Isolated Abdominal Aortic Rupture in a Child due to All-Terrain Vehicle Accident

BAAI is a rare but challenging traumatic lesion. Since BAAI is difficult to suspect and diagnose, frequently lethal and associated to multiorgan injuries, its management is objective of research and discussion. REBOA is an accepted practice in ruptured abdominal aortic aneurysm. Conversely, blunt aortic injuries are the currently most cited contraindications for the use of REBOA in trauma, together with thoracic lesions. We reported a case of BAAI safely managed in our Trauma Center at Maggiore Hospital in Bologna (Italy) utilizing REBOA as a bridge to endovascular repair, since there were no imminent indications for laparotomy. Despite formal contraindication to placing REBOA in aortic rupture, we hypothesized that this approach could be feasible and relatively safe when introduced in a resuscitative damage control protocol.

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Abstract 283: Platelet Inhibition Increases Angiotensin II-induced Abdominal Aortic Aneurysm Incidence and Rupture in Mice

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.33.suppl_1.a283 ◽

2013 ◽

Vol 33 (suppl_1) ◽

Author(s):

A. Phillip Owens ◽

Yacine Boulaftali ◽

Wolfgang Bergmeier ◽

James P Luyendyk ◽

Nigel Mackman

Keyword(s):

Angiotensin Ii ◽

Mouse Model ◽

Milk Fat ◽

Aortic Rupture ◽

Plasma Cholesterol ◽

Dabigatran Etexilate ◽

Aortic Aneurysms ◽

Thrombin Inhibitor ◽

Drug Bioavailability ◽

Abdominal Aortic

Objective Platelets play a central role in both hemostasis and thrombosis. The coagulation protease thrombin activates platelets by cleavage of protease-activated receptors (PAR1 and PAR4 in humans, and PAR3 and PAR4 in mice). Circulating thrombin is increased in patients with abdominal aortic aneurysms (AAAs). We recently demonstrated that PAR4 deficiency in mice increased the incidence of aneurysm (P = 0.001) and rupture-induced death (P = 0.003) in an angiotensin II (AngII) infusion model of AAA. Furthermore, platelet depletion significantly increased rupture in this model (P = 0.048). The purpose of this study was to examine clinically used anti-platelet drugs in this mouse model of AAA. Methods and Results Male Ldlr -/- mice (8-12 weeks in age) were fed a fat and cholesterol-enriched diet (21% milk fat, 0.2% cholesterol). Groups of mice received either aspirin (30 mg/L via drinking water [ASA]), or diet supplemented with the direct thrombin inhibitor dabigatran etexilate (10 g/kg chow [DE]) or the P2Y 12 inhibitor clopidogrel (50 mg/kg/day [Plavix]) 1 week prior to and throughout AngII (1,000 ng/kg/min) infusion for 28 days. Drug bioavailability was confirmed with all treatments. Medial diameters in the suprarenal aortic region were increased significantly from baseline to day 28 in all groups infused with AngII, as measured by in vivo ultrasound. Medial diameters were not different in any of the treatment groups compared with placebo controls. However, DE (87% vs. 47%) and Plavix (82% vs. 40%) significantly increased the incidence of AAA versus placebo groups (P < 0.05). ASA also increased the incidence of AAA (93% vs. 70% P = NS). Importantly, all treatments had a significant increase in aortic rupture-induced death versus placebo groups (P < 0.05; DE [67% vs. 7%]; Plavix [41% vs. 0%]; and ASA [64% vs. 10%]). None of the treatments affected total plasma cholesterol, lipoprotein-cholesterol distributions, or AngII-induced increases in systolic blood pressure. Conclusion This study indicates that the presence of functional platelets reduces the formation and rupture of AAA in this mouse model. This suggests that inhibition of platelet function may be detrimental to patients with existing AAAs, a conclusion that will be addressed in future mouse studies.

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A case of traumatic thoracic aorta rupture - A life threatening emergency

Journal of Cardiovascular and Thoracic Research ◽

10.15171/jcvtr.2019.41 ◽

2019 ◽

Vol 11 (3) ◽

pp. 248-250

Author(s):

Rupesh Kumar ◽

Javid Raja ◽

Ganesh Kumar Munirathinam ◽

Anand Kumar Mishra ◽

Rana Sandeep Singh ◽

...

