SEARCH · PubMed Health

Results for “VASA VASORUM”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources

PubMed1989

[The microcirculatory system and smooth muscle cells of major arteries in various rheumatic diseases].

The microcirculatory bed (MCB) and smooth muscle cells (SMC) of the main arteries were examined in subjects who had died from rheumatic disease (33 cases), systemic lupus erythematosus (n = 28), and systemic sclerosis (n = 8) at the age of 12 to 69 years. Adventitial film preparations impregnated with silver nitrate by the method of Kupriyanov and other techniques were applied to comparatively characterize pathological and adaptive changes in MCB of vasa vasorum. In each disease, there were impaired smooth cells along with formed SMC deficit that was mostly pronounced in lupus. The medial SMC were shown to contribute to the degradation of the basic substance and reparative and synthetic processes. It was found that the immune complexes might be accepted both by the vasa vasorum system and the luminal surface of large arteries.

Adolescent↗

PubMed1992

Dissecting intramural haematoma of the coronary artery with intimal tears.

A dissecting intramural haematoma of the coronary artery is an infrequent cause of sudden and unexpected death. Most cases are women and in a significant number of these women, the haematoma occurred at term to 80 days postpartum. Because the intimal rupture and communication with the lumen were not found in most of the cases, the site of rupture has been considered to be a vasa vasorum. The authors report on a case of one woman who was at a later postpartum period (106 days). The microscopic finding of the dissected coronary artery revealed two intimal tears in a section. The case showed that the dissecting intramural haematoma of the coronary artery is caused not only by the rupture of the vasa vasorum but also by the rupture of the intima.

Adult↗

PubMed2004

Immunocytochemical study on endothelial integrity of saphenous vein grafts harvested by minimally invasive surgery with the use of vascular mayo stripers. A randomized controlled trial.

OBJECTIVES: The aim of this study is to compare the endothelial integrity of saphenous vein grafts harvested by minimally invasive surgery and veins harvested conventionally for coronary artery bypass surgery in 200 participants who were assigned to interventions by using random allocation. DESIGN: Randomized controlled trial. Methods. Immunocytochemistry with anti-CD 31 antibodies and anti-nitric oxide synthase (NOS) antibodies were employed to identify the endothelial integrity. RESULTS: The CD 31 immunostaining showed that the endothelial cell integrity of the minimally invasive harvested veins was preserved in 82+/-13% of the circumference of luminal endothelium, while in conventionally harvested grafts it was reduced to 64+/-15% (p=0.05).> This was associated with the lack of CD 31 expression in vasa vasorum (10 and 18%) in both groups, respectively, (p=0.02). The NOS immunostaining revealed that the endothelial integrity of the minimally invasive harvested grafts was preserved in 96+/-4% of the luminal endothelium circumference as compared to 74+/-10% in conventionally harvested grafts (p=0.05). The percentage of cases with the lack of NOS expression in all vasa vasorum was 12 and 21%, in G1 and G2, respectively, (p=0.02). CONCLUSION: The endothelial integrity of saphenous vein grafts harvested by minimally invasive surgery is better preserved than with the grafts obtained by the conventional manner. This could play an important role in improving vein graft patency rates.

Aged↗

PubMed2005

Does sac size matter? Findings based on surgical exploration of excluded abdominal aortic aneurysms.

