Spondylitis and Aortic aneurysm

Spondylitis and Aortic aneurysm

The aim of a study of Patelis et al. from Greece was to assess any relation between spondylitis and aortic aneurysmal disease by reviewing the current literature.

Systematic serching was undertaken using MEDLINEEMBASE and CENTRAL databases till May 2019, for articles reporting on patients suffering from spondylitis and aortic aneurysm.

The most involved aortic segment was infrarenal aorta (56.9%). The lumbar vertebrae were more frequently affected (79.7%). Commonest symptoms were back pain (79.1%), fever (33.7%) and lower limb pain (29.1%). 55.8% of cases were diagnosed using computed tomography. The pathology was attributed to infectious causes in 25.1% of cases. 53.4% of patients were treated only for the aneurysm, 27.9% for both pathologies, while two patients solely for the vertebral disease. Endovascular aneurysm repair was chosen in 12.8% of cases. The 30-day mortality was 8.1% (7/86); mostly from vascular complications.

A synchronous spondylitis and aortic aneurysm may share common etiopathology, when an infectious or inflammatory cause is presented. The lumbar vertebrae are more frequently affected. Low quality data do not allow safe conclusion to suggest the best treatment option 1).

Inflammatory conditions are a rare cause of aortic aneurysms, accounting for 3% to 10% of cases. Patients with ankylosing spondylitis uncommonly present with ascending aortic aneurysms related to long-standing, aggressive disease. Miller et al. reviewed the case of a young man with ankylosing spondylitis exhibiting complex inflammatory aortic aneurysms atypically involving the abdominal and descending thoracic aorta, as well as ectasia of medium-sized visceral vessels. Inflammatory aneurysms require a multidisciplinary approach incorporating diagnostic modalities to confirm etiology, targeted immunosuppressive therapy to control disease activity, and aneurysm repair. Evidence suggests that endovascular approaches should be considered first-line therapy for patients requiring reconstruction when anatomy is appropriate 2).

A 69-year-old man was admitted with low back pain and signs of nerve root compression. A computed tomography (CT) scan showed abscess formation in the left psoas region, spondylodiscitis L3-L4 and a ruptured abdominal aortic aneurysm. The aortic aneurysm was replaced with a bifurcated vascular graft. One week later, laminectomy at the L4-level was done. In a small abscess, Mycobacterium bovis was found. The condition was considered to be a mycobacterial spondylitis secondary to BCG instillations of the urinary bladder for carcinoma. The patient received antituberculous medication for 9 months. Subsequently bone transplantation and internal fixation of the spine became necessary. Three years after surgery he is in good condition and there are no signs of graft infection on CT. Spondylitis and mycotic aortic aneurysm should be kept in mind in patients who have been treated for carcinoma of the bladder with BCG instillations 3).

Ankylosing spondylitis (AS) is a rheumatic disease characterized by consolidation of the articulating surfaces and inflammation of the vertebral column. Because of its associated spine stiffness and secondary osteoporosis, patients with this disorder are at increased risk of vertebral fractures. Ankylosing spondylitis presents a significant challenge to spine surgeons because of its complex effects on the spine, extraarticular organ manifestations, and potential neurological and functional sequelae. Traumatic thoracic and lumbar spine injuries in this patient population may be associated with injury to the aorta either due to direct mechanical trauma or to blunt forces associated with the spine fracture. This complication and association is thought to be the result of pathophysiological changes that cause the aorta to become firmly adherent to the anterior longitudinal ligament. The authors present a case of AS in a patient with a thoracic spine fracture and in whom a delayed thoracic aortic pseudoaneurysm ruptured. To the best of the authors’ knowledge, only five cases of this complex condition have been reported since 1980. Recognition of the potential for aortic injury in patients with AS should prompt early investigation of the aorta in cases involving numerous fractures and assist in surgical planning to avoid this lethal injury 4).


Patelis N, Nana P, Spanos K, Tasoudis P, Brotis A, Bisdas T, Kouvelos G. The association of Spondylitis and Aortic Aneurysm Disease. Ann Vasc Surg. 2021 May 2:S0890-5096(21)00371-X. doi: 10.1016/j.avsg.2021.04.020. Epub ahead of print. PMID: 33951524.

