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PubMed2006

Neovascularization in human atherosclerosis.

In the absence of disease, microvessels provide vessel wall nutrients to the tunica media, while the intima is fed by oxygen diffusion from the lumen. As disease evolves and the tunica intima thickens, oxygen diffusion is impaired, and microvessels become the major source for nutrients to the vessel wall. Microvessels serve as a port of entry for inflammatory cells, from the systemic circulation to the nascent atherosclerotic lesion. As disease progress, microvessels also play a role in intraplaque hemorrhage, lipid core expansion, and plaque rupture. In addition, microvessels are also involved in stent restenosis, and plaque regression. Therefore, microvessels are a pivotal component of atherosclerosis, and proper patient risk-stratification in the near future may include the detection of increased neovascularization in atherosclerotic lesions. This review divided in two parts summarizes the current understanding of atherosclerosis neovascularization, starting with the normal anatomy and physiology and progressing to more advanced stages of the disease. We will review the structure and function of vasa vasorum in health and disease, the mechanisms responsible for the angiogenic process, the role of the immune system, including inflammation and Toll-like receptors, and the pathology of microvessels in early atherosclerotic plaques. Furthermore, the review addresses the advanced stages of atherosclerosis, summarizing the progressive role for microvessels during disease progression, red blood cell extravasation, lipid core expansion, plaque rupture, healing, repair, restenosis, and disease regression, offering the clinician a state-of-the-art, "bench to bedside" approach to neovascularization in human atherosclerosis.

Animals↗
PubMed1994

Poststenotic dilatation in arteries and the role of turbulence.

A hypothesis is presented on the origin of PSD, the dilatation which occurs in an artery distal to a site of stenosis. The fact that turbulent flow is associated with both PSD and with experimentally induced varicosities suggested that similar mechanisms are involved. That is the basis for a proposal that PSD originates as an active dilator response of the artery wall to circulating NE released in excess from a section of the vasa vasorum (VV) network of the affected artery. Turbulence is believe to be the cause of that excess through multiplying the volume of blood and, consequently, the amount of circulating NE flowing from an artery to its VV. There is published evidence that turbulence does increase flow to the VV of an artery and evidence is presented that if norepinephrine is injected rapidly into a small canine muscular artery, with the aim of creating turbulence in the artery, the injection is promptly followed by localised dilator effects in the artery which, overall, is constricted by the drug.

Animals↗
PubMed1980

Microvasculature of the rat lung as revealed by scanning electron microscopy of corrosion casts.

The pulmonary microvasculature of rats was studied by injection replicas prepared from Mercox. This medium enabled us to easily obtain consistant, stable and complete injected replicas of the pulmonary vasculature. The pulmonary arteries repeated branching as far as the pulmonary arterioles, and then formed rich, basket-like anastomosing capillary networks in the alveolar walls. These capillary networks were collected into the tributaries of the pulmonary veins. The walls of the pulmonary veins, down to small branches of approximately 100 micrometers in diameter, were surrounded by one to three layers of circular or obliquely oriented capillaries with longitudinal connections. The pulmonary artery had only a single layer of capillary network in the adventitia. The vasa vasorum of the pulmonary vessels were collected into venules. They were confluent to the bronchial veins outside the lung and into the tributaries of the pulmonary veins within the lung. The bronchial tree was supplied by the bronchial arteries which form the coarse capillary plexus extending as far as the terminal bronchioles. The trachea and the proximal parts of the bronchi drained into the bronchial veins connected with the superior vena cava. The distal parts of the bronchial tree drained into the tributaries of the pulmonary veins, or adjacent capillary networks in and around the alveolar walls.

Animals↗
PubMed1999

Morphology and histology of human and canine internal thoracic arteries.

