Aortic Tortuosity Research Articles

Antegrade thoracic endovascular aortic repair using an ascending aortofemoral through-and-through wire technique for a severely tortuous aorta associated with rickets

BackgroundSevere aortic tortuosity of the access route often prevents successful complete exclusion of an aneurysm in thoracic endovascular aortic repair (TEVAR).Case presentationWe performed antegrade TEVAR on a 79-year-old man with right hemiparesis. We deployed the stent graft from the ascending aorta with a tube graft conduit to treat a descending thoracic aortic aneurysm associated with rickets and multiple comorbidities. Although the application of a ministernotomy diminished the potential advantages of endovascular treatment in view of less invasive surgery, antegrade TEVAR using an ascending aortofemoral through-and-through wire technique was a good option in this patient because a conventional retrograde approach was not feasible due to his severely tortuous aorta.ConclusionsTo avoid device-related complications, it is crucial to make a prudent preoperative decision on a patient-by-patient basis, taking into account the appropriate access site, adjuvant guidewire technique, and adjunctive surgical interventions.

The Impact of Aortic Tortuosity on Delayed Type I or III Endoleak after Endovascular Aortic Repair

Endovascular aneurysm repair (EVAR) becomes the treatment of choice for patients with abdominal aortic aneurysm (AAA). Type I or III endoleak is related to high risk of rupture and reintervention, but little is known about the delayed presentation of these. We sought to evaluate the delayed type I or III endoleak after EVAR and assess the early morphological portending factors. We retrospectively reviewed a database of 249 patients who underwent endovascular repair with a Zenith AAA stent graft (Cook Medical, Bloomington, IN) in a single institute from October 2005 to December 2013. Age, aneurysm size, angulation, tortuosity index (TI), and follow-up evaluations were recorded and analyzed. Patients having <1year of follow-up were excluded. One hundred eighteen patients were included in this study. There was no delayed type Ia endoleak. Ten patients (9.3%) were found to have a delayed type Ib or III endoleak. The mean diagnosis time was 49.1months (range, 22-91months) after EVAR. All of them were treated with endovascular repair except one had combined open revision. Three of the patients (30%) with delayed endoleaks presented with a ruptured aneurysm, and two of them (20%) died after reintervention. Postoperative TI was found to be the most significant morphological factor associated with increased risk of type Ib or III endoleak. Delayed type Ib or III endoleak was not rare in our study population and was found to have a high risk of rupture and mortality. Aneurysm tortuosity is associated with increased risk of endoleaks, and postoperative TI can be an indicator in the early period of follow-up.

Aortic knob width reflects left ventricular diastolic function assessed by gated myocardial perfusion single photon emission computed tomography in patients with normal myocardial perfusion.

Aortic knob width on chest radiography represents the extent of aortic dialation and tortuosity of the aortic arch. We tested the hypothesis that aortic knob width reflected left ventricular (LV) diastolic function assessed by gated myocardial perfusion single photon emission computed tomography (SPECT) in patients with normal myocardial perfusion. One hundred and thirty patients with preserved LV ejection fraction and normal myocardial perfusion were enrolled in this study. Aortic knob width was measured along the horizontal line from the point of the lateral edge of the trachea to the left lateral wall of the aortic knob. The peak filling rate (PFR) and the one-third mean filling rate (1/3 MFR) were obtained as LV diastolic parameters. There were 114 male and 16 female patients. Age ranged from 43 to 88 years (69.9 ± 8.9 years). Aortic knob width ranged from 24.2 to 53.4mm (37.6 ± 5.7mm). There was a significant correlation between age and aortic knob width (r = 0.34, p < 0.001). Aortic knob width was inversely correlated with both PFR (r = -0.53, p < 0.001) and 1/3 MFR (r = -0.42, p < 0.001). Multivariate linear regression analysis revealed that serum creatinine (β = -0.16, p = 0.045) and aortic knob width (β = -0.45, p < 0.001) were significant predictors of PFR, and that age (β = -0.20, p = 0.02) and aortic knob width (β = -0.33, p < 0.001) were significant predictors of 1/3 MFR. Our data suggested that aortic knob width on chest radiography was a simple marker of LV diastolic function in patients with normal myocardial perfusion.

