Progressive aneurysm development following hemodynamic insult

Meng, Hui; Metaxa, Eleni; Gao, Ling; Liaw, Nicholas; Natarajan, Sabareesh K.; Swartz, Daniel D.; Siddiqui, Adnan H.; Kolega, John; Mocco, J

doi:10.3171/2010.9.jns10368

Cited by 71 publications

(99 citation statements)

References 45 publications

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“…This is consistent with reports of IA initiation at the BT after both BCCA-L [20][21][22]24 and unilateral CCA ligation. 20,23 Specifically, Meng et al 22 found that the aneurysmal development at the BT continued out to 6 months, even after normalization of the inciting WSS and cessation of adaptive remodeling at 4 to 5 weeks. By comparing the 5-day and 6-month groups in the current study, we also found that the pathologic changes throughout the CoW increased with time.…”

Section: Discussionsupporting

confidence: 93%

“…Our previous studies of BT aneurysm formation in the same model (rabbit BCCA-L) have demonstrated that aneurysmal remodeling is a maladaptive response to elevated hemodynamic stresses. 22,24 Through detailed hemodynamics-histology mapping, we found that IA initiation at the BT (defined by regions of IEL loss) was associated with high WSS combined with positive WSS gradient above a threshold. 24,33 This hemodynamic condition, often associated with bifurcation apices, 34 has been recognized to independently cause de novo IA formation.…”

Section: Discussionmentioning

confidence: 94%

“…In order to gain additional insight into structures observed on the cast surfaces, we compared our cast data with available histologic sections at the BT in rabbits that underwent BCCA-L from our previous studies. 22 We spatially matched SEM images of the endocasts at the BT with representative sections stained with van Gieson's stain for each experimental group.…”

Section: Scanning Electron Microscopy Image Comparison With Histologymentioning

confidence: 99%

“…18 Experimentally, we have performed unilateral and bilateral CCA ligation (BCCA-L) in rabbits and observed a drastic flow increase in the BA 19 and de novo IA initiation at the BT. [20][21][22][23][24] Aneurysm formation was shown to be a direct, maladaptive response to elevated hemodynamic stresses. This localized response was dose dependent on blood flow increase 20 and was sustained beyond the normalization of the inciting hemodynamic insult; that is, after returning wall shear stress (WSS) to baseline levels.…”

Section: Introductionmentioning

confidence: 99%

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Aneurysmal Remodeling in the Circle of Willis after Carotid Occlusion in an Experimental Model

Tutino

Mandelbaum

Choi³

et al. 2013

J Cereb Blood Flow Metab

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Carotid occlusions are associated with de novo intracranial aneurysm formation in clinical case reports, but this phenomenon is not widely studied. We performed bilateral carotid ligation (n ¼ 9) in rabbits to simulate carotid occlusion, and sham surgery (n ¼ 3) for control. Upon euthanasia (n ¼ 3 at 5 days, n ¼ 6 at 6 months post ligation, and n ¼ 3 at 5 days after sham operation), vascular corrosion casts of the circle of Willis (CoW) were created. Using scanning electron microscopy, we quantified gross morphologic, macroscopic, and microscopic changes on the endocasts and compared findings with histologic data. At 5 days, CoW arteries of ligated animals increased caliber. The posterior communicating artery (PCom) increased length and tortuosity, and the ophthalmic artery (OA) origin presented preaneurysmal bulges. At 6 months, calibers were unchanged from 5 days, PComs further increased tortuosity while presenting segmental dilations, and the OA origin and basilar terminus presented preaneurysmal bulges. This exploratory study provides evidence that flow increase after carotid occlusion produces both compensatory arterial augmentation and pathologic remodeling such as tortuosity and saccular/fusiform aneurysm. Our findings may have considerable clinical implications, as these lesser-known consequences should be considered when managing patients with carotid artery disease or choosing carotid ligation as a therapeutic option.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Section: Scanning Electron Microscopy Image Comparison With Histologymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Aneurysmal Remodeling in the Circle of Willis after Carotid Occlusion in an Experimental Model

Tutino

Mandelbaum

Choi³

et al. 2013

J Cereb Blood Flow Metab

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“…5,6 CFD offers an excellent alternative for testing hypotheses statistically by correlating hemodynamic variables and aneurysm rupture by using clinical data. Correlation does not imply causation, but different causative mechanisms lead to different correlations that can be tested by combining hemodynamic models (computational or not) and clinical data.…”

Section: Why There Are a Large Number Of Parameters Publishedmentioning

confidence: 99%

Counterpoint: Realizing the Clinical Utility of Computational Fluid Dynamics—Closing the Gap