BACKGROUND: We evaluated human and canine internal thoracic arteries (ITAs) to determine whether the latter is valid for studies relevant to clinical use. METHODS: We studied 19 human ITAs obtained from 1 female and 14 male victims of recent fatal accidents who had no evidence of cardiovascular disease (mean age = 39+/-19 years; range = 15 to 79 years), and ITAs of 21 randomly-selected mongrel dogs of both sexes, weighing 18-40 kg (average = 24.3+/-5.7 kg). Specimens were fixed in formalin at a controlled pressure of 120 mm Hg, before extensive assessment that included intimal thickening, condition of the internal elastic lamina, and number of medial elastic lamellae and vasa vasorum. RESULTS: The canine morphology and histology were similar to the human ITAs, but there was no intimal hyperplasia, and the media and adventitia were thinner (ITAs of humans older than 40 years had significant increases in medial thickness, as well as in overall length). Morphologically and histologically, the left and right canine ITAs were almost completely the same. CONCLUSIONS: Canine ITAs are valid for bilateral comparative studies and are a useful tissue source and model for clinically-relevant experimental studies.

Adolescent↗
PubMed1983

Effect of aspirin on angioplasty-induced vessel wall hyperemia.

Angioplasty produces a persistent 20-fold increase in blood flow through mural vasa vasorum. To assess the role of prostaglandins in this phenomenon, vessel wall blood flow in experimentally dilated carotid arteries of aspirin treated dogs was measured. Aspirin (10 mg/kg, intravenously) significantly attenuated the increase in blood flow produced by dilation (+283 +/- 91% SE, n = 6) when compared to non-aspirin-treated controls (+2356 +/- 885% SE, n = 10). This suggests that aspirin, by interfering with arachidonate metabolism, may decrease local vasodilation after angioplasty. The effect of aspirin therapy on the long-term success of angioplasty requires further study.

Angioplasty, Balloon↗
PubMed2000

The presence of collagen III and IV in experimental microsurgical anastomoses of arteries.

PURPOSE: This study investigated the distribution of collagen III and IV in experimental microvascular anastomoses and correlated the findings with the quality of the healing process. MATERIALS AND METHODS: A previously excised and reanastomosed section of the left common carotid artery of 21 female Wistar rats were explanted 4 weeks after surgery. Collagens III and IV were identified in perfusion-fixed specimens by immunohistochemistry. RESULTS: The identification and distribution of collagens reflected the quality of each suturing procedure. A myointimal hyperplasia was present, extending into the vascular lumen, and was closely related to the ends of the vessel segments. The extent of myointimal hyperplasia was dependent on the length and the vitality of the vessel segments. The media was the weakest part of the tissue layers with regard to regenerative potential in the axial direction. The marked cuff of the adventitia around the anastomosis was rich in collagen III-positive vasa vasorum. Collagen IV was distributed in net-like patterns in the media. The distribution pattern in the media was not observed in anastomoses with incomplete approximation and necrotic segment ends. The collagen IV-positive subendothelial basal membrane was incomplete in the aneurysms because of partial necrosis. CONCLUSIONS: The experimental findings support the need for atraumatic suturing in microvascular surgery. Immunohistochemical detection of collagens can be a valuable tool for studying the basic processes of wound healing and the integration of microvascular flaps into their recipient sites.

Anastomosis, Surgical↗
PubMed2003

[Pathogenesis of atherosclerosis in patients with lipid metabolism disturbances: hypothesis on cholesterol utilization and atheromatous plaque formation].

Cholesterol is known to participate in atheromatous plaque formation coming from blood stream and affecting vascular endothelium in environment of elevated low-density lipoproteins (LDL). Nevertheless, the occurrence of single atheromatous plaque evidences the possibility of local lipoprotein accumulation by vascular wall without systemic increase in serum LDLs. The author hypothesizes that in the absence of hypercholesterolemia atheroma can evolve through the utilization of modified LDL and free or etherified cholesterol, that remain in media non-removed by high density lipoproteins (HDL) owing to their structural damage after local vascular wall ischemia caused by vasa vasorum disorders. Disturbances in HDL acceptor function and transport of cholesterol and modified LDL to blood circulation and further into liver are followed by local accumulation of these products in smooth muscle cells. Overloaded by lipids smooth muscle cells move through internal fenestrated membrane thus activating receptor mechanism for transmission of modified lipoproteins to monocytes and capture of endothelial membrane and amorphous lipids by them in local lipid peroxidation area. A framework for hypothesis experimental and clinical testing is suggested.