Superior mesenteric artery syndrome - A clinicoradiologic case report

Superior mesenteric artery (SMA) syndrome is a rare cause of duodenal obstruction due to compression of the third part of duodenum between SMA and aorta. Clinical suspicion and radiological findings are playing important role in the diagnosis of SMA syndrome. We report here the clinicoradiologic findings in a case of 66-year-old Indian male. In our case, abdominal aortic tortuosity in an elderly patient was the cause for SMA syndrome.

Function of Ltbp-4L and fibulin-4 in survival and elastogenesis in mice.

ABSTRACTLTBP-4L and LTBP-4S are two isoforms of the extracellular matrix protein latent-transforming growth factor beta-binding protein 4 (LTBP-4). The mutational inactivation of both isoforms causes autosomal recessive cutis laxa type 1C (ARCL1C) in humans and an ARCL1C-like phenotype in Ltbp4−/− mice, both characterized by high postnatal mortality and severely affected elastogenesis. However, genetic data in mice suggest isoform-specific functions for Ltbp-4 because Ltbp4S−/− mice, solely expressing Ltbp-4L, survive to adulthood. This clearly suggests a requirement of Ltbp-4L for postnatal survival. A major difference between Ltbp4S−/− and Ltbp4−/− mice is the matrix incorporation of fibulin-4 (a key factor for elastogenesis; encoded by the Efemp2 gene), which is normal in Ltbp4S−/− mice, whereas it is defective in Ltbp4−/− mice, suggesting that the presence of Ltbp-4L might be required for this process. To investigate the existence of a functional interaction between Ltbp-4L and fibulin-4, we studied the consequences of fibulin-4 deficiency in mice only expressing Ltbp-4L. Resulting Ltbp4S−/−;Fibulin-4R/R mice showed a dramatically reduced lifespan compared to Ltbp4S−/− or Fibulin-4R/R mice, which survive to adulthood. This dramatic reduction in survival of Ltbp4S−/−;Fibulin-4R/R mice correlates with severely impaired elastogenesis resulting in defective alveolar septation and distal airspace enlargement in lung, and increased aortic wall thickness with severely fragmented elastic lamellae. Additionally, Ltbp4S−/−;Fibulin-4R/R mice suffer from aortic aneurysm formation combined with aortic tortuosity, in contrast to Ltbp4S−/− or Fibulin-4R/R mice. Together, in accordance with our previous biochemical findings of a physical interaction between Ltbp-4L and fibulin-4, these novel in vivo data clearly establish a functional link between Ltbp-4L and fibulin-4 as a crucial molecular requirement for survival and elastogenesis in mice.

Transradial Approach for Noncoronary Interventions: A Single-Center Review of Safety and Feasibility in the First 1,500 Cases

PurposeTo review safety and feasibility in a single center using transradial access (TRA) for noncoronary interventions. Materials and MethodsRetrospective analysis was performed of 946 patients evaluated for 1,531 consecutive TRA procedures from April 2012 to July 2015. Exclusion criteria included sheath > 6 F, Barbeau D waveform, radial artery (RA) diameter < 2 mm on ultrasound, history of severe aortic tortuosity or RA occlusion, and dialysis. TRA was attempted in 936 patients (62% men; median age, 62.4 y) who underwent 1,512 consecutive procedures (chemoembolization [n = 485], yttrium-90 mapping [n = 391] and infusion [n = 293], renal/visceral intervention [n = 172], uterine artery embolization [n = 116], peripheral intervention [n = 43], endoleak repair [n = 10], and other [n = 2]). Patients were evaluated for complications during follow-up at ~30 days. ResultsTechnical success was 98.2% (1,485/1,512). Major complications (0.13%) included pseudoaneurysm (n = 1) and seizure (n = 1). Minor complications (2.38%) included hematoma/bleeding (n = 13), RA occlusion (n = 11), arm pain (n = 6), and RA spasm (n = 6). Univariate analysis demonstrated a lower rate of adverse events in African American patients (hazard ratio [HR], 0.25; 95% confidence interval [CI], 0.07–0.86; P = .027). Twenty-seven cases (1.8%) required crossover to transfemoral access (TFA). Crossover rates were higher in female patients (P = .0055), height < 1.7 m (P = .024), renal/visceral interventions (P = .0003), and endoleak interventions (P = .0357). Multivariate analysis demonstrated intervention type to be the only significant predictor of TFA crossover (renal/visceral [HR, 4.48; 95% CI, 1.84–10.9; P = .001]; endoleak repair [HR, 9.54; 95% CI, 1.09–83.8; P = .042]). ConclusionsTRA was safe and well tolerated in a heterogeneous patient population across a range of peripheral vascular interventions.

