35-155) months. The aorta showed aneurysmal dilation with an average maximum short-axis diameter of 58.9 (41-91) mm. Two cases needed emergency surgery due to rupture and impending rupture. There were no postoperative deaths. Complete thrombosis within the false lumen was achieved in 6 cases (75%), but 2 cases had incomplete thrombosis, requiring additional treatment. The mean maximum diameter showed a significant decrease at 6 months, 1 year and 2 years postoperatively compared to preoperative measurements (P < .05). CONCLUSION: We showed the results of false lumen occlusion treatment using the AFX VELA cuff. We observed favorable clinical outcomes and remodeling effects. While the long-term durability and efficacy of this technique in aortic remodeling will need to be monitored with further observation, the use of this cuff is considered a reliable approach to false lumen occlusion treatment.

Initial Thoracic Endovascular Aortic Repair vs Medical Therapy for Acute Uncomplicated Type B Aortic Dissection.

Importance: Thoracic endovascular aortic repair (TEVAR) has increasingly been used for uncomplicated type B aortic dissection (uTBAD) despite limited supporting data. Objective: To assess whether initial TEVAR following uTBAD is associated with reduced mortality or morbidity compared with medical therapy alone. Design, Setting, and Participants: This cohort study included Centers for Medicare & Medicaid Services inpatient claims data for adults aged 65 years or older with index admissions for acute uTBAD from January 1, 2011, to December 31, 2018, with follow-up available through December 31, 2019. Exposures: Initial TEVAR was defined as TEVAR within 30 days of admission for acute uTBAD. Main Outcomes and Measures: Outcomes included all-cause mortality, cardiovascular hospitalizations, aorta-related and repeated aorta-related hospitalizations, and aortic interventions associated with initial TEVAR vs medical therapy. Propensity score inverse probability weighting was used. Results: Of 7105 patients with eligible index admissions for acute uTBAD, 1140 (16.0%) underwent initial TEVAR (623 [54.6%] female; median age, 74 years [IQR, 68-80 years]) and 5965 (84.0%) did not undergo TEVAR (3344 [56.1%] female; median age, 76 years [IQR, 69-83 years]). Receipt of TEVAR was associated with region (vs South; Midwest: adjusted odds ratio [aOR], 0.66 [95% CI, 0.53-0.81]; P < .001; Northeast: aOR, 0.63 [95% CI, 0.50-0.79]; P < .001), Medicaid dual eligibility (aOR, 0.76; 95% CI, 0.63-0.91; P = .003), hypertension (aOR, 1.26; 95% CI, 1.03-1.54; P = .03), peripheral vascular disease (aOR, 1.24; 95% CI, 1.02-1.49; P = .03), and year of admission (2012, 2013, 2014, and 2015 were associated with greater odds of TEVAR compared with 2011). After inverse probability weighting, mortality was similar for the 2 strategies up to 5 years (hazard ratio [HR], 0.95; 95% CI, 0.85-1.06), as were aorta-related hospitalizations (HR, 1.12; 95% CI, 0.99-1.27), aortic interventions (HR, 1.01; 95% CI, 0.84-1.20), and cardiovascular hospitalizations (HR, 1.05; 95% CI, 0.93-1.20). In a sensitivity analysis that included deaths within the first 30 days, initial TEVAR was associated with lower mortality over a period of 1 year (adjusted HR [aHR], 0.86; 95% CI, 0.75-0.99; P = .03), 2 years (aHR, 0.85; 95% CI, 0.75-0.96; P = .008), and 5 years (aHR, 0.87; 95% CI, 0.80-0.96; P = .004). Conclusions and Relevance: In this study, 16.0% of patients underwent initial TEVAR within 30 days of uTBAD, and receipt of initial TEVAR was associated with hypertension, peripheral vascular disease, region, Medicaid dual eligibility, and year of admission. Initial TEVAR was not associated with improved mortality or reduced hospitalizations or aortic interventions over a period of 5 years, but in a sensitivity analysis that included deaths within the first 30 days, initial TEVAR was associated with lower mortality. These findings, along with cost-effectiveness and quality of life, should be assessed in a prospective trial in the US population.

Effect of Anastomosis Angles on Retrograde Perfusion and Hemodynamics of Hybrid Treatment for Thoracoabdominal Aortic Aneurysm.