Cholesterol, HDL↗
PubMed2004

Molecular imaging of atherosclerotic plaques using a human antibody against the extra-domain B of fibronectin.

Current imaging modalities of human atherosclerosis, such as angiography, ultrasound, and computed tomography, visualize plaque morphology. However, methods that provide insight into plaque biology using molecular tools are still insufficient. The extra-domain B (ED-B) is inserted into the fibronectin molecule by alternative splicing during angiogenesis and tissue remodeling but is virtually undetectable in normal adult tissues. Angiogenesis and tissue repair are also hallmarks of advanced plaques. For imaging atherosclerotic plaques, the human antibody L19 (specific against ED-B) and a negative control antibody were labeled with radioiodine or infrared fluorophores and injected intravenously into atherosclerotic apolipoprotein E-null (ApoE-/-) or normal wild-type mice. Aortas isolated 4 hours, 24 hours, and 3 days after injection exhibited a selective and stable uptake of L19 when using radiographic or fluorescent imaging. L19 binding was confined to the plaques as assessed by fat staining. Comparisons between fat staining and autoradiographies 24 hours after 125I-labeled L19 revealed a significant correlation (r=0.89; P<0.0001). Minimal antibody uptake was observed in normal vessels from wild-type mice receiving the L19 antibody and in atherosclerotic vessels from ApoE-/- mice receiving the negative control antibody. Immunohistochemical studies revealed increased expression of ED-B not only in murine but also in human plaques, in which it was found predominantly around vasa vasorum and plaque matrix. In summary, we demonstrate selective targeting of atheromas in mice using the human antibody to the ED-B domain of fibronectin. Thus, our findings may set the stage for antibody-based molecular imaging of atherosclerotic plaques in the intact organism.

Adult↗
PubMed2003

Mechanisms and consequences of large artery rigidity.

In this review paper, the classical and more recently described mechanisms responsible for the structural and functional characteristics of large artery rigidity are described. Mostly important, these characteristics appear to be non-specific to the primary disease process involved in arterial hypertension, diabetes mellitus, dyslipidemia, congestive heart failure, chronic uremia, and perhaps senescence, including vascular dementia. Nonspecific in terms of aetiology, the vasculopathy encountered in these diseases exhibits common structural and functional abnormalities. The identification of such abnormalities could well become the target of potent nonpharmacological and (or) pharmacological interventions capable of preventing or retarding morbidity and mortality. The structural characteristics responsible for large artery rigidity include smooth muscle cell hypertrophy, matrix collagen deposition, and recently described, dysfunction in proteoglycan metabolism. Functional abnormalities, such as bradykinin-dependent hyper-reactivity of smooth muscle cells and vasa vasorum microcirculation network disturbances, also appear to alter aortic wall rigidity. The physiopathology of target organ damage is then revisited, based on endothelial dysfunction, documented in large and resistance arteries, as well as in microcirculation networks, where altered permeability to macromolecules leads to interstitial matrix disorganization and cell damage. The clinical evaluation of large artery rigidity is described, and one of the noninvasive methods, evaluation of pulse-wave velocity, is validated in normal conditions and in disease processes. Finally, non-pharmacological and pharmacological therapeutic measures are presented, and includes physical exercise to reduce insulin resistance, and renin-angiotensin-II-aldosterone modulators.

Animals↗
PubMed1981

The morphology of the human newborn ductus arteriosus: a reappraisal of its structure and closure with special reference to prostaglandin E1 therapy.