Cebral¹,

Meng²

2012

AJNR Am J Neuroradiol

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ith great interest, we read the stimulating editorial by Dr Kallmes, who raises important questions regarding the potential utility of computational fluid dynamics (CFD) in guiding neurointerventional and neurosurgical treatment of cerebral aneurysms. We believe that Dr Kallmes' opinion is representative of that of most avant-garde clinicians who have collaborated with computational scientists or engineering researchers. These clinicians not only appreciate the aesthetic and intuitive aspects of CFD simulations but also recognize their enormous potential for providing objective, quantitative, and mechanism-based parameters to stratify aneurysm rupture risk and help aneurysm management. Recently clinical journals such as the American Journal of Neuroradiology have seen an increasing number of articles about CFD. It is sobering to reflect on where we are and where we should be heading.Dr Kallmes' main points are the following: 1) CFD involves assumptions that might make results questionable; 2) a large number of hemodynamic parameters have surfaced in recent publications, which are confusing and confounding; 3) to change the current situation of isolated groups working on a small number of cases, cross-disciplinary collaboration on a large amount of clinical data is required to realize the clinical utility of CFD; and 4) CFD researchers need to close the gaps in information and address the conflicting information and confounding variables. These are excellent points (despite a few minor misconceptions), with which we emphatically agree.We wish to express our thoughts in response to Dr Kallmes' points. CFD holds great promise for revealing aneurysm pathophysiology and for becoming a tool that the neurointerventionalists could expect to use routinely someday to assess patients' aneurysm rupture risk and to guide treatment. However, an aneurysm is a complex problem. To make CFD work for clinical practice, computational scientists/engineers and clinicians have to work much closer together. We are fully on board with Dr Kallmes in his call for multidisciplinary collaboration to build a large clinical data base for CFD and to realize its clinical utility. How Much Detail Should Clinicians Know about CFD and Its Assumptions?Dr Kallmes raises an important question about whether clinicians need to know the details of CFD computations. We are of the opinion that though clinicians do not need to understand all the details of how CFD calculations are performed, just as they do not know all the details about the medical imaging equipment they use, it is very important that they at least understand the approximations, assumptions, and limitations of these techniques, just as they do with medical imaging systems.Dr Kallmes mentions some typical approximations made in most CFD studies, apparently implying that because of these, the CFD methodology is inaccurate and unreliable. CFD has played an indispensible role in almost every aspect of technology that we enjoy in modern life, including aircraft design, food processing, and wea...

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Hypertension and Estrogen Deficiency Augment Aneurysmal Remodeling in the Rabbit Circle of Willis in Response to Carotid Ligation

Tutino

Mandelbaum

Takahashi

et al. 2015

The Anatomical Record

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Increased cerebral blood flow has been shown to induce pathological structural changes in the Circle of Willis (CoW) in experimental models. Previously, we reported flow-induced aneurysm-like remodeling in the CoW secondary to flow redistribution after bilateral common carotid artery (CCA) ligation in rabbits. In the current study, we tested the hypothesis that loading rabbits with biological risk factors for vascular disease would increase flow-induced aneurysmal remodeling in the CoW. In the same series as the previously-reported bilateral CCA-ligation-alone (n=6) and sham surgery (n=3) groups, eight additional female rabbits (the experimental group in this study) were subjected to two risk factors for intracranial aneurysm (hypertension and estrogen deficiency) and then bilateral CCA ligation. Upon euthanasia at 6 months, vascular corrosion casts of the CoW were created and analyzed by scanning electron microscopy for morphological changes and aneurysmal damage. In rabbits with hypertension and estrogen deficiency, arterial caliber increased throughout the CoW, similar to rabbits with CCA ligation alone. However, aneurysmal remodeling (i.e. local bulging) in the CoW was significantly greater than in CCA-ligation-only rabbits and was more widespread, presenting in regions that did not show aneurysmal changes after CCA ligation alone. Furthermore, hypertension and estrogen deficiency caused greater increases in vessel length and tortuosity. These results suggest that hypertension and estrogen deficiency make the CoW more vulnerable to flow-induced aneurysmal remodeling and tortuosity. We propose they do so by lowering the tolerance of vascular tissue to hemodynamic forces caused by CCA ligation, thus lowering the threshold necessary to incite vascular damage.

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Progressive aneurysm development following hemodynamic insult

Abstract: Hemodynamic insult can elicit a pathological vascular response leading to a self-sustaining aneurysmal remodeling that does not require persistence of the original inciting factor to continue its pathological progression.

Cited by 71 publications

References 45 publications

Aneurysmal Remodeling in the Circle of Willis after Carotid Occlusion in an Experimental Model

Aneurysmal Remodeling in the Circle of Willis after Carotid Occlusion in an Experimental Model

Counterpoint: Realizing the Clinical Utility of Computational Fluid Dynamics—Closing the Gap

Hypertension and Estrogen Deficiency Augment Aneurysmal Remodeling in the Rabbit Circle of Willis in Response to Carotid Ligation

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