PURPOSE: To prospectively examine the outcomes of excluded abdominal aortic aneurysms (AAA) that continue to expand without evidence of endoleak. METHODS: From 1984 to 1998, 1218 patients underwent operative retroperitoneal exclusion of AAA and aortoiliac reconstructions. During the procedure, the aneurysm sac was ligated proximally, as well as distally, which created an ideal in-vivo model of excluded AAA sacs with or without endoleaks. From January 2002 to June 2003, 15 of these patients were identified as having an increase in AAA sac size with or without an endoleak on duplex ultrasonography. These patients were prospectively evaluated by computed tomography and diagnostic arteriography. Patients with a demonstrable endoleak underwent embolization, and the remainder underwent open surgical exploration. RESULTS: Eight patients had arteriographically demonstrated endoleaks that were treated with coil embolization. The remaining 7 patients (6 men; mean age 76 years, range 68-81) without a demonstrable endoleak underwent elective surgical exploration and sac endoaneurysmorrhaphy. The mean time interval between the original surgery and aneurysm sac exploration was 76 months (range 52-92); during this time, the mean aneurysm sac size increased by 2.7 cm (range 1.3-5.2). The mean sac pressure was 53 mmHg, and the sac walls were noticeably thickened, with markedly dilated vasa vasorum. The sac contained yellow, fibrinous material with clear serous fluid (5 patients without any evidence of retrograde flow) or liquefied thrombus with serosanguinous fluid (2 patients with retrograde flow from lumbar arteries). No AAA sacs were pulsatile. CONCLUSIONS: Continued expansion of excluded AAA sacs can occur from causes other than a missed endoleak. Exudation of fluid from thickened sac wall and vasa vasorum, as well as local enzymatic activity, might lead to the formation of a sac hygroma. Furthermore, these findings raise questions as to the need for surgical exploration of all patients with an enlarging AAA sac in the setting of low sac pressures and no definable endoleak.

Aged↗

PubMed1996

Binding of [3H]-5-hydroxytryptamine to human coronary artery and bypass graft vessels.

OBJECTIVES: 5-Hydroxytryptamine (5-HT) has a wide range of vascular effects mediated via specific receptors and it has been suggested to be a mediator in ischemic heart disease. The aim of the present study was to localise the 5-HT receptors within the vessel wall. METHODS: Epicardial coronary arteries obtained from patients undergoing cardiac transplantation, internal mammary arteries from heart donors and saphenous veins from patients undergoing coronary bypass surgery, were sectioned and incubated with [3H]-5-HT for in vitro receptor autoradiography. RESULTS: Microscopic analysis of high resolution autoradiographic images revealed a similar pattern of [3H]-5-HT binding in epicardial coronary and internal mammary artery, where it predominated in the lamina muscularis. In the saphenous vein, binding increased towards the adventitia which showed dense, displaceable binding to the vasa vasorum as well as to nerve-like structures, from which binding was only partially displaced. Computer-assisted densitometric analysis of low resolution autoradiographs revealed a high degree of specific binding to all vessels examined. CONCLUSIONS: The distribution of the [3H]-5-HT binding is different in the saphenous vein compared to epicardial coronary and internal mammary artery. The dense binding to vasa vasorum in the saphenous vein suggests a role for 5-HT in closure of these nutrient vessels, which could contribute to the formation of atherosclerotic changes in saphenous vein grafts.

Adult↗

PubMed2006

Endothelial alpha(v)beta3 integrin-targeted fumagillin nanoparticles inhibit angiogenesis in atherosclerosis.

OBJECTIVE: Angiogenic expansion of the vasa vasorum is a well-known feature of progressive atherosclerosis, suggesting that antiangiogenic therapies may stabilize or regress plaques. Alpha(v)beta3 integrin-targeted paramagnetic nanoparticles were prepared for noninvasive assessment of angiogenesis in early atherosclerosis, for site-specific delivery of antiangiogenic drug, and for quantitative follow-up of response. METHODS AND RESULTS: Expression of alpha(v)beta3 integrin by vasa vasorum was imaged at 1.5 T in cholesterol-fed rabbit aortas using integrin-targeted paramagnetic nanoparticles that incorporated fumagillin at 0 microg/kg or 30 microg/kg. Both formulations produced similar MRI signal enhancement (16.7%+/-1.1%) when integrated across all aortic slices from the renal arteries to the diaphragm. Seven days after this single treatment, integrin-targeted paramagnetic nanoparticles were readministered and showed decreased MRI enhancement among fumagillin-treated rabbits (2.9%+/-1.6%) but not in untreated rabbits (18.1%+/-2.1%). In a third group of rabbits, nontargeted fumagillin nanoparticles did not alter vascular alpha(v)beta3-integrin expression (12.4%+/-0.9%; P>0.05) versus the no-drug control. In a second study focused on microscopic changes, fewer microvessels in the fumagillin-treated rabbit aorta were counted compared with control rabbits. CONCLUSIONS: This study illustrates the potential of combined molecular imaging and drug delivery with targeted nanoparticles to noninvasively define atherosclerotic burden, to deliver effective targeted drug at a fraction of previous levels, and to quantify local response to treatment.