The ductus arteriosus was examined in 103 fetuses and infants to define the normal structure, development, and morphologic features of the functional and anatomic phases of ductal closure. New contributions include ultrastructural observations and the light microscopic definition of the junctional regions of the ductus with the pulmonary artery and aorta. Observations relating to ductal closure include hyperemia of the ductal vasa vasorum, the presence of longitudinal muscle bands in the inner media, necrosis of the inner ductal wall, and organization of intraluminal thrombi. We found that a ductus arteriosus that fails to close normally is liable to show morphologic lesions, including intimal fibrinous deposits, medial hemorrhages, and dissecting aneurysms. The findings were used comparatively to investigate whether prostaglandin E1 infusion, given to maintain ductal patency in 7 infants with ductus dependent congenital heart disease, was associated with specific morphologic features. We could not delineate specific changes attributable to its use.

Age Factors↗
PubMed1999

Estrogen and progesterone receptors in normal and varicose saphenous veins.

The presence of estrogen and progesterone receptors was investigated in the walls of normal and varicose veins. Cryostat sections from the saphenous veins of 29 normal individuals, and varicose and normal vein segments of 32 patients with varicose veins, were stained with anti-estrogen or anti-progesterone receptor antibodies. Nuclear stain intensity was scored by three independent observers. Receptors to both hormones were detected in the nuclear regions of the intima and media in females and males. In the adventitia, estrogen and the progesterone receptors were found only in nuclei of the vasa vasorum. Estrogen receptor levels were lower in non-varicose segments of varicose veins compared with normal veins. In varicose segments, estrogen receptors were more abundant than in the non-varicose parts of the same vein, especially in females. Similarly, progesterone receptor levels in the non-varicose portions were higher in females. These gender differences may be related to hormonal action. However, these differences may also be age related. These findings may be related to the involvement of sex-hormones in varicosis, by mechanisms as yet unknown.

Adult↗
PubMed1997

Intermediate filament proteins in adult human arteries.

BACKGROUND: The cytoskeleton of cells in blood vessel walls contains desmin, vimentin, and cytokeratins. The distribution of these proteins in human vessels is not fully known. We have mapped the distribution of intermediate filament proteins in human arterial walls. METHODS: Monoclonal antibodies targeted at the intermediate filament proteins desmin, vimentin, and cytokeratins were used, and the distribution of these proteins was studied by immunohistochemistry. RESULTS: In the muscular arteries, most smooth muscle cells in the media expressed both desmin and vimentin; in the elastic arteries, the proportion of desmin-labelled cells was lower and preferentially located to the periphery of the media. In general, the desmin immunoreactivity within the intima was weak, but some smooth muscle cells and smooth muscle cells in the musculoelastic layer showed strong immunoreactivity. The vasa vasorum exhibited a heterogeneous desmin-labelling pattern. The vimentin antibodies labelled the endothelium and showed a heterogeneous staining pattern in the other layers of the arterial wall. Cytokeratin was detected in occasional cells in the media of muscular arteries, in many adluminal cells and cell clusters in the coronary intima, and in smooth muscle cells in the media of the elastic arteries. CONCLUSIONS: Vimentin is widely distributed in vascular smooth muscle cells, whereas the distribution of desmin and cytokeratin varies. Each artery studied had an intermediate filament pattern typical for the anatomical location. There were no interindividual variations in the distribution of intermediate filament proteins.

Adult↗
PubMed2005

Metalloproteinase-2 and -9 in giant cell arteritis: involvement in vascular remodeling.