Miller RJH, Moore R, Kim B, Mosher D, Alvarez N. Inflammatory aortic aneurysm in a young patient with ankylosing spondylitis. J Vasc Surg. 2017 Aug;66(2):600-604. doi: 10.1016/j.jvs.2016.09.044. Epub 2016 Dec 14. PMID: 27988155.

Dahl T, Lange C, Ødegård A, Bergh K, Osen SS, Myhre HO. Ruptured abdominal aortic aneurysm secondary to tuberculous spondylitis. Int Angiol. 2005 Mar;24(1):98-101. PMID: 15877007.

Lifshutz J, Lidar Z, Maiman D. Thoracic aortic pseudoaneurysm after spine trauma in ankylosing spondylitis. Case report. J Neurosurg Spine. 2005 Feb;2(2):218-21. doi: 10.3171/spi.2005.2.2.0218. PMID: 15739538.

Posterior communicating artery aneurysm recurrence

Posterior communicating artery aneurysm recurrence

Seven of eight aneurysms (87.5%) were ruptured. Stent assisted coiling was used in one case that a stent was deployed via PCoA-ipsilateral P2 segment. The dual-microcatheter technique was used in one case. The remaining six cases were treated by coiling alone. One patient (12.5%) suffered perioperative complication, of which a coil herniated into parent vessel during the procedure without symptomatic stroke or other adverse event after the procedure. The initial embolization results showed complete occlusion in five cases and residual neck in three. Six patients (75%) had a mean of 15-month angiographic follow-up and two of them revealed recurrence (33.3%) 1)

Dome size, aneurysm neck width, aneurysm volume, and Pcom diameter were associated with recurrence after coil embolization for IC-PC ANs. In particular, Pcom diameter could be an independent risk factor for recurrence 2)).

Lee et al. from the Chuncheon Army Hospital and St. Mary’s Hospital in Seoul, demonstrated that fetal posterior cerebral artery may be an independent risk factor for the recurrence of posterior communicating artery aneurysms. Therefore, fetal-type posterior cerebral artery can be considered as an important risk factor for posterior communicating artery aneurysm recurrences, along with other known risk factors such as size, ruptured status, endovascular treatment, and incomplete occlusion 3).

In 2010 Golshani et al. from the Division of Vascular and Interventional Radiology, Duke University Medical CenterDurham published that coiled posterior communicating artery aneurysms have a particularly high risk of recurrence and must be followed closely. Posterior communicating artery aneurysms with an elongated fundus, true posterior communicating artery aneurysms, and aneurysms associated with a fetal posterior communicating artery may have better outcome with surgical clipping in terms of completeness of occlusion and preservation of the posterior communicating artery. However, as endovascular technology improves, endovascular treatment of posterior communicating artery aneurysms may become equivalent or preferable in the near future 4).


Liu J, Zhang Y, Li W, Wang K, Zhang Y, Yang X. Treatment of true posterior communicating artery aneurysms: Endovascular experience in a single center. Interv Neuroradiol. 2020 Feb;26(1):55-60. doi: 10.1177/1591019919874603. Epub 2019 Sep 5. PMID: 31488022; PMCID: PMC6998000.

Shinya Fukuta, Chiyoe Hikita, Mitsuhiro Iwasaki, Masahiro Maeda, Yasufumi Inaka, Hidekazu Yamazaki, Hiroaki Sato, Masafumi Morimoto, Hidenori Oishi, Risk factors for recurrence after coil embolization for internal carotid artery-posterior communicating artery aneurysms, Interdisciplinary Neurosurgery, Volume 24, 2021, 101097, ISSN 2214-7519, https://doi.org/10.1016/j.inat.2021.101097. (https://www.sciencedirect.com/science/article/pii/S2214751921000098

Lee HJ, Choi JH, Shin YS, Lee KS, Kim BS. Risk Factors for the Recurrence of Posterior Communicating Artery Aneurysm: The Significance of Fetal-Type Posterior Cerebral artery. J Stroke Cerebrovasc Dis. 2021 Apr 26;30(7):105821. doi: 10.1016/j.jstrokecerebrovasdis.2021.105821. Epub ahead of print. PMID: 33915389.

Golshani K, Ferrell A, Zomorodi A, Smith TP, Britz GW. A review of the management of posterior communicating artery aneurysms in the modern era. Surg Neurol Int 22-Dec-2010;1:88

Intracranial aneurysm pathogenesis

Intracranial aneurysm pathogenesis

Until now, the exact etiology of intracranial aneurysms formation remains unclear.

