A comparison of acute vascular damage caused by ADAPT versus a stent retriever device after thrombectomy in acute ischemic stroke: a histological and ultrastructural study in an animal model

2016 ◽  
Vol 9 (8) ◽  
pp. 743-749 ◽  
Author(s):  
S Peschillo ◽  
F Diana ◽  
J Berge ◽  
P Missori
Keyword(s):  
Arterial Wall ◽  
Elastic Fibers ◽  
Cell Alignment ◽  
Internal Elastic Lamina ◽  
Endothelial Lining ◽  
Tissue Samples ◽  
First Pass ◽  
Stent Retrievers ◽  
Ultrastructural Damage ◽  
Elastic Lamina

BackgroundIt has been amply demonstrated that endovascular procedures can be successful treatment for stroke, both in terms of revascularization and clinical outcome. There is not, however, a published comparison of any histological or ultrastructural damage to the vessels that may be caused by a direct aspiration first pass technique (ADAPT) or stent retrievers (SR) used in these procedures. This study analyses and compares acute damage to the arterial wall caused by ADAPT or SR.Material and methodsDamage to the walls of swine extracranial arteries was evaluated after ADAPT with the Penumbra system or thrombectomy with an SR (Solitaire 6×30). The procedures were performed after injecting thrombi into the selected arteries (arteries with diameters similar to those of the human internal carotid artery and first segment of the middle cerebral artery). After the procedures, the animal was euthanized and 12 arterial samples were obtained for analysis by optical and electronic microscopy.ResultsTissue samples from the vessels treated with SR showed almost complete loss of endothelium, thickening of the internal elastic lamina, and degeneration of the elastic fibers of the bordering lamina media and adventitia. In contrast, tissue samples of the vessels treated with ADAPT had a clear integral internal elastic lamina and uninterrupted endothelial lining, although cell alignment was altered and there were surface lacerations due to manipulation of the samples.ConclusionsBoth techniques caused acute damage to the vessel walls, however, thrombectomy with SR appeared to be more harmful to all layers of the arterial wall, particularly the endothelium.

scholarly journals Elastic Fibers of the Internal Elastic Lamina Are Unraveled But Not Created With Expanding Arterial Diameter in Arteriogenesis

2020 ◽  
Vol 1 ◽  
pp. 247
Author(s):  
Derek Afflu ◽  
Dylan D. McCreary ◽  
Nolan Skirtich ◽  
Kathy Gonzalez ◽  
Edith Tzeng ◽  
...  
Keyword(s):  
Elastic Fibers ◽  
Internal Elastic Lamina ◽  
Arterial Diameter ◽  
Elastic Lamina

Postnatal alterations in elastic fiber organization precede resistance artery narrowing in SHR

2006 ◽  
Vol 291 (2) ◽  
pp. H804-H812 ◽  
Author(s):  
José M. González ◽  
Ana M. Briones ◽  
Beatriz Somoza ◽  
Craig J. Daly ◽  
Elisabet Vila ◽  
...  
Keyword(s):  
Time Course ◽  
Elastic Fiber ◽  
Elastic Fibers ◽  
Early Event ◽  
Resistance Artery ◽  
Internal Elastic Lamina ◽  
Wall Stiffness ◽  
Fiber Deposition ◽  
Fiber Organization ◽  
Elastic Lamina

Resistance artery narrowing and stiffening are key elements in the pathogenesis of essential hypertension, but their origin is not completely understood. In mesenteric resistance arteries (MRA) from spontaneously hypertensive rats (SHR), we have shown that inward remodeling is associated with abnormal elastic fiber organization, leading to smaller fenestrae in the internal elastic lamina. Our current aim is to determine whether this alteration is an early event that precedes vessel narrowing, or if elastic fiber reorganization in SHR arteries occurs because of the remodeling process itself. Using MRA from 10-day-old, 30-day-old, and 6-mo-old SHR and normotensive Wistar Kyoto rats, we investigated the time course of the development of structural and mechanical alterations (pressure myography), elastic fiber organization (confocal microscopy), and amount of elastin (radioimmunoassay for desmosine) and collagen (picrosirius red). SHR MRA had an impairment of fenestrae enlargement during the first month of life. In 30-day-old SHR, smaller fenestrae and more packed elastic fibers in the internal elastic lamina were paralleled by increased wall stiffness. Collagen and elastin levels were unaltered at this age. MRA from 6-mo-old SHR also had smaller fenestrae and a denser network of adventitial elastic fibers, accompanied by increased collagen content and vessel narrowing. At this age, elastase digestion was less effective in SHR MRA, suggesting a lower susceptibility of elastic fibers to enzymatic degradation. These data suggest that abnormal elastic fiber deposition in SHR increases resistance artery stiffness at an early age, which might participate in vessel narrowing later in life.

scholarly journals Adaptive Remodeling of Internal Elastic Lamina and Endothelial Lining During Flow-Induced Arterial Enlargement

