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Physiological Reviews Jan 2005Intimal thickening, the accumulation of cells and extracellular matrix within the inner vessel wall, is a physiological response to mechanical injury, increased wall... (Review)
Review
Intimal thickening, the accumulation of cells and extracellular matrix within the inner vessel wall, is a physiological response to mechanical injury, increased wall stress, or chemical insult (e.g., atherosclerosis). If excessive, it can lead to the obstruction of blood flow and tissue ischemia. Together with expansive or constrictive remodeling, the extent of intimal expansion determines final lumen size and vessel wall thickness. Plaque rupture represents a failure of intimal remodeling, where the fibrous cap overlying an atheromatous core of lipid undergoes catastrophic mechanical breakdown. Plaque rupture promotes coronary thrombosis and myocardial infarction, the most prevalent cause of premature death in advanced societies. The matrix metalloproteinases (MMPs) can act together to degrade the major components of the vascular extracellular matrix. All cells present in the normal and diseased blood vessel wall upregulate and activate MMPs in a multistep fashion driven in part by soluble cytokines and cell-cell interactions. Activation of MMP proforms requires other MMPs or other classes of protease. MMP activation contributes to intimal growth and vessel wall remodeling in response to injury, most notably by promoting migration of vascular smooth muscle cells. A broader spectrum and/or higher level of MMP activation, especially associated with inflammation, could contribute to pathological matrix destruction and plaque rupture. Inhibiting the activity of specific MMPs or preventing their upregulation could ameliorate intimal thickening and prevent myocardial infarction.
Topics: Animals; Arteriosclerosis; Blood Vessels; Gene Expression Regulation, Enzymologic; Humans; Matrix Metalloproteinases; Rupture; Tunica Intima
PubMed: 15618476
DOI: 10.1152/physrev.00048.2003 -
Journal of Medical Radiation Sciences Mar 2017The aim of this study was to assess if the complex anatomy of aortic aneurysm and aortic dissection can be accurately reproduced from a contrast-enhanced computed...
INTRODUCTION
The aim of this study was to assess if the complex anatomy of aortic aneurysm and aortic dissection can be accurately reproduced from a contrast-enhanced computed tomography (CT) scan into a three-dimensional (3D) printed model.
METHODS
Contrast-enhanced cardiac CT scans from two patients were post-processed and produced as 3D printed thoracic aorta models of aortic aneurysm and aortic dissection. The transverse diameter was measured at five anatomical landmarks for both models, compared across three stages: the original contrast-enhanced CT images, the stereolithography (STL) format computerised model prepared for 3D printing and the contrast-enhanced CT of the 3D printed model. For the model with aortic dissection, measurements of the true and false lumen were taken and compared at two points on the descending aorta.
RESULTS
Three-dimensional printed models were generated with strong and flexible plastic material with successful replication of anatomical details of aortic structures and pathologies. The mean difference in transverse vessel diameter between the contrast-enhanced CT images before and after 3D printing was 1.0 and 1.2 mm, for the first and second models respectively (standard deviation: 1.0 mm and 0.9 mm). Additionally, for the second model, the mean luminal diameter difference between the 3D printed model and CT images was 0.5 mm.
CONCLUSION
Encouraging results were achieved with regards to reproducing 3D models depicting aortic aneurysm and aortic dissection. Variances in vessel diameter measurement outside a standard deviation of 1 mm tolerance indicate further work is required into the assessment and accuracy of 3D model reproduction.
Topics: Aorta; Aortic Aneurysm; Contrast Media; Humans; Image Processing, Computer-Assisted; Models, Anatomic; Printing, Three-Dimensional; Tomography, X-Ray Computed; Tunica Intima
PubMed: 28134482
DOI: 10.1002/jmrs.212 -
Brain and Behavior Nov 2017To analyze the risk factors of carotid plaque (CP) and carotid common artery intima-media thickening (CCAIMT) and the association between the risk factors and CP numbers...
INTRODUCTION
To analyze the risk factors of carotid plaque (CP) and carotid common artery intima-media thickening (CCAIMT) and the association between the risk factors and CP numbers and the side of the CCAIMT in a high-stroke-risk population.
METHODS
Carotid ultrasonography was conducted in 2025 participants with high stroke risk. Participants were divided into different groups according to the results of the ultrasound. The risk factors and blood biochemical indices were recorded.