Time-dependent and site-dependent morphological changes and the level of degradation molecules may be indicative of the vulnerability of aneurysm rupture 1).

Miyata et al. proposed the contribution of a structural change in an adventitia, i.e., vasa vasorum formation, to the rupture of IAs 2).

Intracranial aneurysm risk factors.

see Intracranial aneurysm genetics.

see Intracranial aneurysm pathophysiology.

see Intracranial aneurysm hemodynamics.

In addition to ambiental factors (smoking, excessive alcohol consumption and hypertension), epidemiological studies have demonstrated a familiar influence contributing to the pathogenesis of intracranial aneurysms, with increased frequency in first- and second-degree relatives of people with subarachnoid hemorrhage.

Data suggest that macrophage-derived Matrix metalloproteinase 2 and Matrix metalloproteinase 9, may play an important role in the progression of intracranial aneurysms. The findings will shed a new light into the pathogenesis of cerebral aneurysms and highlight the importance of inflammatory response causing the degeneration of extracellular matrix in the process of this disease 3).

Investigations strongly suggest that the pathophysiology is closely associated with chronic inflammation in vascular walls. Nuclear factor kappaB (NF-kappaB) has a key role in the formation and progression.

Children with Sickle Cell Disease (SCD) are at risk for developing multiple intracranial aneurysms, and a high index of suspicion must be maintained during the interpretation of routine magnetic resonance imaging or angiography of the brain 4).

Dental bacterial DNA can be found using a quantitative polymerase chain reaction in both ruptured and unruptured aneurysm walls, suggesting that bacterial DNA plays a role in the pathogenesis of cerebral aneurysms in general, rather than only in ruptured aneurysms 5).

Thrombospondin type-1 domain-containing protein 1 is a protein that in humans is encoded by the THSD1 gene.

The protein encoded by this gene contains a type 1 thrombospondin domain, which is found in thrombospondin, a number of proteins involved in the complement pathway, as well as extracellular matrix proteins. Alternatively spliced transcript variants encoding distinct isoforms have been observed.

As illustrated by THSD1 research, cell adhesion may play a significant role in IA 6).

A study discovered that harmful variants in THSD1 (Thrombospondin type-1 domain-containing protein 1) likely cause intracranial aneurysm and subarachnoid hemorrhage in a subset of both familial and sporadic patients with supporting evidence from two vertebrate models 7).

A report identified THSD1 mutations in familial and sporadic IA patients and shows that THSD1 loss results in cerebral bleeding in 2 animal models. This finding provides new insight into IA and subarachnoid hemorrhage pathogenesis and provides new understanding of THSD1 function, which includes endothelial cell to extracellular matrix adhesion 8).

Toll‑like receptor (TLR) 2/4 serves an important regulatory role in nerve tissue injury. However, the downstream and potential mechanisms remain to be elucidated. The present study was designed to investigate the roles of the TLR2/4‑major myeloid differentiation response gene 88 (MyD88)‑NF‑κB signaling pathway in the development of an intracranial aneurysm. The expression of TLR2, TLR4, and MyD88 in the blood of normal controls and patients with intracranial aneurysms were detected by quantitative PCR and ELISA. Human brain vascular smooth muscle cells were treated by Angiotensin II (Ang II) to evaluate the involvement of the TLR2/4‑MyD88‑NF‑κB signaling pathway in the process. The in vitro experiment was divided into four groups: The control group, an Ang Ⅱ group, an Ang Ⅱ + small interfering (si)RNA control group, and an Ang Ⅱ + TLR2‑group. Cell viability, migration, apoptosis, and expression of TLR2, TLR4, MyD88, NF‑κB, and phosphorylated (p‑)p65 expression was detected. The results demonstrated that the expression of TLR2, TLR4, MyD88, and NF‑κB at mRNA and protein levels in patients with an intracranial aneurysm was significantly higher compared with corresponding protein in normal controls (P&lt;0.05). <em>In vitro</em> experiments demonstrated that Ang Ⅱ treatment increased the cell proliferation and migration rate but reduced the apoptotic rate compared with the control (P&lt;0.05). The expression of TLR2, TLR4, MyD88, NF‑κB, and p‑p65 was significantly increased in the Ang II group (vs. control; P&lt;0.05). By contrast, TLR2‑short interfering RNA reduced the cell proliferation and migration rate and reduced the expression of TLR2, TLR4, MyD88, NF‑κB, and p‑p65 (vs. Ang Ⅱ + short interfering RNA control; P&lt;0.05). In conclusion, the data of the present study indicated that the TLR2/4‑MyD88‑NF‑κB signaling pathway is involved in the intracranial aneurysm pathogenesis 9).