Angiogenesis Inhibitors↗

PubMed2000

Coexpression of cyclooxygenase-2 and matrix metalloproteinases in human aortic atherosclerotic lesions.

Inflammation appears to have a major role in the development of atherosclerosis. Cyclooxygenase-2 (COX-2) is involved in the inflammatory response via the generation of prostanoids that, in turn, are involved in the production of matrix metalloproteinases (MMPs). This study aimed to investigate atherosclerosis in human aortas for in situ tissue distribution of COX-2, MMPs including MMP-9 and membrane type 1 MMP (MT1-MMP), and tissue inhibitor of metalloproteinase-2 (TIMP-2). Immunohistochemical studies were performed on atherosclerotic lesions of aortas from patients with aortic aneurysms (n = 4) and dissections (n = 3) by using antibodies to COX-2, MMP-9, MT1-MMP, and TIMP-2. Control tissues were obtained from traumatically dissected aortas (n = 2). All specimens from diseased aortas had atherosclerotic lesions ranging from fatty streak to atheromatous plaques. In control, there was no expression of COX-2, MMP-9, and MT1-MMP in all aortic layers. Immunoreactivity for COX-2 was predominantly noted in macrophages and smooth muscle cells (SMCs) of the intima including atherosclerotic plaque itself and the medial layer of the plaque base, as well as in SMCs and endothelial lining of the vasa vasorum in the adventitia. Immunoreactivity for MMP-9 and MT1-MMP was found in the same distribution as that of COX-2. Additionally, the expression of TIMP-2 increased in relation to MMP-9 expression. This study demonstrates that COX-2 is coexpressed with MMP-9 and MT1-MMP, not only by macrophages and SMCs in atherosclerotic lesions, but also in endothelial lining of the vasa vasorum of human aortas. Thus, vascular inflammatory reactions may influence extracellular matrix remodeling by coactivation of MMPs in the development of atherosclerosis and, in turn, the progression of disease.

Animals↗

PubMed1984

Endothelial seeding of Dacron and polytetrafluoroethylene grafts: the cellular events of healing.

To detect cellular differences in the healing of polytetrafluoroethylene (e-PTFE) and Dacron grafts up to 7 months after implantation, we studied 108 aortic graft interpositions in dogs. Each prosthesis was alternately prepared by endothelial seeding or by an unseeded control method. The grafts were perfusion fixed and studied with light, scanning, and transmission electron microscopy at intervals from before to 221 days after implantation. Seeding resulted in the development of an extensive endothelial flow surface in two out of three of the e-PTFE and none out of four of the Dacron grafts by 10 days after implantation (p = 0.053). After 30 days a microfibrillar subendothelial matrix ranging from 5 to 11 mu formed in all but three grafts with endothelial coverage. The inner capsule of mature Dacron grafts was significantly thicker (169 +/- 143 mu) than in e-PTFE grafts (22 +/- 32 mu; p = 0.002). Seeded and unseeded Dacron grafts had predominantly fibroblasts in the outer capsule of the graft by 10 days. Surface endothelium, vasa vasorum, fibroblasts, and myointimal cells appeared in the inner capsule between 10 and 30 days after implantation. In Dacron grafts, fibroblasts and myointimal cells predominated in the inner capsule at 30 days, with smooth muscle cells not being definitely identifiable until after 150 days. Neither fibroblasts nor myointimal cells were common (present but sparse in one of four e-PTFE grafts) at 30 days, and transmural vasa vasorum were never seen. The seeded endothelial cells migrated rapidly from the sites of initial adhesion near the e-PTFE onto the flow surface. Only one of four of the unseeded e-PTFE grafts had surface endothelium after 30 days, and only moderate coverage developed during 180 days. We conclude that endothelial healing is more rapid in seeded e-PTFE grafts than in seeded Dacron grafts and occurs by a different mechanism.

