Endovascular Therapy of Spontaneous Aortocaval Fistulae Associated with Abdominal Aortic Aneurysms

León, Luis R.; Arslan, Bülent; Ley, Eleazar; Labropoulos, Nicos

doi:10.2310/6670.2007.00011

Cited by 19 publications

(13 citation statements)

References 34 publications

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“…Several reports have described successful EVAR of AAA with spontaneous aortocaval fistula. [239][240][241] Primary aortoenteric fistula. Primary aortoenteric fistula is a rare event often characterized by a classical triad of gastrointestinal bleeding, pain, and a pulsating mass that, in fact, is present in only a minority of patients.…”

Section: Unusual Aneurysmsmentioning

confidence: 99%

The care of patients with an abdominal aortic aneurysm: The Society for Vascular Surgery practice guidelines

Chaikof

Brewster

Dalman

et al. 2009

Journal of Vascular Surgery

625

520

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DEFINITION OF THE PROBLEM Purpose of these guidelinesThe Clinical Practice Council of the Society for Vascular Surgery charged a writing committee with the task of updating practice guidelines, initally published in 2003, for surgeons and physicians who are involved in the preoperative, operative, and postoperative care of patients with abdominal aortic aneurysms (AAA). 1 This document provides recommendations for evaluating the patient, including risk of aneurysm rupture and associated medical co-morbidities, guidelines for selecting surgical or endovascular intervention, intraoperative strategies, perioperative care, long-term follow-up, and treatment of late complications.Decision making related to the care of patients with AAA is complex. Aneurysms present with varying risks of rupture and patient specific factors influence anticipated life expectancy, operative risk, and the need to intervene. Careful attention to the choice of operative strategy, as influenced by anatomic features of the AAA, along with optimal treatment of medical co-morbidities is critical to achieving excellent outcomes. Moreover, appropriate postoperative patient surveillance and timely intervention in the case of a late complication is necessary to minimize subsequent aneurysm-related death or morbidity. All of these clinical decisions are determined in an environment where cost-effectiveness will ultimately dictate the ability to provide optimal care to the largest possible segment of the population. Currently available clinical data sets have been reviewed in formulating these recommendations. However, an important goal of this document is to clearly identify those areas where further clinical research is necessary. Methodology and evidenceA comprehensive review of the available clinical evidence in the literature was conducted in order to generate a concise set of recommendations. The strength of any given recommendation and the quality of evidence was scored based on the GRADE system (Table I). 2 When the benefits of an intervention outweighed its risks, or, alternatively, risks outweighed benefits, a strong recommendation was noted. However, if benefits and risks were less certain, either because of low quality evidence or because high quality evidence suggests benefits and risks are closely balanced, a weak recommendation was recorded. The quality of evidence that formed the basis of these recommendations was scored as high, moderate, or low. Not all randomized controlled trials are alike and limitations may compromise the quality of their evidence. In addition, if there is a large magnitude of effect, the quality of evidence derived from observational studies may be high. Thus, quality of evidence was scored as high when additional research is considered very unlikely to change confidence in the estimate of effect; moderate when further research is likely to have an important impact in the estimate of effect; or low when further research is very likely to change the estimate of the effect.

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Section: Unusual Aneurysmsmentioning

confidence: 99%

The care of patients with an abdominal aortic aneurysm: The Society for Vascular Surgery practice guidelines

Chaikof

Brewster

Dalman

et al. 2009

Journal of Vascular Surgery

625

520

View full text Add to dashboard Cite

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“…Although gene expression profiling in LV eccentric hypertrophy resulting from volume overload has been studied recently in an aortocaval fistula rat model (25), very little is known about the mechanisms of LV hypertrophy and extracellular matrix (ECM) remodeling associated with a more clinically common form of LV volume overload, namely AR. Aortocaval fistula models relate to a clinically rather rare complication of aortic aneurysm or secondary to abdominal trauma in humans (21). Moreover, aortocaval fistulae result in a global form of volume overload affecting all right and left heart chambers, resulting in rapid and massive congestive heart failure.…”

mentioning

confidence: 99%

Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the β-adrenergic and renin-angiotensin systems