Yamaguchi T, Miyamoto T, Kitazato KT, Shikata E, Yamaguchi I, Korai M, Shimada K, Yagi K, Tada Y, Matsuzaki Y, Kanematsu Y, Takagi Y. Time-dependent and site-dependent morphological changes in rupture-prone arteries: ovariectomized rat intracranial aneurysm model. J Neurosurg. 2019 Sep 13:1-9. doi: 10.3171/2019.6.JNS19777. [Epub ahead of print] PubMed PMID: 31518986.

Miyata H, Imai H, Koseki H, Shimizu K, Abekura Y, Oka M, Kawamata T, Matsuda T, Nozaki K, Narumiya S, Aoki T. Vasa vasorum formation is associated with rupture of intracranial aneurysms. J Neurosurg. 2019 Aug 16:1-11. doi: 10.3171/2019.5.JNS19405. [Epub ahead of print] PubMed PMID: 31419795.

Aoki T, Kataoka H, Morimoto M, Nozaki K, Hashimoto N. Macrophage-derived matrix metalloproteinase-2 and -9 promote the progression of cerebral aneurysms in rats. Stroke. 2007 Jan;38(1):162-9. Epub 2006 Nov 22. PubMed PMID: 17122420.

Saini S, Speller-Brown B, Wyse E, Meier ER, Carpenter J, Fasano RM, Pearl MS. Unruptured Intracranial Aneurysms in Children With Sickle Cell Disease: Analysis of 18 Aneurysms in 5 Patients. Neurosurgery. 2015 Feb 12. [Epub ahead of print] PubMed PMID: 25710108.

Pyysalo MJ, Pyysalo LM, Pessi T, Karhunen PJ, Lehtimäki T, Oksala N, Öhman JE. Bacterial DNA findings in ruptured and unruptured intracranial aneurysms. Acta Odontol Scand. 2016 May;74(4):315-20. doi: 10.3109/00016357.2015.1130854. Epub 2016 Jan 18. PubMed PMID: 26777430.

Xu Z, Rui YN, Hagan JP, Kim DH. Intracranial Aneurysms: Pathology, Genetics, and Molecular Mechanisms. Neuromolecular Med. 2019 May 4. doi: 10.1007/s12017-019-08537-7. [Epub ahead of print] Review. PubMed PMID: 31055715.

Rui YN, Xu Z, Fang X, Menezes MR, Balzeau J, Niu A, Hagan JP, Kim DH. The Intracranial Aneurysm Gene THSD1 Connects Endosome Dynamics to Nascent Focal Adhesion Assembly. Cell Physiol Biochem. 2017;43(6):2200-2211. doi: 10.1159/000484298. Epub 2017 Oct 25. PubMed PMID: 29069646.

Santiago-Sim T, Fang X, Hennessy ML, Nalbach SV, DePalma SR, Lee MS, Greenway SC, McDonough B, Hergenroeder GW, Patek KJ, Colosimo SM, Qualmann KJ, Hagan JP, Milewicz DM, MacRae CA, Dymecki SM, Seidman CE, Seidman JG, Kim DH. THSD1 (Thrombospondin Type 1 Domain Containing Protein 1) Mutation in the Pathogenesis of Intracranial Aneurysm and Subarachnoid Hemorrhage. Stroke. 2016 Dec;47(12):3005-3013. Epub 2016 Nov 15. Erratum in: Stroke. 2017 Aug;48(8):e240. PubMed PMID: 27895300; PubMed Central PMCID: PMC5134902.

Zhang X, Wan Y, Feng J, Li M, Jiang Z. Involvement of TLR2/4‑MyD88‑NF‑κB signaling pathway in the pathogenesis of intracranial aneurysm. Mol Med Rep. 2021 Jan 26. doi: 10.3892/mmr.2021.11869. Epub ahead of print. PMID: 33655339.
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