Browsing by Subject "Aneurysm"

Now showing 1 - 9 of 9
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    Endovascular approach to thrombosed limb of aortoiliac endoprosthetic stent graft following abdominal endovascular aneurysm repair
    (Elsevier, 2022-07-20) Willhite, Sydney R.; Warner, Adam C.; Hain, Julius S.; Nickerson, Margaret C.; Peterson, David A.; Cuddy, Duangnapa S.; Graduate Medical Education, School of Medicine
    The increasing use of endovascular aneurysm repair to treat abdominal aortic aneurysms has mandated solutions to the limitations of this operation, including the requirement for additional procedures. A 64-year-old man had presented with symptomatic thrombosis of the left iliac limb after endovascular aneurysm repair. We have reported the use of an innovative endovascular repair for our patient.
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    Exome Sequencing Identifies Candidate Genetic Modifiers of Syndromic and Familial Thoracic Aortic Aneurysm Severity
    (Springer Nature, 2017-08) Landis, Benjamin J.; Schubert, Jeffrey A.; Lai, Dongbing; Jegga, Anil G.; Shikany, Amy R.; Foroud, Tatiana; Ware, Stephanie M.; Hinton, Robert B.; Pediatrics, School of Medicine
    Thoracic aortic aneurysm (TAA) is a genetic disease predisposing to aortic dissection. It is important to identify the genetic modifiers controlling penetrance and expressivity to improve clinical prognostication. Exome sequencing was performed in 27 subjects with syndromic or familial TAA presenting with extreme phenotypes (15 with severe TAA; 12 with mild or absent TAA). Family-based analysis of a subset of the cohort identified variants, genes, and pathways segregating with TAA severity among three families. A rare missense variant in ADCK4 (p.Arg63Trp) segregated with mild TAA in each family. Genes and pathways identified in families were further investigated in the entire cohort using the optimal unified sequence kernel association test, finding significance for the gene COL15A1 (p = 0.025) and the retina homeostasis pathway (p = 0.035). Thus, we identified candidate genetic modifiers of TAA severity by exome-based study of extreme phenotypes, which may lead to improved risk stratification and development of new medical therapies.
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    Left colic artery aneurysm
    (Elsevier, 2020-10) Kota, Albert A.; Wang, Keisin; Leckie, Katherine; King, Justin; Maijub, John; Motaganahalli, Raghu L.; Medicine, School of Medicine
    An aneurysm of the inferior mesenteric artery is a rarely described clinical presentation. We have presented the case of a ruptured aneurysm originating from a branch of the inferior mesenteric artery that might represent an aneurysm of the left colic artery or the arc of Riolan. Aneurysms of this anatomic location can develop secondary to mesenteric occlusive disease, alterations in mesenteric blood flow from previous operations, or connective tissue disease. In the present case, a patient with a ruptured inferior mesenteric artery branch aneurysm had presented with intra-abdominal hemorrhage, which was successfully treated with endovascular embolization.
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    Myeloid cells induce neurofibromatosis type 1 aneurysm formation through inflammation and oxidative stress
    (2014-06) Downing, Brandon David; Kapur, Reuben; Yoder, Mervin C.; Conway, Simon J.; Ingram Jr., David A.
    Neurofibromatosis Type 1 (NF1) is a genetic disorder resulting from mutations in the NF1 tumor suppressor gene. Neurofibromin is the protein product of NF1 and functions as a negative regulator of Ras activity in both hematopoietic and vascular wall cells, which are critical for maintaining blood vessel homeostasis. NF1 patients are predisposed to chronic inflammation and premature cardiovascular disease, including development of large arterial aneurysms, which may result in sudden death secondary to their rupture. However, the molecular pathogenesis of NF1 aneurysm formation is completely unknown. Utilizing a novel model of Nf1 murine aneurysm formation, we demonstrate that heterozygous inactivation of Nf1 (Nf1+/-) results in enhanced aneurysm formation with myeloid cell infiltration and increased reactive oxygen species in the vessel wall. Using cell lineage-restricted transgenic mice, we show that loss of a single Nf1 allele in myeloid cells is sufficient to recapitulate the Nf1+/- aneurysm phenotype in vivo. Additionally, oral administration of simvastatin, a statin with antioxidant and anti-inflammatory effects, significantly reduced aneurysm formation in Nf1+/- mice. Finally, the antioxidant apocynin was administered orally and also resulted in a significant reduction of Nf1+/- aneurysms. These data provide genetic and pharmacologic evidence that neurofibromin-deficient myeloid cells are the central cellular triggers for aneurysm formation in a novel model of NF1 vascular disease, implicated oxidative stress as the key biochemical mechanisms of NF1 aneurysm formation and provide a potential therapeutic target for NF1 vasculopathy.