Champetier¹,

Bojmehrani²,

Beaudoin³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the ␤-adrenergic and renin-angiotensin systems. Am J Physiol Heart Circ Physiol 296: H669 -H677, 2009. First published December 26, 2008 doi:10.1152/ajpheart.01046.2008.-Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV), which results in dilation, eccentric hypertrophy, and eventually loss of function. Little is known about the impact of AR on LV gene expression. We, therefore, conducted a gene expression profiling study in the LV of rats with acute and severe AR. We identified 64 genes that were specifically upregulated and 29 that were downregulated out of 21,910 genes after 2 wk. Of the upregulated genes, a good proportion was related to the extracellular matrix. We subsequently studied a subset of 19 genes by quantitative RT-PCR (qRT-PCR) to see if the modulation seen in the LV after 2 wk persisted in the chronic phase (after 6 and 12 mo) and found that it did persist. Knowing that the adrenergic and renin-angiotensin systems are overactivated in our animal model, we were interested to see if blocking those systems using metoprolol (25 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) and captopril (100 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) would alter the expression of some upregulated LV genes in AR rats after 6 mo. By qRT-PCR, we observed that upregulations of LV mRNA levels encoding for procollagens type I and III, fibronectin, atrial natriuretic peptide, transforming growth factor-␤2, and connective tissue growth factor were totally or partially reversed by this treatment. These observations provide a molecular rationale for a medical strategy aiming these systems in the medical treatment of AR and expand the paradigm in the study of this form of LV volume overload. heart hypertrophy; gene expression; renin-angiotensin system; adrenergic system SEVERE AORTIC VALVE REGURGITATION (AR) is associated with a long asymptomatic period during which the left ventricle (LV) progressively dilates and hypertrophies in response to a chronic volume overload. This process is accompanied by a decrease in LV function, occurrence of symptoms, and eventually heart failure (4, 7). No drug has yet been clearly shown in humans to be effective to slow LV dilation, hypertrophy, and loss of systolic function or to have any impact on morbidity or mortality in chronic AR (5, 15).At the microscopic level, AR is associated with cardiomyocyte elongation and excessive but mostly noncollagen myocardial fibrosis (fibronectin) (6, 23). Although gene expression profiling in LV eccentric hypertrophy resulting from volume overload has been studied recently in an aortocaval fistula rat model (25), very little is known about the mechanisms of LV hypertrophy and extracellular matrix (ECM) remodeling associated with a more clinically common form of LV volume overload, namely AR. Aortocaval fistula models relate to a clinically rather rare complication of aortic aneurysm or secondary to abdominal trauma in humans (21). Moreover, aortocaval ...

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“…Leon et al 7 mentions that the symptoms related to an arteriovenous fistula vary according to the size of the fistula. Patients with a small fistula could be asymptomatic.…”

Section: Discussionmentioning

confidence: 99%

Bridging stent repair of type III endoleak causing aortocaval fistula after branched aortic endovascular repair

Khan

Vasudevan

2017

Journal of Vascular Surgery Cases, Innovations and Techniques

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A 62-year-old man presented to our department with abdominal pain and diarrhea for 3 weeks on a background of previous branched endovascular repair for a thoracoabdominal aneurysm. A triple-phase computed tomography scan of his abdomen and pelvis showed a large aortocaval fistula caused by a type III endoleak from a dislodged superior mesenteric artery stent. He was successfully treated with a BeGraft (Bentley Innomed, Hechingen, Germany) by using an endovascular technique.

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Endovascular Therapy of Spontaneous Aortocaval Fistulae Associated with Abdominal Aortic Aneurysms

Cited by 19 publications

References 34 publications

The care of patients with an abdominal aortic aneurysm: The Society for Vascular Surgery practice guidelines

The care of patients with an abdominal aortic aneurysm: The Society for Vascular Surgery practice guidelines

Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the β-adrenergic and renin-angiotensin systems

Bridging stent repair of type III endoleak causing aortocaval fistula after branched aortic endovascular repair

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