BACKGROUND: Hemodynamic effects on the retrograde visceral reconstruction (RVR) for thoracoabdominal aortic aneurysms treatment by anastomotic angle remains unclear. This study aims to qualitatively and quantitatively investigate the effects of different anastomotic angles on hemodynamics and patency. METHODS: Three RVR models with 45°, 60° and 90° anastomotic angles were reconstructed respectively by manipulating apostoperative patient-specific model. The manipulated models of the RVRs were numerically simulated and analyzed in terms of hemodynamics including theinstant and cumulative patency, flow pattern and indicators based on wall shear stress (WSS). RESULTS: Although a smaller anastomotic angle may decrease the patency rate of common iliac arteries, it can improve the visceral perfusion during a cardiac cycle. More importantly, RVR with the smallest anastomotic angle experienced a minimal low time-averaged wall shear stress, high oscillatory shear index and relative residence time in the anastomosis region, whereas the largest anastomotic angle can introduce more unfavorable WSS in the graft trunk. Furthermore, a spiral flow pattern was observed in the proximal graft trunk of all three models, where no high-risk shear distribution was detected in this region. CONCLUSION: A smaller anastomotic angle may have more benefits of hemodynamic environment in RVR, especially the WSS distribution and flow pattern in the graft trunk. We may also suggest that additional stents or an extended cuff for the graft can be used to induce spiral flow intentionally, which can further improve local hemodynamic environment and long-term prognosis.

New mechanistic insights to PLOD1-mediated human vascular disease.

Heritable thoracic aortic disease and familial thoracic aortic aneurysm/dissection are important causes of human morbidity/mortality, most without identifiable genetic cause. In a family with familial thoracic aortic aneurysm/dissection, we identified a missense p. (Ser178Arg) variant in PLOD1 segregating with disease, and evaluated PLOD1 enzymatic activity, collagen characteristics and in human aortic vascular smooth muscle cells, studied the effect on function. Comparison with homologous PLOD3 enzyme indicated that the pathogenic variant may affect the N-terminal glycosyltransferase domain, suggesting unprecedented PLOD1 activity. In vitro assays demonstrated that wild-type PLOD1 is capable of processing UDP-glycan donor substrates, and that the variant affects the folding stability of the glycosyltransferase domain and associated enzymatic functions. The PLOD1 substrate lysine was elevated in the proband, however the enzymatic product hydroxylysine and total collagen content was not different, albeit despite collagen fibril narrowing and preservation of collagen turnover. In VSMCs overexpressing wild-type PLOD1, there was upregulation in procollagen gene expression (secretory function) which was attenuated in the variant, consistent with loss-of-function. In comparison, si-PLOD1 cells demonstrated hypercontractility and upregulation of contractile markers, providing evidence for phenotypic switching. Together, the findings suggest that the PLOD1 product is preserved, however newly identified glucosyltransferase activity of PLOD1 appears to be affected by folding stability of the variant, and is associated with compensatory vascular smooth muscle cells phenotypic switching to support collagen production, albeit with less robust fibril girth. Future studies should focus on the impact of PLOD1 folding/variant stability on the tertiary structure of collagen and ECM interactions.

Prognostic Implications of Bicuspid and Tricuspid Aortic Valve Phenotype on Progression of Moderate Aortic Stenosis and Ascending Aorta Dilatation.

