scholarly journals Postoperative Aortic Neck Dilation: Myth or Fact?

2018 ◽  
Vol 27 (02) ◽  
pp. 110-113 ◽  
Author(s):  
A.S. Ribner ◽  
A.K. Tassiopoulos

AbstractThe abdominal aorta is the most common site of an aortic aneurysm. The visceral and most proximal infrarenal segment (aneurysm neck) are usually spared and considered more resistant to aneurysmal degeneration. However, if an abdominal aortic aneurysm (AAA) is left untreated, the natural history of the aortic neck is progressive dilatation and shortening. This may have significant implications for patients undergoing endovascular repair of AAAs (EVAR) as endograft stability and integrity of the repair are dependent on an intact proximal seal zone. Compromised seal zones, caused by progressive diameter enlargement and foreshortening of the aortic neck, may lead to distal endograft migration, type Ia endoleak, aortic sac repressurization, and, ultimately, aortic rupture.

Vascular ◽  
2021 ◽  
pp. 170853812110528
Author(s):  
Chong Li ◽  
Katherine Teter ◽  
Caron Rockman ◽  
Karan Garg ◽  
Neal Cayne ◽  
...  

Objective Contemporary commercially available endovascular devices for the treatment of abdominal aortic aneurysm (AAA) include standard endovascular aortic repair (sEVAR) or fenestrated EVAR (fEVAR) endografts. However, aortic neck dilatation (AND) can occur in nearly 25% of patients following EVAR, resulting in loss of proximal seal with risk of aortic rupture. AND has not been well characterized in fEVAR, and direct comparisons studying AND between fEVAR and sEVAR have not been performed. This study aims to analyze AND in the infrarenal and suprarenal aortic segments, including seal zone, and quantify sac regression following fEVAR implantation compared to sEVAR. Method A retrospective review of prospectively collected data on 20 consecutive fEVAR patients (Cook Zenith® Fenestrated) and 20 sEVAR (Cook Zenith®) patients was performed. Demographic data, anatomic characteristics, procedural details, and clinical outcome were analyzed. Pre-operative, post-operative (1 month), and longest follow-up CT scan at an average of 29.3 months for fEVAR and 29.8 months for sEVAR were analyzed using a dedicated 3D workstation (iNtuition, TeraRecon Inc, Foster City, California). Abdominal aortic aneurysm neck diameter was measured in 5 mm increments, ranging from 20 mm above to 20 mm below the lowest renal artery. Sub-analysis comparing the fEVAR to the sEVAR group at 12 months and at greater than 30 months was performed. Standard statistical analysis was done. Results Demographic characteristics did not differ significantly between the two cohorts. The fEVAR group had a larger mean aortic diameter at the lowest renal artery, shorter infrarenal aortic neck length, increased prevalence of nonparallel neck shape, and longer AAA length. On follow-up imaging, the suprarenal aortic segment dilated significantly more at all locations in the fEVAR cohort, whereas the infrarenal aortic neck segment dilated significantly less compared to the sEVAR group. Compared to the sEVAR cohort, the fEVAR patients demonstrated significantly greater positive sac remodeling as evident by more sac diameter regression, and elongation of distance measured from the celiac axis to the most cephalad margin of the sac. Device migration, endoleak occurrence, re-intervention rate, and mortalities were similar in both groups. Conclusion Compared to sEVAR, patients undergoing fEVAR had greater extent of suprarenal AND, consistent with a more diseased native proximal aorta. However, the infrarenal neck, which is shorter and also more diseased in fEVAR patients, appears more stable in the post-operative period as compared to sEVAR. Moreover, the fEVAR cohort had significantly greater sac shrinkage and improved aortic remodeling. The suprarenal seal zone in fEVAR may result in a previously undescribed increased level of protection against infrarenal neck dilatation. We hypothesize that the resultant decreased endotension conferred by better seal zone may be responsible for a more dramatic sac shrinkage in fEVAR.