RESULTS
The presence of CP and CCAIMT were 38.9% and 24.8% respectively. Multivariate logistic regression indicated that the risk factors of CP were age, high LDL-C and FBG levels, male gender, stroke, diabetes, hypertension, and tobacco use. Compared with participants without CPs, the participants who were male, and older in age, with risk factors of tobacco use, diabetes, high LDL-C levels, and a family history of hypertension were likely to have a single CP, whereas the participants with risk factors of tobacco use, diabetes, hypertension, male gender, older age, high LDL-C levels, stroke and AF or valvulopathy were prone to have multiple CPs. The risk factors of CCAIMT were male gender, stroke, hypertension, diabetes, AF or valvulopathy, tobacco use and age. Compared with the N-CCAIMT subgroup, the risk factors of left CCAIMT were tobacco use, diabetes, male gender, and age. The risk factors of right CCAIMT were male gender, high FBG levels, age, AF or valvulopathy. The risk factors of dual CCAIMT were high frequency of drinking milk, tobacco use, male gender, age, stroke, and hypertension.
CONCLUSION
These findings revealed the risk factors of CP and CCAIMT, and an association between the risk factors and the CP numbers and the side of the CCAIMT.
Topics: Aged; Carotid Artery Diseases; Carotid Artery, Common; Female; Humans; Logistic Models; Male; Middle Aged; Plaque, Atherosclerotic; Predictive Value of Tests; Risk Assessment; Risk Factors; Stroke; Tunica Intima; Tunica Media; Ultrasonography
PubMed: 29201548
DOI: 10.1002/brb3.847 -
Journal of the American College of... Jun 2004Pulmonary arterial hypertension (PAH) includes various forms of pulmonary hypertension of different etiology but similar clinical presentation and functional... (Review)
Review
Pulmonary arterial hypertension (PAH) includes various forms of pulmonary hypertension of different etiology but similar clinical presentation and functional derangement. Histopathological vascular changes in all forms of PAH are qualitatively similar but with quantitative differences in the distribution and prevalence of pathological changes in various portions of the pulmonary vascular bed. The documentation of these topographic variations in the response of the pulmonary vasculature to injury may be important to understand the pathogenesis of the various subsets of PAH. To standardize the precise histopathological documentation of the pulmonary vasculopathy in PAH we propose a histopathological classification that includes both the predominant segment of the pulmonary vasculature affected and the possible coexistence of pathological changes in other vascular segments.
Topics: Humans; Hypertension, Pulmonary; Lung; Muscle, Smooth, Vascular; Pulmonary Artery; Pulmonary Circulation; Tunica Intima; Vascular Diseases; Vascular Resistance; Vasoconstriction
PubMed: 15194175
DOI: 10.1016/j.jacc.2004.02.033 -
PloS One 2015Kidney transplant recipients have high cardiovascular risk, and vascular inflammation may play an important role. We explored whether the inflammatory state in the... (Clinical Trial)
Clinical Trial Observational Study
BACKGROUND
Kidney transplant recipients have high cardiovascular risk, and vascular inflammation may play an important role. We explored whether the inflammatory state in the vessel wall was related to carotid intima-media thickness (c-IMT) and patient survival following kidney transplantation.
METHODS
In this prospective observational cohort study we measured c-IMT and expression of proinflammatory cytokines and adhesion molecules in the inferior epigastric artery in 115 kidney transplant candidates. Another c-IMT measurement was done 1-year post-transplantation in 107. By stepwise multiple regression analysis we explored factors associated with baseline c-IMT and their changes over time. Multivariate Cox regression analysis was constructed to identify risk factors for mortality.
RESULTS
A worse cardiovascular profile (older age, smoker, diabetic, carotid plaque, systolic blood pressure and vascular calcification) and higher VCAM-1 levels were found in patients in the highest baseline c-IMT tertile, who also had a worse survival. Factors independently related to baseline c-IMT were age (β=0.369, P<0.0001), fasting glucose (β=0.168, P=0.045), smoking (β=0.228, P=0.003) and VCAM-1 levels (β=0.244, P=0.002). Independent factors associated with c-IMT measurement 1-year post-transplantation were baseline c-IMT (β=-0.677, P<0.0001), post-transplant diabetes (β=0.225, P=0.003) and triglycerides (β=0.302, P=0.023). Vascular VCAM-1 levels were associated with increased risk of mortality in bivariate and multivariate Cox regression. Notably, nearly 50% of patients showed an increase or maintenance of high c-IMT 1 year post-transplantation and these patients experienced a higher mortality (13 versus 3.5%; P=0.021).