Animals↗

PubMed1981

[Immunological implications in the pathogenesis of Horton arteritis].

Fragments of temporal artery obtained by surgical biopsy from 3 patients suffering from Horton arteritis were employed for immunopathologic studies by direct immunofluorescence. In 2 of the cases, granular deposition of IgM, C1q and C3 but not of albumin were observed in the wall of vasa vasorum of the temporal artery. Elution techniques determined the disappearance of the immunoreactants. In one case in which biopsy fragments of temporal artery were obtained prior to and after steroid treatment it was observed that IgM and complement, previously present, disappeared after such treatment. The data reported indicate that indeed immunologic factors play a role in the pathogenesis of the disease and that the immunoreagents present on the wall of vasa vasorum are not evidence of increased vascular permeability but indicate an active immunologic process which takes place in them.

Albumins↗

PubMedDate not supplied

Neurocompensatory responses to balloon-catheter-induced injury of the rat carotid artery.

Percutaneous transluminal angioplasty relieves discrete arterial stenosis but causes extensive vascular injury. There is denudation of the endothelium and variable medial disruption, but the effect on adventitial structures has not been studied in detail. We have investigated the innervation of the left and right carotid arteries after unilateral balloon-catheter-induced injury. Immunohistochemical examination of the arteries 1 day after Fogarty-catheter-induced injury of the left common carotid artery revealed a reduction in the density of protein gene product 9.5 (PGP)-, substance P (SP)- and calcitonin-gene-related peptide (CGRP)-containing nerves close to the medial smooth muscle of the injured vessel. At the same time, on the side contralateral to the injury, there was a substantial increase in the density of PGP-, SP- and CGRP-containing nerves innervating the carotid artery and vasa vasorum compared to controls. Immunoassay data from these vessels showed a selective increase in SP and CGRP contents of the contralateral carotid artery (SP, controls 0.02 +/- 0.01, operated 0.59 +/- 0.32 pmol/cm; CGRP, controls 0.03 +/- 0.01, operated 0.14 +/- 0.03 pmol/cm, n = 6, p < 0.05). Neuropeptide Y levels were unchanged. Twenty-eight days after surgery, at which time a neointima was present, peptide levels were no different from controls, and the innervation of both the left and right carotid arteries and vasa vasorum was indistinguishable from the controls. In conclusion, balloon-catheter-induced injury includes damage to the perivascular nerves and induces a transient increase in the density of sensory neuropeptide-containing nerves innervating the contralateral, uninjured side. This novel observation may reflect neurocompensatory responses to vascular injury.

Animals↗

PubMed2006

A numerical study on the influence of vulnerable plaque composition on intravascular thermography measurements.

Intracoronary thermography is a technique that measures lumen wall temperatures for vulnerable plaque detection. In this paper the influence of vulnerable plaque composition on lumen wall temperatures was studied numerically. Concerning the vulnerable plaque heat generation, the location of the heat source and its heat production were varied. Concerning the heat transfer, the thermal properties of the lipid core and the location of the vasa vasorum were studied. The heat source location was the main determinant of the lumen wall temperature distribution. The strongest effect was noted when the heat producing macrophages were located in the shoulder region leading to focal spots of higher temperature. The maximal lumen wall temperature was mainly determined by the heat production of the macrophages and the cooling effect of blood. The insulating properties of the lipid core increased lumen wall temperatures when the heat source was located in the cap and the presence of vasa vasorum lowered the temperatures. These results show that the lumen wall temperature distribution is influenced by vulnerable plaque composition and that intracoronary thermography techniques require a high spatial resolution. To be able to couple temperature measurements to plaque vulnerability, intracoronary thermography needs to be combined with an imaging modality.