Studies on the impact of aortic valve anatomy (bicuspid aortic valve [BAV] or tricuspid aortic valve [TAV]) on the progression of moderate aortic stenosis (AS) and ascending aorta (AA) dilatation and its prognostic implications are limited. From 1991 to 2016, 288 asymptomatic patients with moderate AS detected during index echocardiography with at least 1 year of echocardiographic follow-up were retrospectively studied. Baseline clinical and echocardiographic characteristics were compared between patients with BAV (n = 80) and patients with TAV (n = 208). Co-primary outcomes were 1-year hemodynamic and anatomic progression of AS and AA dilatation. Secondary end points were the incidence of AA rapid progressors, all-cause mortality, aortic valve replacement, and congestive heart failure. Determinants of AS progression, AA diameters, AA dilatation, and prognostic outcomes were evaluated. Similar 1-year progression of the aortic valve peak velocity, Vmax (9 ± 18 vs 9 ± 23 cm/s), mean gradient (1.5 ± 2.3 vs 1.3 ± 3.2 mm Hg), and aortic valve area (AVA) (-0.04 ± 0.09 vs -0.05 ± 0.10 cm2) were noted for BAV and TAV groups, respectively. One-year progressions of AA were similar at Valsalva (0.11 ± 0.88 vs 0.14 ± 1.10 mm) and tubular levels (0.12 ± 0.68 vs 0.30 ± 1.51 mm) in BAV and TAV groups, respectively. A trend toward increased rapid AA progression in patients with BAV (31.3%) was observed compared with patients with TAV (14.8%, p = 0.099). BAV was associated with progression of Vmax (ß = 0.17, p = 0.036), the dimensionless index (ß = -0.17, p = 0.008), and AVA (ß = -0.14, p = 0.048), but not mean gradient after adjusting for age, baseline severity indexes, gender, hypertension, diabetes, and body surface area. Although BAV was a determinant of larger baseline AA diameter, there was no significant association between BAV and AA rapid progressors. Adjusted Kaplan-Meier curves demonstrated no differences in congestive heart failure, aortic valve replacement, or mortality between valve morphology. In conclusion, there was a similar 1-year disease progression in terms of AVA, Vmax, mean gradient, and AA diameters between patients with BAV and patients with TAV. BAV was associated with a significant increase in Vmax, dimensionless index, and AVA after adjusting for important confounders. Close and prolonged follow-up is warranted in both groups of patients.

Aortic distensibility in Marfan syndrome: a potential predictor of aortic events?

OBJECTIVES: Patients with Marfan syndrome (MFS) are prone to develop aortic aneurysms due to fragmentation of elastic fibres, resulting in reduced distensibility of the aorta. Reduced distensibility was previously shown to predict progressive descending aorta dilatation. Here, we investigated longitudinal changes in distensibility, as a potential predictor of aortic events. METHODS: This retrospective study included all patients with MFS with at least four cardiac magnetic resonance examinations performed between 1996 and 2012. Aortic distensibility was assessed, in the ascending (level 1), proximal descending (level 2) and distal descending (level 3) aorta. Changes in distensibility were studied using linear mixed-effects regression models. RESULTS: In total, 35 patients with MFS (age at inclusion 28 (IQR 23-32) years, 54% men) were included. Mean aortic distensibility was already low (between 2.9×10-3/mm Hg/year and 6.4×10-3/mm Hg/year) at all levels at baseline, and significantly decreased over time at levels 2 and 3 (respectively, p=0.012 and p=0.002). The rate of distensibility loss per year (×10-3/mm Hg/year) was 0.01, 0.03 and 0.06×10-3/mm Hg at levels 1, 2 and 3, respectively. At inclusion, men exhibited very low distensibility, whereas women showed moderately reduced distensibility, gradually decreasing with age.Aortic dilatation rate at level 2 was associated with reduced aortic distensibility. However, we could not demonstrate a direct correlation between distensibility and clinical events during a follow-up of 22 years. CONCLUSION: Patients with MFS display reduced aortic distensibility already at an early age, inversely relating to aortic dilatation rate. However, in this selected patient group, distensibility seems less suitable as an individual predictor of aortic events.

Inflammasomes in the Pathophysiology of Aortic Disease.

Aortic diseases comprise aneurysms, dissections, and several other pathologies. In general, aging is associated with a slow but progressive dilation of the aorta, along with increased stiffness and pulse pressure. The progression of aortic disease is characterized by subclinical development or acute presentation. Recent evidence suggests that inflammation participates causally in different clinical manifestations of aortic diseases. As of yet, diagnostic imaging and surveillance is mainly based on ultrasonography, computed tomography (CT), and magnetic resonance imaging (MRI). Little medical therapy is available so far to prevent or treat the majority of aortic diseases. Endovascular therapy by the introduction of covered stentgrafts provides the main treatment option, although open surgery and implantation of synthetic grafts remain necessary in many situations. Because of the risks associated with surgery, there is a need for identification of pharmaceutical targets interfering with the pathophysiology of aortic remodeling. The participation of innate immunity and inflammasome activation in different cell types is common in aortic diseases. This review will thus focus on inflammasome activities in vascular cells of different chronic and acute aortic diseases and discuss their role in development and progression. We will also identify research gaps and suggest promising therapeutic targets, which may be used for future medical interventions.

Single vs Serial Assessments of Arterial Hemodynamics to Predict Thoracic Aortic Aneurysm Expansion.