Increased aortic tortuosity indicates a more severe aortic phenotype in adults with Marfan syndrome

BackgroundPatients with Marfan syndrome (MFS) have a highly variable occurrence of aortic complications. Aortic tortuosity is often present in MFS and may help to identify patients at risk for aortic complications. Methods3D-visualization of the total aorta by MR imaging was performed in 211 adult MFS patients (28% with prior aortic root replacement) and 20 controls. A method to assess aortic tortuosity (aortic tortuosity index: ATI) was developed and reproducibility was tested. The relation between ATI and age, and body size and aortic dimensions at baseline was investigated. Relations between ATI at baseline and the occurrence of a clinical endpoint (aortic dissection, and/or aortic surgery) and aortic dilatation rate during 3years of follow-up were investigated. ResultsATI intra- and interobserver agreements were excellent (ICC: 0.968 and 0.955, respectively). Mean ATI was higher in 28 age-matched MFS patients than in the controls (1.92±0.2 vs. 1.82±0.1, p=0.048). In the total MFS cohort, mean ATI was 1.87±0.20, and correlated with age (r=0.281, p<0.001), aortic root diameter (r=0.223, p=0.006), and aortic volume expansion rate (r=0.177, p=0.026). After 49.3±8.8months follow-up, 33 patients met the combined clinical endpoint (7 dissections) with a significantly higher ATI at baseline than patients without endpoint (1.98±0.2 vs. 1.86±0.2, p=0.002). Patients with an ATI>1.95 had a 12.8 times higher probability of meeting the combined endpoint (log rank-test, p<0.001) and a 12.1 times higher probability of developing an aortic dissection (log rank-test, p=0.003) compared to patients with an ATI<1.95. ConclusionsIncreased ATI is associated with a more severe aortic phenotype in MFS patients.

Impact on outcomes by measuring tortuosity with reporting standards for thoracic endovascular aortic repair

In this study, we assessed the association between the tortuosity of the thoracic aorta as measured by the reporting standards for thoracic endovascular aortic repair (TEVAR), described by the Society for Vascular Surgery, and midterm outcomes after TEVAR for atherosclerotic aneurysms. We analyzed 77 consecutive patients who underwent TEVAR for atherosclerotic aneurysms from November 2006 through May 2013 in a single institution. The preoperative aortic tortuosity index (TI) was calculated by computed tomography aortography, and patients were divided into low-tortuosity (TI ≤ 1.29) and high-tortuosity (TI > 1.29) groups. The relationships between TI and the occurrence of endoleaks, complications, and survival were analyzed. The mean follow-up period was 29± 26months. During this period, endoleaks occurred in 19 patients. Patients in the high-tortuosity group were at greater risk for endoleaks (odds ratio, 9.95; 95% confidence interval, 2.06-48.1; P= .004) and stroke (odds ratio, 13.2; 95% confidence interval, 1.03-169; P= .047) than those in the low-tortuosity group. The overall survival at 1, 3, and 5years was 73%, 69%, and 63%, respectively, for the high-tortuosity group and 92%, 92%, and 86%, respectively, for the low tortuosity group. Our findings demonstrated that high tortuosity of the thoracic aorta is associated with higher rates of endoleaks and lower survival in patients undergoing TEVAR for atherosclerotic aneurysms. Patients with aneurysms in a highly tortuous aorta may therefore need greater attention in preoperative planning, perioperative procedures, and follow-up examinations.

