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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Herpes simplex virus (HSV) infection may be involved in various endothelial-injury syndromes, including vasculitis and atherosclerosis. In a previous study, it was reported that HSV-infected human umbilical endothelial cells are more vulnerable to detachment mediated by granulocyte-secreted proteases. To elucidate the molecular basis of this observation, the authors examined the interaction of infected endothelial cells with the purified basement membrane proteins, fibronectin, laminin, and type IV collagen. HSV-infected endothelial cells exhibited defects in their ability to adhere, spread, and migrate on all three matrix components. This defective adhesion could be partially overcome by increasing concentrations of fibronectin; in contrast, no abrogation of deficient binding occurs with increased levels of laminin or collagen type IV. This suggests that endothelial cells may use different surface constituents for binding to the three proteins and use multiple "receptors" for adhesion to the fibronectin molecule--"receptors" that are variably affected by HSV infection. The authors investigated this supposition by assaying adhesion of normal and infected endothelial cells to two non-overlapping cell-adhesion promoting fragments of fibronectin: 1) a 75 kd motility-promoting fragment which contains the arginyl-glycyl-aspartylserine (RGDS) adhesion sequence, and 2) a 33 kd carboxyl-terminal heparin binding fragment, which promotes cell adhesion by an RGDS-independent mechanism. Normal endothelial cells adhered and spread on both purified fragments. In contrast, while infected endothelial cells could adhere, albeit rather poorly, to high coating concentrations of the 75 kd fragment, these cells did not bind to the 33 kd heparin binding fragment of fibronectin at all. These results support the concept that endothelial cells adhere to multiple domains of fibronectin, and that HSV infection preferentially abrogates binding to the heparin-binding domain, while leaving relatively intact receptors for the RGDS-containing domain. In support, soluble RGDS significantly blocked fibronectin adhesion of infected, but not control, endothelial cells. It is concluded that HSV infection inhibits the interaction of endothelial cells with basement membrane proteins and weakens their tethering to substratum. This tethering is inadequate for proper cell spreading or movement to occur and may result in both excessive endothelial lift-off and impaired vascular repair in HSV infections.
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PMID:Herpes simplex virus inhibits endothelial cell attachment and migration to extracellular matrix proteins. 253 23

Vascular problems involving the brachiocephalic vessels may occur from atherosclerosis, trauma, vasculitis, infection, and procedures for congenital heart disease. A wide variety of symptoms and signs may result from such disorders. This study is a report of five unusual manifestations of brachiocephalic vascular diseases. Diagnosis, management, and previous surgical experience is discussed relating to each case illustrating the complexity and variability of brachiocephalic vascular pathology.
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PMID:Unusual manifestations of brachiocephalic vascular disease. 264 19

The generation of toxic oxygen metabolites is more usually associated with inflammation. However, pathological free radical reactions can cause tissue damage by adversely affecting prostacyclin (PGI2) synthesis allowing initiation of coagulation. We have assessed changes in the red cell defence to toxic oxygen metabolite generation, viz measurement of glutathione concentration (GSH) and superoxide dismutase activity (SOD). GSH and SOD were measured in 20 patients with peripheral arterial disease, 22 patients with vasculitis, and 11 patients with angina, and compared to 17 matched controls. The 53 subjects with arterial disease had significantly lower SOD levels: in contrast GSH levels were significantly higher. Extracellularly plasma thiol levels (PSH) were low and caeruloplasmin (Cp) levels were high. We suggest that free radical pathology exists not only in inflammatory vascular disease but also in atherosclerosis.
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PMID:Free radical pathology in chronic arterial disease. 270 21