BACKGROUND: Thoracic aortic aneurysm (TAA) is a highly morbid disease. We have previously shown that baseline hemodynamic measures reflecting aortic function are associated with future TAA expansion. However, whether serial arterial hemodynamic assessment further improves TAA growth assessment remains unknown. Therefore, we aimed to compare single vs serial arterial hemodynamic assessments in the evaluation of future TAA growth. METHODS: Eighty-six unoperated participants with TAA underwent noninvasive arterial hemodynamic assessment using arterial tonometry and echocardiography at baseline and after 1 year. Aortic diameter was measured serially with the use of standard imaging modalities. Stepwise multivariable linear regression was used to assess associations of baseline and 1-year change (Δ) in arterial hemodynamic measures with TAA growth. RESULTS: Mean age was 62.7 ± 11.0 years; 79% were male. Mean aneurysm growth was 0.48 ± 0.54 mm/year after a follow-up of 2.96 ± 1.03 years. Yearly changes in arterial hemodynamic measures ranged from -3.2% to +4.2%. Linear regression results showed that while baseline arterial hemodynamic measures were independently associated with aneurysm growth (carotid-femoral pulse wave velocity: ß ± SE = 0.038 ± 0.013; aortic characteristic impedance: ß ± SE = 0.002 ± 0.001; proximal aortic compliance: ß ± SE = -0.011 ± 0.006; forward pressure wave amplitude: ß ± SE 0.009 ± 0.002; reflected pressure wave amplitude: ß ± SE = 0.017 ± 0.006; P < 0.05 for each), the 1-year Δ in these measures did not incrementally add to aneurysm growth assessment (P > 0.05 for each Δ). CONCLUSIONS: Although baseline measures of aortic function independently predict TAA expansion, 1-year changes in these measures do not improve this prediction. Thus, for TAA risk assessment purposes, a baseline assessment of aortic function may suffice, which simplifies its use for potential predictive algorithms.

Evaluation of physician-modified endografts for the treatment of thoraco-abdominal and pararenal aortic pathologies at a single institution.

BACKGROUND: This study aimed to describe the outcomes of high-risk patients with symptomatic or impending ruptured pararenal aneurysm and thoraco-abdominal aortic aneurysm with comorbidities unsuitable for conventional open surgery, using physician-modified endografts (PMEGs). METHODS: A single-center retrospective analysis was conducted on 59 patients (mean age: 75 years; 47 males) treated with PMEGs between 2017 and 2020. Data on baseline characteristics, procedures, and clinical follow-up were collected to retrospectively analyze early (technical success, perioperative mortality, and major adverse events) and late (patency, endoleak, intervention, aneurysm thrombosis, and survival) outcomes. RESULTS: Technical success was achieved in 96.6% (57/59) of cases. The 30-day mortality rate was 5.1% (3/59). Five patients suffered renal failure and required temporary or permanent dialysis, one developed respiratory failure, and one suffered bowel ischemia. The major stroke rate was 3.4%, the spinal cord injury rate was 0%, and the myocardial infarction rate was 3.4%. During a mean follow-up period of 18.8±9.2 months, one patient suffered upper gastrointestinal bleeding and died after 7 postoperative months. Primary branch patency was observed in 97.2% of target vessels. Estimated freedom from reintervention was 88.1% and 87.5% at 6 months and 1 year, respectively. Five cases of endoleak (one type I, one type II, and three type III) were detected, and 7.1% required reintervention. The aneurysmal lumen thrombosis rate at 1 year was 89.6%. The estimated overall survival rate was 94.9% and 92.9% at 6 and 12 months, respectively. CONCLUSIONS: When used by experienced teams under appropriate anatomical conditions, PMEGs are a safe and effective alternative to open surgery. However, further technical advancement and larger studies with long-term follow-up periods are warranted.

MicroRNAs involve in bicuspid aortic aneurysm: pathogenesis and biomarkers.

The incidence of bicuspid aortic valves (BAV) is high in the whole population, BAV-related thoracic aortic aneurysm (TAA) is accompanied by many adverse vascular events. So far, there are two key points in dealing with BAV-related TAA. First is fully understanding on its pathogenesis. Second is optimizing surgical intervention time. This review aims to illustrate the potential role of miRNAs in both aspects, that is, how miRNAs are involved in the occurrence and progression of BAV-related TAA, and the feasibilities of miRNAs as biomarkers.