A novel application of CT angiography to detect extracoronary vascular abnormalities in patients with spontaneous coronary artery dissection

BackgroundSpontaneous coronary artery dissection (SCAD) is associated with extracoronary vascular abnormalities, which depending on type and location may warrant treatment or provide additional diagnostic or prognostic information about this uncommon entity. Fibromuscular dysplasia (FMD), aneurysms, and dissections have been detected in multiple vascular territories by magnetic resonance angiography, CT angiography (CTA), and catheter angiography. The optimal modality to detect extracoronary vascular abnormalities is unknown. We highlight the technique and feasibility of a novel CTA protocol to detect extracoronary vascular abnormalities in these patients, incorporating patient safety and convenience. MethodsThe complete CTA protocol consisting of a single CTA of the neck, chest, abdomen, and pelvis was performed on 39 SCAD outpatients. All examinations were performed with 200 mL of low-osmolar contrast agent and used radiation dose modulation techniques. Average volume CT dose index was 9 mGy for the chest, abdomen, and pelvis portions and 21 mGy for the neck portion. Studies were independently reviewed by 2 senior vascular radiologists. ResultsTwo patients had nondiagnostic CTA neck evaluation because of technical acquisition errors. Extracoronary vascular abnormalities were detected in 27 of 39 patients (69%). Catheter angiography detected brachial artery FMD in 1 patient, a vascular bed not included in the SCAD CTA protocol. Extracoronary vascular abnormalities were common, including FMD, aneurysms, dissection, and aortic tortuosity, and were seen in the iliac (36%), carotid and/or vertebral (31%), splanchnic (10%), and renal (26%) arteries and in the thoracic and/or abdominal aorta (10%). ConclusionsThe frequency of extracoronary vascular abnormalities and extent of territories identified the CTA protocol in our cohort are high. A tailored CTA may be the optimal imaging technique for detecting extracoronary vascular abnormalities in patients with suspected underlying vasculopathy. Although the clinical significance of extracoronary vascular abnormalities remains unclear, detection of these abnormalities has identified patients in whom cerebral imaging and serial monitoring have been recommended.

Absence of Cardiovascular Manifestations in a Haploinsufficient Tgfbr1 Mouse Model

Loeys-Dietz syndrome (LDS) is an autosomal dominant arterial aneurysm disease belonging to the spectrum of transforming growth factor β (TGFβ)-associated vasculopathies. In its most typical form it is characterized by the presence of hypertelorism, bifid uvula/cleft palate and aortic aneurysm and/or arterial tortuosity. LDS is caused by heterozygous loss of function mutations in the genes encoding TGFβ receptor 1 and 2 (TGFBR1 and −2), which lead to a paradoxical increase in TGFβ signaling. To address this apparent paradox and to gain more insight into the pathophysiology of aneurysmal disease, we characterized a new Tgfbr1 mouse model carrying a p.Y378* nonsense mutation. Study of the natural history in this model showed that homozygous mutant mice die during embryonic development due to defective vascularization. Heterozygous mutant mice aged 6 and 12 months were morphologically and (immuno)histochemically indistinguishable from wild-type mice. We show that the mutant allele is degraded by nonsense mediated mRNA decay, expected to result in haploinsufficiency of the mutant allele. Since this haploinsufficiency model does not result in cardiovascular malformations, it does not allow further study of the process of aneurysm formation. In addition to providing a comprehensive method for cardiovascular phenotyping in mice, the results of this study confirm that haploinsuffciency is not the underlying genetic mechanism in human LDS.

Impact of Aortorenal Morphology on Renal Artery Stent Procedures: Significance of Aortic Tortuosity and Renal Artery Derivation