Animals↗

PubMed2006

The "in situ" expression of human leukocyte antigen class I antigens is not altered by cryopreservation in human arterial allografts.

This study was aimed to establish whether the cryopreservation procedure we currently use in clinics can modify arterial homograft antigenicity. To this purpose, we performed an immunohistochemical study on fresh and cryopreserved human arterial homografts to visualize the expression of HLA class I heavy and light chains "in situ" by using the HC-10 and Namb-1 monoclonal antibodies. Human femoral arteries and thoracic aortas were harvested from 18 heart-beating donors and sampled before and after cryopreservation. Arterial segments were frozen in liquid nitrogen vapors in a controlled rate freezing system. After thawing, samples were processed for routine immunohistochemistry. To standardize immunostaining, flow-cytometry indirect immunofluorescence analysis was performed on HUVEC; immunohistochemistry of human ovarian cortical vessels was performed as an additional positive control. Negative controls were performed by omitting tissue incubation with primary antibodies. HLA-class I antigens were markedly expressed by endothelial cells lining surface intima and adventitial vasa vasorum; a moderate expression was found in medial smooth muscle cells. Except for the surface unreactivity caused by loss of endothelium, results from cryopreserved arterial allografts were strictly comparable to those observed in fresh, unfrozen tissues. These results support the view that cryopreserved arterial allografts are immunogenic as their fresh counterparts; apart from smooth muscle cells which retained a moderate expression of HLA class I antigens following cryopreservation, our study suggests that the highly HC-10 positive endothelial cells we found to line the rich adventitial network of vasa vasorum are expected to be one of the major targets of the serological response in the recipient.

Adult↗

PubMed1998

Mapping of vascular dendritic cells in atherosclerotic arteries suggests their involvement in local immune-inflammatory reactions.

OBJECTIVE: We previously demonstrated that vascular dendritic cells (VDCs) are present in the intima of large arteries and that their numbers are increased in atherosclerotic lesions. This study was undertaken to determine whether VDCs are involved in immune-mediated reactions in atherogenesis. METHODS: Specimens of carotid artery and aorta were obtained at operation. VDCs were identified with anti-CD1a or with S-100. Co-localisation of VDCs with different intimal cells, including T-cells and macrophages, was studied using a double immunostaining procedure. In areas where the co-localising cells were detected, the peculiarities of expression of HLA-DR, ICAM-1, VCAM-1 were examined. RESULTS: In all the atherosclerotic plaques, VDCs were seen in contact with T-cells, but these co-localising cells were irregularly distributed and were mainly found in zones of neovascularisation containing inflammatory infiltrates. In other areas, T-cell/VDC co-localisation was rarely detected but VDCs were often found in contact with macrophages. VDCs were detected also in the media beneath atherosclerotic lesions and in the adventitia, where they were mostly around vasa vasorum, especially in areas exhibiting signs of acute inflammation. In these areas VDCs expressed ICAM-1, VCAM-1 and were in contact with T-cells. In both plaques and in the adventitia, the areas with co-localising VDCs and T-cells corresponded to the areas with HLA-DR expression. CONCLUSIONS: The results suggest that VDCs are involved in T-cell activation in atherogenesis. There are two regions within the arterial wall where VDC/T-cell co-localisation mostly occurs, namely, in zones of neovascularisation containing inflammatory infiltrates located within atherosclerotic lesions, and in areas with inflammatory infiltrates around vasa vasorum in the adventitia. Possibly, some intimal VDCs migrate through the media and adventitia to adjacent lymph nodes where they present atherosclerosis associated antigens. We also speculate that VDC/macrophage contacts are essential in processing immune information in atherogenesis.