2019 ◽  
Vol 53 (7) ◽  
pp. 599-601
Author(s):  
Pagliariccio Gabriele ◽  
Gatta Emanuele ◽  
Carlo Grilli Cicilioni ◽  
Schiavon Sara ◽  
Carbonari Luciano

Introduction: A 90-year-old patient was admitted with a hemorrhagic shock from a huge ruptured abdominal aortic aneurysm with an unfavourable infrarenal aortic neck and a horseshoe kidney (HSK). Report: We decided on an open surgical approach: the HSK isthmus was sectioned with an Endo GIA 45 mm, and we performed a suprarenal aortic cross-clamping and an aortic graft reconstruction. Postoperatively, no urinary leakage was detected, and renal function showed no impairment. The patient died on the 10th postoperative day from pneumonia. Conclusion: We believe that the sectioning of the HSK isthmus with Endo GIA is a fast and simple maneouvre.


2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier

Introduction: Abdominal aortic aneurysm is a devastating disease since it can lead to aortic rupture and instantaneous death. We previously demonstrated that IL-6 secreted from the aortic wall is necessary for the development of abdominal aortic aneurysm and dissection (AAD). Since IL-6 is a NF-kB/RelA dependant gene, we investigated the role of aortic wall- NF-kB/RelA signaling in the development of AAD. Methods and Results: To test the role of aortic wall-RelA, we utilized Cre-Lox technology to delete RelA from aortic cells. Tamoxifen-inducible, Col1a2-promoter driven Cre mice (Col1a2-Cre) were crossed with mT/mG Cre-reporter mice to determine which aortic cells undergo genetic recombination after Cre activation. Flow cytometry analysis of the aortic wall indicated that 88% of the genetically recombined cells were SMCs and 8% were fibroblasts. Next, RelA floxed (RelA f/f) mice, generated in our lab, were crossed with Col1a2-Cre mice. RelA f/f Cre+ and RelA f/f Cre- were stimulated with tamoxifen for 10 days to generate aortic-RelA deficient (Ao-RelA-/-) or wild-type (Ao-RelA+/+) transgenics. Flow cytometry, qRT-PCR, and immunohistochemistry analysis suggested a depletion of aortic-RelA greater than 60%. To test the role of Ao-RelA in AAD, Ao-RelA -/- (n= 20) and Ao-RelA +/+ (n=14) mice were infused with angiotensin II for 7 days. Surprisingly, 20% of Ao-RelA-/- mice died from development of AAD and aortic rupture while no deaths were observed in Ao-RelA+/+ group. In addition, 40% of Ao-RelA-/- mice developed AAD compared to 14% of Ao-RelA+/+ mice. There was no significant difference in TUNEL staining or ERTR7+ fibroblast population between the two groups. Conclusion: Our studies suggest that aortic wall-RelA may be necessary for protection from AAD.


2011 ◽  
Vol 93 (4) ◽  
pp. e1-e2 ◽  
Author(s):  
Rachael O Forsythe ◽  
Victoria Lavin ◽  
Simon CA Fraser ◽  
Alan McNeill

Abdominal aortic aneurysm (AAA) rupture commonly presents with abdominal or lower back pain and haemodynamic instability. There have been case reports of co-existing left testicular pain; however, very few cases describe right testicular pain as the sentinel symptom. We discuss the case of a 75-year-old man who presented to the on-call urologists with a 6-day history of right testicular pain. On examination, a painless AAA was detected. The patient was stable and a CT scan demonstrated a large AAA extending into the right iliac vessels, with suggestion of leakage. Attempted emergency repair was unsuccessful and the patient died in theatre. This atypical presentation of occult aneurysm leak highlights the need for clinical vigilance in the older patient with seemingly benign groin symptoms, including isolated right testicular pain.