Keyword(s):

Motor Vehicle ◽

Motor Vehicle Accident ◽

Aortic Rupture ◽

Medical Attention ◽

Vehicle Accident ◽

Complete Tear ◽

Life Threatening ◽

Injury Treatment ◽

Aorta Rupture ◽

Aortic Transection

Traumatic aortic transection is a life threatening emergency where there is a near-complete tear through all the layers of the aorta due to trauma. This condition is most often lethal and requires immediate medical attention. Symptoms of an aortic rupture may include severe chest pain, back pain, abdominal pain and signs of external chest injury. Treatment should be prompt in hemodynamically unstable patient in the form of endovascular or open surgical technique. We present a twenty nine year old male with aortic transection following motor vehicle accident where an interposition tube graft was placed after trimming the lacerated segments of the aorta under cardiopulmonary bypass. The patient is doing well with two years of follow up at our institution.

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GSDMD Deficiency Protects Against Aortic Rupture

10.1101/2021.01.08.425983 ◽

2021 ◽

Author(s):

Dien Ye ◽

Deborah Howatt ◽

Zhenyu Li ◽

Alan Daugherty ◽

Hong S. Lu ◽

...

Keyword(s):

Drinking Water ◽

Viral Vectors ◽

Aortic Rupture ◽

Initial Study ◽

Aortic Aneurysms ◽

Aortic Dilation ◽

Abdominal Aortic ◽

Aortic Pathologies ◽

Deficient Mice ◽

Macrophage Accumulation

Objective: Aortic ruptures are fatal consequences of aortic aneurysms with macrophage accumulation being a hallmark at the site of ruptures. Pyroptosis is critical in macrophage-mediated inflammation. This study determined effects of pyroptosis on aortic dilation and rupture using GSDMD deficient mice. Approach and Results: In an initial study, male Gsdmd+/+ and Gsdmd-/- mice in C57BL/6J background (8 to 10 weeks old) were infected with adeno-associated viral vectors encoding mouse PCSK9D377Y gain-of-function mutation and fed a Western diet to induce hypercholesterolemia. After two weeks of AAV infection, angiotensin II (AngII, 1,000 ng/kg/min) was infused. During the 4 weeks of AngII infusion, 5 of 13 Gsdmd+/+ mice died of aortic rupture, whereas no aortic rupture occurred in Gsdmd-/- mice. In surviving mice, no differences in either ascending or abdominal aortic dilation were observed between Gsdmd+/+ and Gsdmd-/- mice. To determine whether protection of GSDMD deficiency against aortic rupture is specific to AngII infusion, we subsequently examined aortic pathologies in mice administered beta-aminopropionitrile (BAPN). BAPN (0.5% wt/vol) was administered in drinking water to male Gsdmd+/+ and Gsdmd-/- mice (4 weeks old) for 4 weeks. Six of 13 Gsdmd+/+ mice died of aortic rupture, whereas no aortic rupture occurred in Gsdmd-/- mice. In mice survived, no differences of diameters in the ascending, arch, or abdominal aortic regions were observed between Gsdmd+/+ and Gsdmd-/- mice. Conclusions: GSDMD deficiency protects against AngII or BAPN-induced aortic ruptures in mice.

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Traumatic abdominal aortic rupture treated by endovascular stent placement in an 11-year-old boy

Journal of Pediatric Surgery Case Reports ◽

10.1016/j.epsc.2013.03.010 ◽

2013 ◽

Vol 1 (4) ◽

pp. 56-59 ◽

Cited By ~ 3

Author(s):

Véronique Andrey ◽

Vincent Bettschart ◽

Nicolas Ducrey ◽

Christophe Constantin ◽

Bernard Genin

Keyword(s):

Stent Placement ◽

Aortic Rupture ◽

Endovascular Stent ◽

Abdominal Aortic ◽

Endovascular Stent Placement

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Abstract 522: TGF-beta Neutralization Augments Development of Angiotensin II-induced Aneurysms in Both Ascending and Abdominal Aortic Regions

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.33.suppl_1.a522 ◽

2013 ◽

Vol 33 (suppl_1) ◽

Author(s):

Xiaofeng Chen ◽

Debra L Rateri ◽

Deborah A Howatt ◽

Anju Balakrishnan ◽

Jessica J Moorleghen ◽

...