1999 ◽  
Vol 19 (10) ◽  
pp. 2298-2307 ◽  
Author(s):  
Hirotake Masuda ◽  
Yong-Jie Zhuang ◽  
Tej M. Singh ◽  
Koichi Kawamura ◽  
Masayo Murakami ◽  
...  
Keyword(s):  
Internal Elastic Lamina ◽  
Endothelial Lining ◽  
Elastic Lamina

A New Biomechanical Approach to Assessing the Fragility of the Internal Elastic Lamina of the Arterial Wall

1993 ◽  
Vol 30 (2) ◽  
pp. 143-155 ◽  
Author(s):  
Neil D. Broom ◽  
Glenn Ramsey ◽  
Richard Mackie ◽  
Barry J. Martin ◽  
William E. Stehbens
Keyword(s):  
Arterial Wall ◽  
Internal Elastic Lamina ◽  
Biomechanical Approach ◽  
Elastic Lamina

Finite Element Modeling of Cerebral Angioplasty Using a Multi-Mechanism Structural Damage Model

2009 ◽  
Author(s):  
Dalong Li ◽  
Anne M. Robertson
Keyword(s):  
Structural Damage ◽  
Arterial Wall ◽  
Damage Model ◽  
Transluminal Angioplasty ◽  
Controlled Study ◽  
Internal Elastic Lamina ◽  
The Media ◽  
Observed Damage ◽  
Percutaneous Transluminal ◽  
Elastic Lamina

Percutaneous transluminal angioplasty (PTA) can lead to vascular damage when used to treat atherosclerotic obstructions and vasospasm in cerebral vessels [1–3]. In a controlled study of angioplasty in normal arteries of mongrel dogs, changes to the arterial wall due to over inflation were studied at two dilation levels (24%,50%) [4]. Damage to the wall was progressive — increasing with inflation level. At 25% inflation, localized fractures and stretching of the internal elastic lamina (IEL) were observed. Damage to the media was limited to the inner one-third of the wall. At 50% inflation, further radial damage was seen including extensive damage to the IEL, dissection of the media, distorted SMC and disorganized collagen fibers. At six months, the media exhibited signs of repair such as increased collagen content while the IEL showed no recovery.

Recurrence of Cerebral Aneurysm after Initial Neck Clipping

Neurosurgery ◽  
1982 ◽  
Vol 11 (6) ◽  
pp. 764-768 ◽  
Author(s):  
Kunihiko Ebina ◽  
Mikio Suzuki ◽  
Akira Andoh ◽  
Kazuko Saitoh ◽  
Takashi Iwabuchi
Keyword(s):  
Computed Tomography ◽  
Cerebral Aneurysm ◽  
Arterial Wall ◽  
Muscle Layer ◽  
Parent Artery ◽  
Internal Elastic Lamina ◽  
High Resolution Computed Tomography ◽  
Aneurysm Neck ◽  
Thin Walled ◽  
Elastic Lamina

Abstract Neck clipping has generally been believed to be among the most reliable of the operative modalities for cerebral aneurysm. However, recurrences with catastrophic outcome have been known to occur. We recently treated two patients who each had a new aneurysm at the site of the initial clipping. In both cases, the recurrence was found several years after the aneurysm neck had been closed successfully with a silver clip, which had been confirmed by intraoperative inspection and by postoperative angiographic studies demonstrating disappearance of the aneurysm. Histological examination of the recurrent aneurysm showed that the arterial wall had apparently been damaged by the clip edge, which resulted in thinning and disruption of both the muscle layer and the internal elastic lamina. Therefore, local fragility of the arterial wall adjacent to the aneurysm seems to have been the cause of the formation of a new aneurysm. The need to reinforce the thin-walled parent artery and the usefulness of high resolution computed tomography for the early detection of recurrent aneurysms are emphasized.

Abstract T P419: Pathological Arterial Wall Correlates of Lumen-based Remodeling: Results From the Brain Arterial Remodeling Study

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Jose Gutierrez ◽  
Mitchell S Elkind ◽  
James Goldman ◽  
Lawrence Honig ◽  
Susan Morgello ◽  
...  
Keyword(s):  
Vascular Disease ◽  
Arterial Wall ◽  
Cerebral Arteries ◽  
Internal Elastic Lamina ◽  
Cross Sectional ◽  
Luminal Stenosis ◽  
The Media ◽  
The Relationship ◽  
The Brain ◽  
Elastic Lamina