1984 ◽  
Vol 01 (3) ◽  
pp. 429-433 ◽  
Author(s):  
Patrick J. O'Hara ◽  
Gregory P. Borkowski ◽  
Norman R. Hertzer ◽  
Peter B. O'Donovan ◽  
Susan L. Brigham ◽  
...  

BMJ Open ◽  
2019 ◽  
Vol 9 (7) ◽  
pp. e027291
Author(s):  
Wing Cheuk Chan ◽  
Dean Papaconstantinou ◽  
Doone Winnard ◽  
Gary Jackson

ObjectivesTo describe the proportions of people dying from abdominal aortic aneurysm (AAA) who might have benefited from a formal screening programme for AAA.DesignRetrospective cross-sectional review of deaths.Setting and study populationsAll AAA deaths registered in New Zealand from 2010 to 2014 in the absence of a national AAA screening programme.Main outcome measuresKnown history of AAA prior to the acute event leading to AAA death, prognosis limiting comorbidities, history of prior abdominal imaging and a validated multimorbidity measure (M3-index scores).Results1094 AAA deaths were registered in the 5 years between 2010 and 2014 in New Zealand. Prior to the acute AAA event resulting in death, 31.3% of the cohort had a known AAA diagnosis, and 10.9% had a previous AAA procedure. On average, the AAA diagnosis was known 3.7 years prior to death. At least 77% of the people dying from AAA also had one or more other prognosis limiting diagnosis. The hazard of 1-year mortality associated with the non-AAA related comorbidities for the AAA cohort aged 65 or above were 1.5–2.6 times higher than to the age matched general population based on M3-index scores. In 2014, overall AAA deaths accounted for only 0.7% of total deaths, and 1.0% of deaths among men aged 65 or above in New Zealand. At most, 20% of people dying from AAA in New Zealand between 2010 and 2014 might have had the potential to derive full benefit from a screening programme. About 51% of cases would have derived no or very limited benefit from a screening programme.ConclusionFalling AAA mortality, and high prevalence of competing comorbidities and/or prior AAA diagnosis and procedure raises the question about the likely value of a national AAA screening programme in a country such as New Zealand.


2019 ◽  
Vol 116 (26) ◽  
pp. 13006-13015 ◽  
Author(s):  
Wang Wang ◽  
Mengcheng Shen ◽  
Conrad Fischer ◽  
Ratnadeep Basu ◽  
Saugata Hazra ◽  
...  

Abdominal aortic aneurysm (AAA) remains the second most frequent vascular disease with high mortality but has no approved medical therapy. We investigated the direct role of apelin (APLN) in AAA and identified a unique approach to enhance APLN action as a therapeutic intervention for this disease. Loss of APLN potentiated angiotensin II (Ang II)-induced AAA formation, aortic rupture, and reduced survival. Formation of AAA was driven by increased smooth muscle cell (SMC) apoptosis and oxidative stress inApln−/yaorta and in APLN-deficient cultured murine and human aortic SMCs. Ang II-induced myogenic response and hypertension were greater inApln−/ymice, however, an equivalent hypertension induced by phenylephrine, an α-adrenergic agonist, did not cause AAA or rupture inApln−/ymice. We further identified Ang converting enzyme 2 (ACE2), the major negative regulator of the renin-Ang system (RAS), as an important target of APLN action in the vasculature. Using a combination of genetic, pharmacological, and modeling approaches, we identified neutral endopeptidase (NEP) that is up-regulated in human AAA tissue as a major enzyme that metabolizes and inactivates APLN-17 peptide. We designed and synthesized a potent APLN-17 analog, APLN-NMeLeu9-A2, that is resistant to NEP cleavage. This stable APLN analog ameliorated Ang II-mediated adverse aortic remodeling and AAA formation in an established model of AAA, high-fat diet (HFD) inLdlr−/−mice. Our findings define a critical role of APLN in AAA formation through induction of ACE2 and protection of vascular SMCs, whereas stable APLN analogs provide an effective therapy for vascular diseases.


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