BACKGROUND: Both matrix metalloproteinase-2 (MMP-2) and -9 (MMP-9) have been postulated to play roles in the pathophysiology of giant cell arteritis (GCA) because of their ability to degrade elastin. Understanding the specific mediators of arterial damage in GCA could lead to new therapeutic targets in this disease. METHODS AND RESULTS: Temporal artery biopsy specimens were obtained from 147 consecutive patients suspected of GCA. Clinical and histopathological data were collected according to protocol. Using immunohistochemistry, we compared the expression of MMP-2 and MMP-9 in the temporal artery biopsies of both GCA cases (n=50) and controls (n=97). MMP-9 was found more frequently in positive than in negative temporal artery biopsies (adjusted odds ratio [OR], 3.20; P=0.01). In contrast, the frequency of MMP-2 was not significantly different between positive and negative biopsies (adjusted OR, 2.18; P=0.22). Both MMP-2 and MMP-9 were found in macrophages and giant cells near the internal elastic lamina and in smooth muscle cells and myofibroblasts of the media and intima. MMP-9 was also found in the vasa vasorum. MMP-9 but not MMP-2 was associated with internal elastic lamina degeneration, intimal hyperplasia, and luminal narrowing, even after adjustment for possible confounding variables. CONCLUSIONS: MMP-9 appears more likely than MMP-2 to be involved in the pathophysiology of GCA. MMP-9 not only participates in the degradation of elastic tissue but also is associated with intimal hyperplasia, subsequent luminal narrowing, and neoangiogenesis. The expression of MMP by smooth muscle cells implicates these cells as potential secretory cells in GCA.

Aged↗
PubMed2003

Increased expression of thrombospondin-1 in vessel wall of diabetic Zucker rat.

BACKGROUND: Thrombospondin-1 (TSP-1) expression in the vascular wall has been related to the development of atherosclerotic lesions and restenosis. TSP-1 promotes the development of neointima and has recently been associated with atherogenesis at a genetic level. Because TSP-1 expression is responsive to glucose stimulation in mesangial cells, we hypothesized that glucose may stimulate its production by vascular cells. Thus, TSP-1 expression in the blood vessel wall may increase, providing a molecular link between diabetes and accelerated vascular lesion development. METHODS AND RESULTS: To determine whether the expression level of TSP-1 in vessel wall is increased in diabetes, aorta and carotid arteries of Zucker rats were used for immunostaining, Western blotting, and in situ RNA hybridization. A significant increase in TSP-1 expression was found in the adventitia of blood vessels from diabetic rats. Consistent with the well-known antiangiogenic effect of TSP-1, the number of vasa vasorum was reduced in aortas from diabetic rats. In cultured endothelial cells, vascular smooth muscle cells, and fibroblasts, TSP-1 expression increased in response to glucose stimulation (>30-fold). After balloon catheter injury to carotid arteries, expression of TSP-1 protein and mRNA was higher at all time points in the vessels of diabetic rats. CONCLUSIONS: Increased expression of TSP-1 in blood vessels in diabetes may represent a new link between diabetes, atherogenesis, and accelerated restenosis. This increase in TSP-1 production may be a direct response of vascular cells to glucose.

Animals↗
PubMed1987

Anatomical studies to support the expanded use of the internal mammary artery graft for myocardial revascularization.

The internal mammary artery pedicle graft is frequently used for coronary bypass. Five internal mammary artery pedicle grafts, harvested but not utilized for coronary bypass, underwent histological examination. The histological studies demonstrated that the vasa vasorum were confined to the adventitia and did not penetrate the media of the internal mammary artery. These observations indicate that the media is nourished entirely from the lumen and suggest that harvesting the internal mammary artery as a free graft would not subject the wall of the artery to ischemic injury. Subsequent to these studies, we used the right internal mammary artery as a free graft to revascularize the distal circumflex coronary artery in 12 patients. The free graft was anastomosed to marginal branches of the circumflex and was then brought up to the left internal mammary artery pedicle graft and anastomosed end-to-side. This procedure has not resulted in excessive postoperative bleeding or sternal infections, and has relieved the anginal syndrome in all 12 patients.

Aged↗
PubMed2005

Transcription factor SOX18 is expressed in human coronary atherosclerotic lesions and regulates DNA synthesis and vascular cell growth.