CONCLUSION
A worse cardiovascular profile and a higher vascular VCAM-1 protein levels at time of KT are related to subclinical atheromatosis. This could lead to a higher post-transplant mortality. Pre-transplant c IMT, post-transplant diabetes and triglycerides at 1-year post-transplantation may condition a high c-IMT measurement post-transplantation, which may decrease patient survival.
Topics: Adult; Carotid Intima-Media Thickness; Female; Humans; Kidney Transplantation; Male; Middle Aged; Predictive Value of Tests; Survival Rate; Tunica Intima; Vascular Cell Adhesion Molecule-1
PubMed: 26066045
DOI: 10.1371/journal.pone.0129083 -
Journal of Vascular Surgery Jun 2007Since its discovery, nitric oxide (NO) has emerged as a biologically important molecule and was even named Molecule of the Year by Science magazine in 1992. Specific to... (Review)
Review
Since its discovery, nitric oxide (NO) has emerged as a biologically important molecule and was even named Molecule of the Year by Science magazine in 1992. Specific to our interests, NO has been implicated in the regulation of vascular pathology. This review begins with a summary of the molecular biology of NO, from its discovery to the mechanisms of endogenous production. Next, we turn our attention to describing the arterial injury response of neointimal hyperplasia, and we review the role of NO in the pathophysiology of neointimal hyperplasia. Finally, we review the literature regarding NO-based therapies. This includes the development of inhalational-based NO therapies, systemically administered L-arginine and NO donors, NO synthase gene therapy, locally applied NO donors, and NO-releasing prosthetic materials. By reviewing the current literature, we emphasize the tremendous clinical potential that NO-based therapies can have on the development of neointimal hyperplasia.
Topics: Administration, Inhalation; Animals; Apoptosis; Arginine; Arteries; Blood Platelets; Cardiovascular Agents; Cell Proliferation; Chemotaxis, Leukocyte; Drug Carriers; Endothelial Cells; Extracellular Matrix; Genetic Therapy; Humans; Hyperplasia; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Nitric Oxide; Nitric Oxide Donors; Nitric Oxide Synthase; Platelet Adhesiveness; Platelet Aggregation; Tunica Intima
PubMed: 17544026
DOI: 10.1016/j.jvs.2007.02.027 -
Circulation Research Feb 2010
Topics: Animals; Aorta; Atherosclerosis; CD11c Antigen; Dendritic Cells; Lipid Metabolism; Lipids; Mice; Models, Biological; Tunica Intima
PubMed: 20133906
DOI: 10.1161/CIRCRESAHA.109.212191 -
Journal of Anatomy Feb 2009Internal elastic lamina (IEL) hole (fenestration) characteristics and myoendothelial gap junction (MEGJ) density were examined in selected resistance and conduit... (Comparative Study)
Comparative Study
Internal elastic lamina (IEL) hole (fenestration) characteristics and myoendothelial gap junction (MEGJ) density were examined in selected resistance and conduit arteries of normal and diseased rat and mouse models, using conventional, ultrastructural and confocal microscopy methods. Selected vessels were those commonly used in functional studies: thoracic aorta, proximal and distal mesenteric, caudal, saphenous, middle-cerebral and caudal cerebellar artery. Rat and mouse strains and treatment groups examined were Dahl, Sprague Dawley, Wistar Kyoto, Wistar, spontaneously hypertensive (SHR), deoxycorticosterone (DOC) treated rat; and apolipoprotein E knockout, C57/BL6 and BALB/c mice. Vessel size (as IEL circumference), IEL hole and MEGJ density were quantified. In mesenteric arteries, the width of IEL holes and the percent of IEL occupied by holes were also determined. IEL hole density varied significantly within and between mesenteric artery beds, even among normotensive rat strains. Among the hypertensive rats (SHR and DOC), hole density in some vessels was higher in the normotensives than in the hypertensives within each strain, whereas in Dahl rats, hole density was similar between hypertensives and normotensives. Hole density was not correlated with the formation of intimal lesions in superior mesenteric artery. There was no positive general correlation between IEL hole and MEGJ density in resistance and conduit vessels. However, there was a positive correlation between the size of some resistance arteries and MEGJ density, although such a relationship did not hold for conduit vessels or during development, and there was no such relationship between vessel size and IEL hole density. Whilst IEL holes are obviously required for MEGJ communication, their presence is not an indication of contact-mediated communication, but rather may be related to the presence of sites for the low resistance passage of diffusion-mediated release of vasoactive endothelial and smooth muscle substances.