To clarify the impact of aortorenal morphology on renal artery stenting procedures. A retrospective study evaluated 142 consecutive renal artery stenting procedures performed for de novo atherosclerotic renal artery stenosis in 119 patients (62 men; mean age 72±9 years, range 41-93). All procedures were done via a transfemoral approach without distal protection. Aortorenal morphology was classified into 3 types based on the relationship between abdominal aortic tortuosity and renal artery derivation. Using a straight reference line centered on the most angulated point of the inner curve of the infrarenal abdominal aorta, type 1 referred to a renal artery ostium that was more than half of the aortic diameter distance from the reference line in the greater curvature and less than half in the lesser curvature. Type 2 referred to a renal artery ostium that was less than half of the aortic diameter distant from the reference line in the greater curvature and more than half in the lesser curvature. Type 3 referred to a renal artery ostium that was beyond the reference line in the greater curvature or more than one aortic diameter from the reference line in the lesser curvature. The technical success rate, procedure time, final engagement technique, shape of the guide catheter used, and any adverse events were analyzed. Type 1 aortorenal morphology was observed in 91 cases, type 2 in 30, and type 3 in 21. All cases were successfully treated; there were no technical complications, in-hospital cardiovascular events, or deaths. Procedure time differed significantly (p<0.001) among the 3 types (type 1: 19.6±5.6 minutes, type 2: 23.3±6.8 minutes, and type 3: 32.3±9.6 minutes; p<0.05 for type 1 vs. 2, p<0.001 for type 2 vs. 3, and p<0.001 for type 1 vs. 3). There were also significant differences among types in terms of engagement technique and guide catheter shape. Aortorenal morphology was significantly associated with procedure time and the selection of engagement technique and guide catheter shape.

Aortic tortuosity predicts cardiovascular events in Marfan syndrome

Aortic tortuosity predicts cardiovascular events in Marfan syndrome

Bilateral Bochdalek hernias associated with severe aortic tortuosity and aberrant right subclavian artery

Although Bochdalek hernia is the most common congenital diaphragmatic hernia in adults, bilateral occurrence is rare. To the best of our knowledge, only case reports on Bochdalek hernia and its associated pathologies have been previously published. Herein, we present the case of a 27-year-old man with bilateral Bochdalek hernias, which were detected incidentally. The bilateral Bochdalek hernias were found to be associated with severe aortic tortuosity and aberrant right subclavian artery.

The role of diameter versus volume as the best prognostic measurement of abdominal aortic aneurysms

Accurate measurement of abdominal aortic aneurysms is necessary to predict rupture risk and, more recently, to follow aneurysm sac behavior following endovascular repair. Up until this point, aneurysm diameter has been the most common measurement utilized for these purposes. Although aneurysm diameter is predictive of rupture, accurate measurement is hindered by such factors as aortic tortuosity and interobserver variability, and it does not account for variations in morphology such as saccular aneurysms. Additionally, decreases in aneurysm diameter do not completely describe the somewhat complex remodeling seen following endovascular repair of aortic aneurysms. Measurement of aneurysm volume has the advantage of describing aneurysm morphology in a multidimensional fashion, but it has not been readily available or easily measured until recently. This has changed with the introduction of commercially available software tools that permit quicker and easier to perform volume measurements. Whether it is time for volume to replace, or compliment, diameter is the subject of the current debate.

Editors' commentary

Editors' commentary

Predicting the Risk for Acute Type B Aortic Dissection in Hypertensive Patients Using Anatomic Variables

This study sought to identify possible anatomic predictors of acute type B aortic dissection (AAD) in hypertensive patients using multidetector computed tomography angiography (CTA). Although hypertension remains one of the most significant risk factors for AAD development, it is unlikely to be the only risk factor for AAD. Few studies have assessed anatomical predictors of AAD development. CTA of normotensive patients without AAD (group 1, n = 35), hypertensive patients without AAD (group 2, n = 37), and hypertensive patients with AAD (group 3, n = 37) were compared. The length, diameter, volume, and tortuosity of the aorta as well as arch vessel angulation were measured for each patient and normalized to group 1 averages. Stepwise logistic regression identified significant anatomical associations; the model was validated based on 1,000 bootstrapped samples. The demographics of the groups were similar. The length of the proximal and entire aorta, the diameters in the proximal ascending aorta and aortic arch, and the aortic volumes were all greater (p < 0.0001, p = 0.0064 for ascending aortic diameter) in group 3 than in groups 1 and 2, as was entire aortic tortuosity (p < 0.0001). An AAD risk model was developed based on aortic arch diameter, length from the aortic root to the iliac bifurcation, and angulation of the brachiocephalic artery origin from the aorta. The bootstrap estimate of the area under the receiver operating curve was 0.974. Enlargement of the ascending aorta and aortic arch and increased aortic tortuosity reflect an aortopathy which enhances the probability of AAD. A model based on 3 anatomical variables demonstrates significant associations with AAD: it may allow identification by aortic imaging of the hypertensive patient most at risk, and permit implementation of aggressive medical management and consideration of pre-emptive surgery to prevent dissection.