Population-Based Risk Factors for Ascending, Arch, Descending, and Abdominal Aortic Dilations for 60-74-Year-Old Individuals.

BACKGROUND: Aortic dilations (ectasias and aneurysms) may occur on any segment of the aorta. Pathogenesis varies between locations, suggesting that etiology and risk factors may differ. Despite this discrepancy, guidelines recommend screening of the whole aorta if 1 segmental dilation is discovered. OBJECTIVES: The purpose of this study was to determine the most dominant predictors for dilations at the ascending, arch, descending, and abdominal part of the aorta, and to establish comprehensive risk factor profiles for each aortic segment. METHODS: Individuals aged 60-74 years were randomly selected to participate in DANCAVAS I+II (Danish Cardiovascular Multicenter Screening Trials). Participants underwent cardiovascular risk assessments, including blood samples, blood pressure readings, medical records, and noncontrast computed tomography scans. Adjusted odds ratios for potential risk factors of dilations were estimated by multivariate logistic analyses. RESULTS: The study population consisted of 14,989 participants (14,235 men, 754 women) with an average age of 68 ± 4 years. The highest adjusted odd ratios for having any aortic dilation were observed when coexisting aortic dilations were present. Other noteworthy predictors included coexisting iliac dilations, hypertension, increasing body surface area, male sex, familial disposition, and atrial fibrillation, which were present in various combinations for the different aortic parts. Smoking and acute myocardial infarction were inversely associated with ascending and abdominal dilations. Diabetes was a shared protective factor. CONCLUSIONS: Risk factors differ for aortic dilations between locations. The most dominant predictor for having a dilation at any aortic segment is the presence of an aortic dilation elsewhere. This supports current guidelines when recommending a full screening of the aorta if a focal aortic dilation is discovered.

Novel LOX Variants in Five Families with Aortic/Arterial Aneurysm and Dissection with Variable Connective Tissue Findings.

Thoracic aortic aneurysm and dissection (TAAD) is a major cause of cardiovascular morbidity and mortality. Loss-of-function variants in LOX, encoding the extracellular matrix crosslinking enzyme lysyl oxidase, have been reported to cause familial TAAD. Using a next-generation TAAD gene panel, we identified five additional probands carrying LOX variants, including two missense variants affecting highly conserved amino acids in the LOX catalytic domain and three truncating variants. Connective tissue manifestations are apparent in a substantial fraction of the variant carriers. Some LOX variant carriers presented with TAAD early in life, while others had normal aortic diameters at an advanced age. Finally, we identified the first patient with spontaneous coronary artery dissection carrying a LOX variant. In conclusion, our data demonstrate that loss-of-function LOX variants cause a spectrum of aortic and arterial aneurysmal disease, often combined with connective tissue findings.

Association of hemodynamic factors and progressive aortic dilatation following type A aortic dissection surgical repair.

Type A aortic dissection (TAAD) involves the ascending aorta or the arch. Acute TAAD usually requires urgent replacement of the ascending aorta. However, a subset of these patients develops aortic rupture due to further dilatation of the residual dissected aorta. There is currently no reliable means to predict the risk of dilatation following TAAD repair. In this study, we performed a comprehensive morphological and hemodynamic analysis for patients with and without progressive aortic dilatation following surgical replacement of the ascending aorta. Patient-specific models of repaired TAAD were reconstructed from post-surgery computed tomography images for detailed computational fluid dynamic analysis. Geometric and hemodynamic parameters were evaluated and compared between patients with stable aortic diameters (N = 9) and those with aortic dilatation (N = 8). Our results showed that the number of re-entry tears and true/false lumen pressure difference were significantly different between the two groups. Patients with progressive aortic dilatation had higher luminal pressure difference (6.7 [4.6, 10.9] vs. 0.9 [0.5, 2.3] mmHg; P = 0.001) and fewer re-entry tears (1.5 [1, 2.8] vs. 5 [3.3, 7.5]; P = 0.02) compared to patients with stable aortic diameters, suggesting that these factors may serve as potential predictors of aneurysmal dilatation following surgical repair of TAAD.

Anticoagulation and antiplatelet medications do not affect aortic remodeling after thoracic endovascular aortic repair for type B aortic dissection.

OBJECTIVE: 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). METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.