Adult↗

PubMed2006

Angiogenesis in atherosclerosis: gathering evidence beyond speculation.

PURPOSE OF REVIEW: The present review summarizes evidence for several functions of neovascularization in plaque growth that sustain perfusion beyond limits of diffusion from the artery lumen and outer adventitial vasa vasorum, deposit proatherogenic plasma molecules, recruit immune cells and progenitors, and promote intraplaque hemorrhage. Recent approvals of antiangiogenesis drugs for clinical use in cancer and macular degeneration improve the feasibility of testing whether such agents inhibit plaque angiogenesis and incidental atherosclerosis. RECENT FINDINGS: Improvements in large and small animal models of atherosclerosis and knowledge of the molecular regulation of angiogenesis in development and disease have advanced understanding of plaque angiogenesis. Genetic modifications of angiogenesis molecules in mouse strains susceptible to atherosclerosis provide experimental means to identify native molecules that regulate plaque angiogenesis. Studies of plaque angiogenesis are aided by micro-computed tomography techniques that image vasa vasorum anatomy in relation to the atheroma. SUMMARY: Greater knowledge of plaque angiogenesis regulation is needed to design treatments that target the most critical regulatory pathways. Evolutions in angiogenesis inhibitor treatments for cancer and other diseases call for a need to understand the distinct cardiovascular profiles of different agents to rationally combine agents for optimal selectivity and efficacy in the intended vascular bed.

Angiogenesis Inhibitors↗

PubMed2001

Small-vessel vasculitis surrounding a spared temporal artery: clinical and pathological findings in a series of twenty-eight patients.

OBJECTIVE: Occasionally, a temporal artery biopsy reveals small-vessel vasculitis (SVV) surrounding a spared temporal artery, the significance of which is unclear. We analyzed the final diagnosis in a series of patients with this condition and tried to identify histopathologic features with potential usefulness in predicting the ultimate diagnosis. METHODS: We performed a clinical and histopathologic review of 28 patients in whom SVV surrounding a spared temporal artery was the first histologic finding that led to the diagnosis of vasculitis. For comparison purposes, we analyzed the pattern of small vessel involvement in 30 patients with biopsy-proven giant cell arteritis (GCA). RESULTS: GCA was considered the most likely diagnosis in 12 patients, based on the absence of clinical evidence of additional organ involvement and normal findings on muscle biopsy and electrophysiologic study. Three patients had systemic necrotizing vasculitis (SNV), based on the demonstration of typical lesions on subsequent muscle, nerve, or kidney biopsy. After extensive evaluation, 4 patients remained unclassifiable. Nine patients were incompletely studied. Fibrinoid necrosis was significantly more frequent in patients with SNV (P = 0.0022), whereas involvement of vasa vasorum was more frequent in patients classified as having GCA (P = 0.022). No differences in the pattern of small vessel involvement were found in patients with SVV surrounding a spared temporal artery who were classified as having GCA compared with patients with biopsy-proven GCA. Granulocytes were observed at similar frequency in all conditions. CONCLUSION: SVV may be the only abnormal feature in a temporal artery biopsy and the only histologic evidence of vasculitis. The diagnosis of GCA can be reasonably established in most of these patients when there is no apparent evidence of additional organ involvement. However, when fibrinoid necrosis is observed or the temporal artery vasa vasorum are not involved, SNV must be extensively excluded.

Adult↗

PubMed2005

Atherosclerotic plaque progression and vulnerability to rupture: angiogenesis as a source of intraplaque hemorrhage.