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    Neurofibromin Deficient Myeloid Cells are Critical Mediators of Aneurysm Formation In Vivo
    (Ovid Technologies Wolters Kluwer -American Heart Association, 2014-03-18) Li, Fang; Downing, Brandon D.; Smiley, Lucy C.; Mund, Julie A.; DiStasi, Matthew R.; Bessler, Waylan K.; Sarchet, Kara N.; Hinds, Daniel M.; Kamendulis, Lisa M.; Hingtgen, Cynthia M.; Case, Jamie; Clapp, D. Wade; Conway, Simon J.; Stansfield, Brian K.; Ingram, David A.; Department of Pediatrics, IU School of Medicine
    Background Neurofibromatosis Type 1 (NF1) is a genetic disorder resulting from mutations in the NF1 tumor suppressor gene. Neurofibromin, the protein product of NF1, functions as a negative regulator of Ras activity in circulating hematopoietic and vascular wall cells, which are critical for maintaining vessel wall homeostasis. NF1 patients have evidence of chronic inflammation resulting in development of premature cardiovascular disease, including arterial aneurysms, which may manifest as sudden death. However, the molecular pathogenesis of NF1 aneurysm formation is unknown. Method and Results Utilizing an angiotensin II-induced aneurysm model, we demonstrate that heterozygous inactivation of Nf1 (Nf1+/−) enhanced aneurysm formation with myeloid cell infiltration and increased oxidative stress in the vessel wall. Using lineage-restricted transgenic mice, we show loss of a single Nf1 allele in myeloid cells is sufficient to recapitulate the Nf1+/− aneurysm phenotype in vivo. Finally, oral administration of simvastatin or the antioxidant apocynin, reduced aneurysm formation in Nf1+/− mice. Conclusion These data provide genetic and pharmacologic evidence that Nf1+/− myeloid cells are the cellular triggers for aneurysm formation in a novel model of NF1 vasculopathy and provide a potential therapeutic target.
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    A novel approach for treating type II endoleaks utilizing contrast-enhanced ultrasound
    (Elsevier, 2021-06-12) Churchill, Dennis, II.; Motaganahalli, Raghu; LaRoche, Thomas; Ramkaransingh, Jeffrey; Radiology and Imaging Sciences, School of Medicine
    Endoleaks are a frequent and well-known complication after endovascular repair of aortic aneurysms. An endoleak can lead to increased intrasac pressure, sac enlargement, and potential aneurysm rupture. Type II endoleaks result from retrograde filling of aortic branch vessels and can be treated with surgical, endovascular, or direct percutaneous approaches. Direct percutaneous treatment typically involves embolization of the perfused endoleak cavity typically using a translumbar approach with fluoroscopic guidance. We illustrate a novel image-guided approach for percutaneous transabdominal endoleak treatment using contrast-enhanced ultrasound in combination with fluoroscopy.
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    One-Year Results with a Low-Profile Endograft in Subjects with Thoracic Aortic Aneurysm and Ulcer Pathologies
    (Elsevier, 2022-02) Szeto, Wilson Y.; Vallabhajosyula, Prashanth; Matsuda, Hitoshi; Moainie, Sina L.; Sharafuddin, Mel J.; Corvera, Joel; Smolock, Christopher J.; Miyamoto, Shinji; Naslund, Thomas; Ramaiah, Venkatesh; Medicine, School of Medicine
    Objective Evaluate safety and effectiveness of the second generation, low-profile RelayPro thoracic endograft for the treatment of descending thoracic aortic aneurysm or penetrating atherosclerotic ulcer (PAU). Method A prospective, international, non-blinded, non-randomized, pivotal trial analyzed a primary safety endpoint of major adverse events (MAE) at 30 days (death, myocardial infarction, stroke, renal/respiratory failure, paralysis, bowel ischemia, procedural blood loss), and a primary effectiveness endpoint of treatment success at one year (technical success, patency, absence of aneurysm rupture, type I/III endoleaks, stent fractures, reinterventions, aneurysm expansion, and migration) compared to performance goals from the previous generation Relay pivotal study. The study was conducted in 36 centers in the US and Japan and enrolled between 2017 and 2019. Results The study population of 110 patients had a median (IQR) age of 76 (70 – 81) years, n=69 (62.7%) were male, n=43 (39.1%) were Asian, and were treated for 76 fusiform aneurysms (69%), 24 saccular aneurysms (22%), and 10 PAUs (9%). Most patients (82.7%) were treated with a non-bare stent (NBS) configuration. Technical success was 100%: median (IQR) procedure time was 91 (64 – 131) min, deployment time was 16 (10 – 25) min; 50 patients (73.5%) of the US cohort had percutaneous access, while centers in Japan used only surgical cutdown. The 30-day composite MAE rate was 6.4% (95% upper CI 11.6%, p=.0002): 2 strokes, 2 procedural blood losses >1000 mL requiring transfusion, 2 paralysis events, and 1 renal failure. Primary effectiveness was 89.2% (lower 95% CI 81.8%, p=.0185): 9 subjects experienced 11 events (1 aneurysm expansion, 6 secondary interventions, 4 type I endoleaks). There was no loss of stent-graft patency, no rupture, no fractures, and no migration. Conclusions The low-profile RelayPro thoracic endograft met the study primary endpoints and demonstrated satisfactory 30-day safety and 1-year effectiveness for the treatment of patients with aneurysms of the descending thoracic aorta or PAUs. Follow-up is ongoing to evaluate longer term outcomes and durability.