Invited Commentary

Van der Linde and colleagues previously reported a new “aneurysm-osteoarthritis syndrome” [1van de Laar I.M. Oldenburg R.A. Pals G. et al.Mutations in SMAD3 cause a syndromic form of aortic aneurysms and dissections with early-onset osteoarthritis.Nat Genet. 2011; 43: 121-126Crossref PubMed Scopus (492) Google Scholar, 2Van der Linde D, Van de Laar IMBH, Bertoli-Avella AM, et al. Aggressive cardiovascular phenotype of aneurysms-osteoarthritis syndrome caused by pathogenic SMAD3 variants. J Am Coll Cardiol;60:397–403.Google Scholar, 3van de Laar I.M. van der Linde D. Oei E.H. et al.Phenotypic spectrum of the SMAD3-related aneurysms-osteoarthritis syndrome.J Med Genet. 2012; 49: 47-57Crossref PubMed Scopus (192) Google Scholar]. Their data showed that this new syndrome is inherited in an autosomal dominant pattern and is manifest in widespread arterial aneurysms and aortic tortuosity. Their previous work demonstrated a pathophysiology for this disease linked to increased transforming growth factor (TGF)-β signaling in the aortic wall. The syndrome is further characterized by early-onset osteoarthritis. The authors' identification of this new clinical entity represents an advance in our overall understanding of aneurysm disease. In their current article [4van der Linde D. Bekkers J.A. Mattace-Raso F.U.S. et al.Progression rate and early surgical experience in the new aggressive aneurysms-osteoarthritis syndrome.Ann Thorac Surg. 2013; 95: 563-569Abstract Full Text Full Text PDF PubMed Scopus (20) Google Scholar], the authors report the clinical follow-up and surgical outcomes in patients with this disease, including nine valve-sparing aortic root replacements. There was no perioperative or postoperative morbidity or mortality. The aortic tissues did not present any undue level of fragility and were amenable to surgical manipulations. As might be expected in an early clinical report of an uncommon entity, there are shortcomings in the current study. The number of patients is small, and the follow-up interval is short. Specifically, the growth rate assessments—which show aggressive and unpredictably rapid growth in some patients—must be taken with a grain of salt. Differences of only 1 or 2 millimeters in aortic size are nearly impossible to measure, even with modern advanced imaging modalities. The growth rate they calculate (2.5 mm/y) is more than double that in the general population of ascending aneurysms [5Elefteriades J.A. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks.Ann Thorac Surg. 2002; 74: S1877-S1880Abstract Full Text Full Text PDF PubMed Scopus (592) Google Scholar]. The authors found a growth rate of 20.9 mm/y in 1 patient, thus skewing the data severely. The data on changes in carotid distensibility are similarly impaired by the small number of patients and limited follow-up interval. The recommendation for early intervention is preliminary, based on “fast and unpredictable” growth in some patients. This appears a reasonable recommendation at present, but it must be corroborated as additional experience accrues. The authors suggest that the aortic behavior of these patients is similar to that of Loeys-Dietz syndrome. Indeed, the observation of other shared stigmata with Loeys-Dietz (hypertelorism [widely spaced eyes], bifid uvula, scoliosis, abnormal skin texture) makes aneurysms-osteoarthritis syndrome very reminiscent of Loeys-Dietz. Reminescent also are the dominant genetic transmission and the involvement of (TGF)-β pathways in the pathogenesis. One wonders just how clinically distinct aneurysm-osteoarthritis Syndrome is from Loeys-Dietz. We congratulate the authors for the recognition of their new syndromic manifestation of aortic disease. We appreciate their calling this “aneurysm-osteoarthritis syndrome” to the attention of the surgical audience, and their making some pertinent, but very preliminary, clinical observations and corresponding surgical recommendations. Progression Rate and Early Surgical Experience in the New Aggressive Aneurysms-Osteoarthritis SyndromeThe Annals of Thoracic SurgeryVol. 95Issue 2PreviewAneurysms-osteoarthritis syndrome (AOS), caused by SMAD3 mutations, is a recently described autosomal dominant condition characterized by aneurysms throughout the arterial tree in combination with osteoarthritis. The objective of the present study was to evaluate progression rate of aortic dilation and surgical outcome in AOS patients. Full-Text PDF