Observational studies of necrotic core progression identify intraplaque hemorrhage as a critical factor in atherosclerotic plaque growth and destabilization. The rapid accumulation of erythrocyte membranes causes an abrupt change in plaque substrate characterized by increased free cholesterol within the lipid core and excessive macrophage infiltration. Neoangiogenesis is associated closely with plaque progression, and microvascular incompetence is a likely source of intraplaque hemorrhage. Intimal neovascularization is predominantly thought to arise from the adventitia, where there are a plethora of pre-existing vasa vasorum. In lesions that have early necrotic cores, the majority of vessels invading from the adventitia occur at specific sites of medial wall disruption. A breech in the medial wall likely facilitates the rapid in-growth of microvessels from the adventitia, and exposure to an atherosclerotic environment stimulates abnormal vascular development characterized by disorganized branching and immature endothelial tubes with "leaky" imperfect linings. This network of immature blood vessels is a viable source of intraplaque hemorrhage providing erythrocyte-derived phospholipids and free cholesterol. The rapid change in plaque substrate caused by the excessive accumulation of erythrocytes may promote the transition from a stable to an unstable lesion. This review discusses the potential role of intraplaque vasa vasorum in lesion instability as it relates to plaque rupture.

Animals↗

PubMed2000

Thromboangiitis obliterans: classic and new morphological features.

The clinical and pathological concept of thromboangiitis obliterans (TAO, Buerger's disease) is still controversial. While the clinical criteria of TAO are relatively well defined, the etiology is unknown and its diagnosis based on pathology is confusing, since there is no consensus on the precise pathological criteria for TAO. To investigate the morphological features that differentiate TAO from arteriosclerosis obliterans (ASO) or thromboembolism, and to clarify the morphological independence of TAO, we studied 94 amputated specimens of lower extremities, including 31 specimens from patients with a clinical diagnosis of TAO and 31 autopsy specimens as control cases. It was revealed that most of the classic morphological features described by Buerger and others are not helpful when considered independently in the differential diagnosis, except for intact internal elastic lamina. In addition, findings of intimal inflammation, intact media and absence of medial calcification were demonstrated to be common in both TAO and thromboembolism. Statistical analysis in the present study, the most comprehensive thus far, showed that novel findings of onion-like-shaped recanalizing vessels in the occluded arteries, adventitial fibrosis without medial fibrosis, swelling of the endothelium of the vasa vasorum and edema beneath the external elastic lamina were characteristic of TAO and would be helpful in a differential diagnosis. When a combination of these morphological features is present, diagnosis of a presumed overlap of TAO and ASO in the same site of the vessel concerned is possible. Furthermore, comparison of statistical evaluations based on morphological features performed in various diagnostic groups implies that the clinical diagnosis of TAO is currently underestimated because the results of the analysis of morphological features of specimens in which TAO was suspected or specimens selected on the basis of a broad and nonspecific definition of TAO were surprisingly similar to the results in strictly defined TAO cases. Our findings suggest that injury and regeneration of minute vessels such as recanalizing vessels and vasa vasorum play a part in the pathogenesis of TAO.

Adult↗

PubMed2001

Anti-angiogenesis: A new potential strategy to inhibit restenosis.

Microvessels are an integral component of the neointima developing in response to the acute vascular injury resulting from angioplasty. These vessels originate from the vasa vasorum of the adventitia, and as such appear similar to the microvessels present in atherosclerotic plaques. Several angiogenic factors have been found in atherosclerotic plaques and have been associated with increased microvascularity. In addition, most of these agents - either directly or indirectly - also induce smooth muscle cell (SMC) proliferation, an essential component of the developing neointima. We therefore propose: (1) these newly formed blood vessels are necessary for the development, maintenance, and expansion of the neointimal lesions present in restenosis; (2) the initiation, regulation and maintenance of these vessels is, at least in part, due to the coordinate sequential expression of hypoxia-inducible factor 1 (HIF-1), vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), and/or other angiogenic factors such as the fibroblast growth factor (FGF) family of proteins; (3) targeted disruption of the signal transduction pathways modulated by these molecules may reduce vasa vasorum expansion and SMC proliferation. These effects, in turn, may inhibit neointimal expansion and thus the development of restenosis, especially following stenting.

Journal Article↗