Topics: Aging; Animals; Aorta; Endothelium, Vascular; Male; Mesenteric Arteries; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Microscopy, Confocal; Microscopy, Electron, Scanning; Muscle, Smooth, Vascular; Rats; Rats, Inbred Dahl; Rats, Inbred SHR; Rats, Inbred WKY; Rats, Sprague-Dawley; Rats, Wistar; Species Specificity; Tunica Intima
PubMed: 19207987
DOI: 10.1111/j.1469-7580.2008.01020.x -
Annals of Biomedical Engineering Mar 2017Pathologic vascular adaptation following local injury is the primary driver for accelerated intimal hyperplasia and an occlusive phenotype. Smooth muscle cell (SMC)...
Pathologic vascular adaptation following local injury is the primary driver for accelerated intimal hyperplasia and an occlusive phenotype. Smooth muscle cell (SMC) proliferation within the wall, and migration into the developing intima, is a major component of this remodeling response. The primary objective in the current study was to investigate the effect of the local biomechanical forces on early vein graft adaptation, specifically focusing on the spatial and temporal response of SMC proliferation and conversion from a contractile to synthetic architecture. Taking advantage of the differential adaptation that occurs during exposure to divergent flow environments, vein grafts were implanted in rabbits to create two distinct flow environments and harvested at times ranging from 2 h to 28 days. Using an algorithm for the virtual reconstruction of unfixed, histologic specimens, immunohistochemical tracking of DNA synthesis, and high-throughput transcriptional analysis, the spatial and temporal changes in graft morphology, cell proliferation, and SMC phenotype were catalogued. Notable findings include a burst of cell proliferation at 7 days post-implantation, which was significantly augmented by exposure to a reduced flow environment. Compared to the adjacent media, proliferation rates were 3-fold greater in the intima, and a specific spatial distribution of these proliferating cells was identified, with a major peak in the sub-endothelial region and a second peak centering on the internal elastic lamina. Genomic markers of a contractile SMC phenotype were reduced as early as 2 h post-implantation and reached a nadir at 7 days. Network analysis of upstream regulatory pathways identified GATA6 and KLF5 as important transcription factors that regulate this shift in SMC phenotype.
Topics: Animals; Hemodynamics; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Rabbits; Transplants; Tunica Intima; Veins
PubMed: 27624660
DOI: 10.1007/s10439-016-1725-0 -
European Journal of Medical Research Aug 2021Pulmonary artery intimal sarcoma (PAS) is a very rare disease, its prevalence is about 0.001-0.003%. PAS is often misdiagnosed as acute or chronic pulmonary...
BACKGROUND
Pulmonary artery intimal sarcoma (PAS) is a very rare disease, its prevalence is about 0.001-0.003%. PAS is often misdiagnosed as acute or chronic pulmonary thromboembolism due to its clinical presentation and radiological findings. Thus, early diagnosis is very crucial and may improve patient outcome.
CASE PRESENTATION
Here, we report a case in a Chinese male where the symptom presentation was episodes of shortness of breath. Transthoracic echocardiography showed a solid mass in the pulmonary valve orifice, which was demonstrated to be a pulmonary artery intimal sarcoma diagnosed by histopathology. In this case, the initial differential diagnosis included pulmonary embolism. Because the initial symptom of primary pulmonary artery sarcoma is extremely similar to the pulmonary embolism, half of them may be misdiagnosed as pulmonary embolism. Imaging studies are very helpful. Ultrasound and CT are the best due to their resolution and ability to assess the relationship of the mass with the surrounding structures. The final diagnosis is mostly made after surgical excision and this is the most effective treatment. At the same time, radiotherapy and chemotherapy after surgery is also an adjuvant treatment.
CONCLUSION
We report a very rare case of pulmonary artery intimal sarcoma. Due to late diagnosis and delayed treatment in this case, the patient displayed a poor prognostic. Early diagnosis and right treatment can improve the prognosis of PAS and optimize overall health.
Topics: Aged; Diagnosis, Differential; Hemangiosarcoma; Humans; Male; Pulmonary Artery; Pulmonary Embolism; Tomography, X-Ray Computed; Tunica Intima; Ultrasonography; Vascular Neoplasms
PubMed: 34372932
DOI: 10.1186/s40001-021-00568-w