Results of high-risk endovascular procedures in patients with non-dissected thoracic aortic pathology: intermediate outcomes

To investigate mid-term outcome in patients undergoing thoracic endovascular aortic repair (TEVAR) for non-dissected aortic pathology with favourable and unfavourable landing zone and aortic anatomy. Between 2000 and 2011, TEVAR was performed in 208 patients with descending thoracic aortic disease. Of 105 patients with non-dissected thoracic aortic pathology, 69 presented with unfavourable anatomy as defined by short length (<15 mm), large diameter (>42 mm), angulation of >60° of the proximal or distal landing zone or extreme aortic tortuosity. The endpoints perioperative mortality, 1-year survival, endoleak occurrence and incidence of secondary intervention were compared with the remaining 36 patients with favourable anatomy. Median follow-up was 18 months. TEVAR was performed emergently in 24 of 69 (35%) patients with unfavourable anatomy and in 11 of 36 (31%) of those with favourable anatomy (P = 0.68). No patients underwent conversion to open surgery, no periinterventional rupture was observed. Perioperative mortality did not differ between cohorts (1/69 vs 1/36, P = 0.78). Postoperative permanent spinal cord ischaemia occurred in patients with unfavourable anatomy only (2/69 vs 0/36, P = 0.78). Early endoleak and secondary intervention were more frequent in patients with unfavourable anatomy (19/69 vs 7/36 and 13/69 vs 1/36), but not statistically significant (P = 0.5 and P = 0.13, respectively). One-year aorta-related survival rates were similar in both groups (66/69 vs 33/36, P = 0.45). Mid-term outcome after TEVAR does not differ between patients with favourable and unfavourable landing zone anatomy in terms of aorta-related survival. However, the more frequent need for secondary intervention warrants a more rigorous follow-up after TEVAR in patients with unfavourable anatomy.

Differences in Aortic Arch Tortuosity, Neck Size, and Taper in Patients With Traumatic and Aortic Disease

Differences in Aortic Arch Tortuosity, Neck Size, and Taper in Patients With Traumatic and Aortic Disease

Endovascular repair of a native postcoarctation thoracic aortic aneurysm

A 75-year-old woman was referred to our vascular unit for endovascular repair of a postcoarctation thoracic aortic aneurysm. The patient was receiving antihypertensive therapy with four drugs but had presented with several episodes of hypertensive crisis. Other comorbidities included aortic valve insufficiency, left ventricle hypertrophy, thoracic kyphosis and scoliosis, and symptomatic asthma. Aortic imaging with three-dimensional multiplanar computed tomography angiography showed a 65-mm descending thoracic aortic aneurysm. The thoracic aorta presented significant tortuosity. The coarctation lumen diameter was 8 mm (A). Endovascular technical decision making was challenging due to the unknown resistance of the postcoarctation aneurysmal aortic wall to balloon dilatation. The patient was placed under general anesthesia. Open vascular access was performed through the right common femoral and right brachial arteries and percutaneous access through the left common femoral artery. The aortic coarctation was catheterized from the right brachial access, and a 300-cm 0.035-inch ultrastiff guidewire was used to cross the coarctation in a through-and-through fashion to permit the device to pass through the aortic tortuosity. After injection of 5000 IU of heparin, a Gore TAG endograft (W. L. Gore & Associates, Flagstaff, Ariz) was deployed, with a spontaneous increase of the coarctation diameter (B and C). A second device was distally deployed 5 cm above the celiac trunk. A Gore Trilobe balloon catheter was used to seal the overlapping zone between both stent grafts and the distal landing zone. Completion angiograms showed no type I endoleaks. No proximal ballooning was performed because invasive blood pressure monitoring stated a 20% gradient. The patient’s postoperative period was uneventful. Her blood pressure stabilized with therapy with two drugs. Computed tomography imaging after 9 months showed no restenosis and aneurysm exclusion (D).