Keyword(s):

Angiotensin Ii ◽

Transforming Growth Factor Beta ◽

Neutralizing Antibodies ◽

Transforming Growth Factor ◽

Aortic Rupture ◽

Neutralizing Antibody ◽

Normal Diet ◽

Aortic Aneurysms ◽

Tgf Beta ◽

Abdominal Aortic

Introduction and Objectives Angiotensin II (AngII) infusion induces ascending and abdominal aortic aneurysms (AAs) in mice. In a mouse model of Marfan Syndrome expressing Fbn1 C1039G/+ , ascending AAs were reduced by administration of a transforming growth factor-beta (TGF-beta) neutralizing antibody. In contrast, administration of TGF-beta neutralizing antibodies to AngII-infused mice increased aortic rupture. The purpose of this study was to compare the effects of TGF-beta neutralization on formation and progression of AngII-induced ascending and abdominal AAs. Methods and Results Male C57BL/6 mice were fed a normal diet and infused subcutaneously with AngII (1,000 ng/kg/min). Five days prior to initiating infusion, mice were injected i.p. with either a mouse monoclonal TGF-beta antibody (1D11) or an isotype matched IgG at a dose of either 0.3 or 5 mg/kg x 3/per week. 1D11 administration significantly decreased serum TGF-beta concentrations. TGF-beta neutralization at 5 mg/kg greatly increased the incidence of aortic rupture, which was attributed to rupture in both the ascending and abdominal regions. For mice that remained viable after 28 days of infusion, there were equivalent increases in aortic dilation in both the ascending and abdominal regions. Prior to rupture, aortic diameters determined by ultrasound demonstrated no significant effect on AngII-induced dilation of the ascending or abdominal aorta. We also studied the effects of TGF-beta neutralization in mice with established AngII-induced AAs following AngII-infusion for 28 days. C57BL/6 mice were injected with the mouse TGF-beta neutralizing antibody or IgG control (5 mg/kg x 3/per week, n=10 per group), while AngII infusion was continued for a further 28 days. Although TGF-beta antibody administration significantly decreased serum TGF-beta concentrations in mice with established AAs, there was no effect on aortic rupture or dilation of either the ascending or abdominal aortic region. Conclusion TGF-beta inhibition augmented AngII-induced aortic rupture in both the ascending and abdominal regions but had no effect on dilation. Furthermore, TGF-beta neutralization had no effect on either aortic rupture or expansion in established AAs.

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Abstract 667: The Role of Aortic Wall-Nuclear Factor- kappa B (NF-kB) Signaling in Formation of Dissecting Aortic Aneurysms

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.35.suppl_1.667 ◽

2015 ◽

Vol 35 (suppl_1) ◽

Author(s):

Talha Ijaz ◽

Hong Sun ◽

Adrian Recinos ◽

Ronald G Tilton ◽

Allan R Brasier

Keyword(s):

Flow Cytometry ◽

Abdominal Aortic Aneurysm ◽

Aortic Aneurysm ◽

Aortic Wall ◽

Aortic Rupture ◽

Aortic Aneurysms ◽

Tunel Staining ◽

Abdominal Aortic ◽

Significant Difference

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.

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An Abdominal Aortic Rupture Due to Seatbelt Blunt Injury: Report of a Case

Surgery Today ◽

10.1007/s00595-006-3314-6 ◽

2006 ◽

Vol 37 (1) ◽

pp. 86-88 ◽

Cited By ~ 11

Author(s):

Takaki Sugimoto ◽

Atsushi Omura ◽

Takashi Kitade ◽

Hideyuki Takahashi ◽

Takashi Koyama ◽

...

Keyword(s):

Aortic Rupture ◽

Blunt Injury ◽

Abdominal Aortic

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Apelin protects against abdominal aortic aneurysm and the therapeutic role of neutral endopeptidase resistant apelin analogs

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1900152116 ◽

2019 ◽

Vol 116 (26) ◽

pp. 13006-13015 ◽

Cited By ~ 13

Author(s):

Wang Wang ◽

Mengcheng Shen ◽

Conrad Fischer ◽

Ratnadeep Basu ◽

Saugata Hazra ◽

...

Keyword(s):

Abdominal Aortic Aneurysm ◽

Aortic Aneurysm ◽

Aortic Rupture ◽

Critical Role ◽

Neutral Endopeptidase ◽

Negative Regulator ◽

Ang Ii ◽

Direct Role ◽

Abdominal Aortic

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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Abdominal aortic rupture from an impaling osteophyte following blunt trauma

Journal of Vascular Surgery ◽

10.1016/j.jvs.2013.04.062 ◽

2014 ◽

Vol 59 (4) ◽

pp. 1112-1115 ◽

Cited By ~ 3

Author(s):

Seth A. Vernon ◽

William R.C. Murphy ◽

Todd W. Murphy ◽

James M. Haan

Keyword(s):

Blunt Trauma ◽

Aortic Rupture ◽

Abdominal Aortic

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