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    Survivin-induced abnormal ploidy contributes to cystic kidney and aneurysm formation
    (Ovid Technologies Wolters Kluwer -American Heart Association, 2014-02-11) AbouAlaiwi, Wissam A.; Muntean, Brian S.; Ratnam, Shobha; Joe, Bina; Liu, Lijun; Booth, Robert L.; Rodriguez, Ingrid; Herbert, Britney S.; Bacallao, Robert L.; Fruttiger, Marcus; Mak, Tak W.; Zhou, Jing; Nauli, Surya M.; Department of Medical and Molecular Genetics, IU School of Medicine
    BACKGROUND: Cystic kidneys and vascular aneurysms are clinical manifestations seen in patients with polycystic kidney disease, a cilia-associated pathology (ciliopathy). Survivin overexpression is associated with cancer, but the clinical pathology associated with survivin downregulation or knockout has never been studied before. The present studies aim to examine whether and how cilia function (Pkd1 or Pkd2) and structure (Tg737) play a role in cystic kidney and aneurysm through survivin downregulation. METHODS AND RESULTS: Cysts and aneurysms from polycystic kidney disease patients, Pkd mouse, and zebrafish models are characterized by chromosome instability and low survivin expression. This triggers cytokinesis defects and formation of nuclear polyploidy or aneuploidy. In vivo conditional mouse and zebrafish models confirm that survivin gene deletion in the kidneys results in a cystic phenotype. As in hypertensive Pkd1, Pkd2, and Tg737 models, aneurysm formation can also be induced in vascular-specific normotensive survivin mice. Survivin knockout also contributes to abnormal oriented cell division in both kidney and vasculature. Furthermore, survivin expression and ciliary localization are regulated by flow-induced cilia activation through protein kinase C, Akt and nuclear factor-κB. Circumventing ciliary function by re-expressing survivin can rescue polycystic kidney disease phenotypes. CONCLUSIONS: For the first time, our studies offer a unifying mechanism that explains both renal and vascular phenotypes in polycystic kidney disease. Although primary cilia dysfunction accounts for aneurysm formation and hypertension, hypertension itself does not cause aneurysm. Furthermore, aneurysm formation and cyst formation share a common cellular and molecular pathway involving cilia function or structure, survivin expression, cytokinesis, cell ploidy, symmetrical cell division, and tissue architecture orientation.
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    Woven Endobridge device for treatment of dissection-related PICA aneurysm
    (Sage, 2021) Khattar, Nicolas K.; White, Andrew C.; Cruz, Aurora S.; Adams, Shawn W.; Meyer, Kimberly S.; Nauta, Haring J.W.; Ding, Dale; James, Robert F.; Neurological Surgery, School of Medicine
    Ruptured vertebrobasilar dissecting aneurysms require urgent, often challenging treatment as they have with a high re-hemorrhage rate within the first 24 hours. The patient is a 57-year-old woman who presented with severe-sudden onset headache. Further work up showed a ruptured dissecting aneurysm of the caudal loop of the posterior inferior cerebellar artery (PICA) with associated narrowing distally, in the ascending limb. The aneurysm was immediately occluded with a Woven Endobridge (WEB) device (MicroVention, Tustin, CA, USA) while flow diversion treatment of the diseased ascending limb was postponed. Follow-up angiography three months later showed complete occlusion of the aneurysm, as well as healing of the diseased distal vessel, obviating the need for further intervention. WEB embolization of a ruptured dissecting posterior circulation aneurysm provided an excellent outcome for this patient.