OBJECTIVE: SOX18, a member of the SOX gene family (SRY-like 3-hydroxy-3-methylglutaryl box gene), is a transcription factor expressed in the development of blood vessels during embryogenesis. We analyzed SOX18 expression in human coronary atherosclerotic lesions and investigated its potential function in vascular cells. METHODS AND RESULTS: In advanced human coronary atherosclerotic lesions, SOX18 immunostaining was localized in endothelial cells (on the luminal surface, in vasa vasorum, and in intimal neovessels) and in vascular smooth muscle cells (VSMCs) scattered in the intima, colocalizing with proliferating cell nuclear antigen. In cell cultures, SOX18 was mainly localized in subconfluent and denuded areas. Significant SOX18 mRNA levels (by Northern blot analysis and reverse transcription-polymerase chain reaction) were detected in cell cultures from human umbilical vein endothelial cells and human VSMCs. Antisense SOX18 inhibited DNA synthesis ([3H]thymidine incorporation) and vascular cell growth. Antisense SOX18 also significantly reduced VSMC regrowth after injury in an in vitro model of wound repair. CONCLUSIONS: Our results indicate that SOX18 is involved in vascular cell growth and suggest that this transcription factor may play a role in atherosclerosis.

Cell Division↗
PubMed2000

Rupture of pseudointima in an implanted vascular prosthesis: immunohistological study of plasminogen activators and matrix metalloproteinases.

We investigated late-onset anastomotic stenosis in an implanted prosthetic graft. Rupture of the pseudointima and hemorrhaging from the vasa vasorum were observed at the border of the collagenous tissue and fibrin layer. An immunohistological study showed that the fibrin layer was positive for tPA, but weakly positive for PAI-1. Some neutrophils and monocyte/macrophages in the fibrin layer were immunostained for tPA, uPA, uPAR, and MMP-1, -2 and -3. Some spindle-shaped cells surrounding the graft were immunostained for uPA, uPAR, MMP-1, -2, -3, -7 and -9, and TIMP-1 and -2. The endothelial cells of some microvessels were positive for MMP-1 and -2, and tPA. Some multi-nucleated giant cells were immunostained for MMP-7 and-9, tPA, PAI-1, uPA, and uPAR. Overexpressed MMPs and PAs possibly caused instability of the pseudointima.

Aged↗
PubMed2004

Differential effect of experimental hypertension and hypercholesterolemia on adventitial remodeling.

OBJECTIVE: Intima-media remodeling, as frequently assessed by changes in the external elastic lamina-to-lumen area (EELLA), is well-described in coronary artery disease in contrast to adventitial remodeling, especially in the early disease stage. METHOD AND RESULTS: Female domestic pigs were randomized to one of the following 12-week treatment groups: normal diet (N; n=6), high-cholesterol diet (HC; n=6), or renovascular hypertension (HT; n=4). Low-density lipoprotein (LDL) cholesterol serum concentration was higher in HC than in N and HT (395.5+/-106 versus 38.6+/-14 and 37.2+/-6.8 mg/dL; P<0.05 for both). Mean arterial pressure was higher in HT than in N and HC (141.3+/-21 versus 107.4+/-8.9 and 109.4+/-7.8 mm Hg; P<0.05 for both). EELLA ratio, as assessed by morphometry, was similar in N, HC, and HTN (1.03+/-0.32 versus 0.95+/-0.29 and 1.01+/-0.09; P<0.05 for both). Coronary vasa vasorum density, as assessed by 3-dimensional micro-computed tomography, was higher in HC than in N and HT (3.4+/-1.0 versus 1.9+/-0.3 and 2.0+/-1.2; P<0.05 for both). In contrast, immunostaining showed a higher collagen III content and the presence of adventitial myofibroblasts in HT compared with N and HC. CONCLUSIONS: The current study suggests that adventitial remodeling precedes intima and media remodeling of coronary arteries early after exposure to hypercholesterolemia and hypertension, with distinct qualitative differences between them. Intima-media remodeling is well-described in coronary artery disease in contrast to adventitial remodeling. Results of the current study on coronary arteries of pigs, randomized to 12 weeks of normal diet (N), hypercholesterolemic diet (HC), or renovascular hypertensive (HT), indicate that adventitial remodeling precedes intima-media remodeling early after risk factor exposure with distinct qualitative differences.

Actins↗