Background: There is paucity of data about arterial wall characteristics of the smallest and largest caliber cerebral vessels. Determining the relationship between the lumen and the wall might shed new insights into cerebral artery remodeling. Objective: To test the hypotheses that arteries with larger luminal diameters have a thinner wall and that arteries with the smallest lumina have thicker walls. Methods: Cross-sectional segments from large arteries (N=1392) were obtained from the circle of Willis in 196 autopsied brains (mean age 55 ± 17 yrs, 39% with hypertension, 15% with diabetes and 20% with dyslipidemia). Lumen diameter, stenosis percentage, and thicknesses of intima, media, and adventitia were calculated in digital microphotography after staining. Atheromas and internal elastic lamina (IEL) disruption were rated visually. Arteries were categorized into the top 5% (“dilated”) and bottom 5% (“narrowed”) of the luminal diameters, as well as an intermediate category (90% of sample as reference). We used logistic regression to obtain the odds of association (OR, 95% CI) after adjusting for demographic and vascular variables. Results: Narrowed arteries were more frequently found in men (OR 2.7, 95%CI 1.3-5.9) and with dyslipidemia (4.2, 1.6-11.1) while dilated arteries were more frequently found in women (5.6, 2.2-14.0), in smokers (2.6, 1.0-6.5) and those with prior MI (7.7, 1.2-48.7). Narrowed arteries were more likely to have atheromas (20.8, 4.8-90.3), greater luminal stenosis (per %, 1.1, 1.1-1.2), thicker vessel walls (1.3, 1.2-1.4), but thinner medias (0.9, 0.8-1.0). Conversely, larger arteries exhibited less IEL disruption (0.3, 0.1-0.9), atheromas (0.34, 0.1-0.9) and stenosis (0.8, 0.8-0.9), their walls were thinner (0.8, 0.8-0.9) but the media was thicker (1.1, 1.1-1.2). Conclusions: Narrowed cerebral arteries were more likely to have atheromas while dilated arteries had thinner walls and were more frequent in subjects with prior MI. These findings suggest that both extremes of the arterial spectrum might be differentially related with vascular disease, underscoring the need to revisit whether standard preventive measures for vascular disease are equally effective in patients harboring such disparate arterial phenotypes.

scholarly journals EXPERIMENTAL ARTERIOSCLEROSIS

1972 ◽  
Vol 136 (4) ◽  
pp. 769-789 ◽  
Author(s):  
Michael B. Stemerman ◽  
Russell Ross
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Balloon Catheter ◽  
Muscle Cells ◽  
Endothelial Injury ◽  
Macaca Nemestrina ◽  
Elastic Fibers ◽  
Internal Elastic Lamina ◽  
Principal Factors ◽  
Elastic Lamina

Arteriosclerotic lesions have been produced in monkeys (Macaca nemestrina) by selective removal of the vascular endothelium with an intra-arterial balloon catheter. Immediately after de-endothelialization a platelet layer covers the denuded area. This thrombus is gradually removed and by 7 days the vessel appears to be largely reendothelialized. Beginning at day 4, smooth muscle cells undergo modification and migrate through fenestrae in the internal elastic lamina into the intima where they proliferate. By 28 days, the intimal lesion consists of multiple layers of smooth muscle cells surrounded by collagen and elastic fibers and basement-like material. After 3 months the lesions are markedly hyperplastic and contain new extracellular connective tissue elements. In contrast, with no further injury after 6 months the lesion has decreased markedly in size suggesting that it may be reversible in the absence of continued endothelial injury. The importance of endothelial "injury" exposing medial smooth muscle to plasma constituents may be the principal factors associated with the migration and proliferation of the smooth muscle cells into the intima resulting in the lesion. The smooth muscle cells do not contain lipid. The similarities of this lesion to the fibromusculo-elastic lesion or preatherosclerotic intimal hyperplasia in man makes it a useful model for the further study of atherosclerosis.

scholarly journals Magnesium Lithospermate B, an Active Extract ofSalvia miltiorrhiza, Mediates sGC/cGMP/PKG Translocation in Experimental Vasospasm

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Chih-Zen Chang ◽  
Shu-Chuan Wu ◽  
Aij-Lie Kwan
Keyword(s):  
Smooth Muscle ◽  
Gene Family ◽  
Muscle Relaxation ◽  
Rho Kinase ◽  
Smooth Muscle Relaxation ◽  
Internal Elastic Lamina ◽  
Tissue Samples ◽  
Magnesium Lithospermate B ◽  
Elastic Lamina ◽  
Vascular Smooth Muscle Relaxation

Background. Soluble guanylyl cyclases (sGCs) and Ras homolog gene family, member A (rhoA)/Ras homolog gene family kinase(rho-kinase) plays a role in vascular smooth muscle relaxation in subarachnoid hemorrhage (SAH). It is of interest to examine the effect of MLB on rhoA/ROCK and sGC/cGMP/PKG expression.Methods. A rodent SAH model was employed. Tissue samples were for sGCα1, sGCβ1, PKG, rhoA, ROCK (Western blot), and cGMP (ELISA) measurement.Results. MLB morphologically improved convolution of the internal elastic lamina, distortion of endothelial wall, and necrosis of the smooth muscle in the SAH rats. Expressed cGMP, sGCα1, sGCβ1, and PKG in the SAH groups were reduced (P<0.01), and MLB precondition significantly induced cGMP, sGCα1, sGCβ1, and PKG. L-NAME reversed the vasodilation effect of MLB, reduced the bioexpression of PKG and cGMP (P<0.01), and tends to reduce sGCα1 level and induce rhoA, ROCK level in MLB precondition + SAH groups.Conclusion. These results demonstrate that sGC/cGMP/PKG and NO/ET pathways play pivotal roles in SAH-induced vasospasm. Through activating sGC/cGMP/PKG pathway and partially by inactivating rho-kinase in a NO-dependent mechanism, MLB shows promise to be an effective strategy for the treatment of this disease entity.

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