Coronary artery morphologic features of 61 human cardiac allografts of short- and long-term survival were correlated with coexisting myocardial pathologic findings and cause of death. On the basis of distribution of coronary lesions, allografts were divided into two broad groups: those with fibrous or atherosclerotic lesions confined to the proximal region of epicardial arteries and those with diffuse necrotizing vasculitis or atherosclerosis of the entire coronary arterial system. Within the two groups, coronary artery morphologic features varied in a time-dependent fashion. Disease in the proximal region began as concentric fibrous intimal thickening, with atheromatous lesions observed after 1 year after transplantation. Five of 10 (50%) patients with atheromatous plaques in the proximal region of arteries died or underwent retransplantation because of coronary disease, as compared to only 1 of 29 (3%) patients with fibrous intimal thickening only in the proximal region. The earliest form of diffuse disease was a necrotizing vasculitis, which was invariably associated with acute myocardial rejection. Long-term survivors with diffuse disease showed severe fibrous or fibrofatty intimal lesions of the large and small epicardial and intramyocardial arteries. In some, diffuse disease may have resulted from healing of necrotizing vasculitis. Eight of nine (89%) long-term survivors with diffuse coronary artery disease died or required retransplantation because of coronary vascular disease. The coronary artery disease of human cardiac allografts is a heterogeneous phenomenon with variable distribution, morphologic features, severity, clinical significance, and, possibly, pathogenesis.
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PMID:The spectrum of coronary artery pathologic findings in human cardiac allografts. 279 79

The problem of accelerated atherosclerosis in the allograft heart continues to adversely effect the long term survival of transplant patients. Most traditional risk factors influencing atherogenesis do not appear to play an important role in accelerated atherosclerosis. Additional causative factors proposed in recent years are not without controversy. An immune-mediated endothelial damage by cytotoxic B-cell antibodies as the initial injury in the induction of accelerated atherosclerosis has not been confirmed on morphologic grounds. This study is based on six cases (four autopsies and two explanted hearts) from transplant patients whose hearts were examined at different post-transplantation intervals (24 h to 14 mo). Our morphologic findings of a segmental coronary vasculitis involving primarily the outer two-thirds of the media and adventitia suggest that the early vascular manifestations may reflect tissue rejection similar to that seen in the myocardium. Furthermore, our findings from the medium size coronary arteries are suggestive of a cell-mediated immune injury probably directed against the smooth muscle cells of the media. Although the end result (occlusive coronary lesion) may reveal some morphologic similarities in both naturally occurring atherosclerosis and accelerated atherosclerosis, the pathogenetic mechanisms involved in these two conditions may differ.
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PMID:Allograft heart accelerated atherosclerosis: evidence for cell-mediated immunity in pathogenesis. 281 47

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

Factor-VIII-Related antigen (VIII R:Ag) is known to be produced by the blood vessel wall. Noxious stimuli increase endothelial release of VIII R:Ag. It might be expected that the development of vasculitis would be associated with increased levels of VIII R:Ag. To investigate this, eight different groups of subjects were studied: 25 patients with systemic sclerosis, 19 with systemic lupus erythematosus, 15 with rheumatoid arthritis (RA) plus vasculitis, 19 with systemic vasculitis and 14 with atherosclerosis. These groups were compared to 29 patients with primary Raynaud's disease, 15 with RA without vasculitis and 50 controls. Results showed that where there was evidence of vascular disease, then VIII R:Ag was elevated. VIII R:Ag appeared to be a more specific marker for vascular damage than erythrocyte sedimentation rate or C-reactive protein. Longitudinal studies in 11 patients showed good correlation between progression of vascular disease and VIII R:Ag.
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PMID:Vascular damage and factor-VIII-related antigen in the rheumatic diseases. 311 42

We describe five patients aged 50 years or above who had severe atherosclerosis and necrotizing vasculitis. The vasculitis was seen in the small vessels of four patients and in the medium-sized vessels of one. All five patients had multiple necrotic ulcerative skin lesions, and two underwent amputation. Our cases suggest that the relationship between the two disorders changes and exacerbates the clinical and pathological expression of each disease.
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PMID:Necrotizing vasculitis and atherosclerosis. 196 35

Anatomical studies have demonstrated the high incidence of vasculitis in SLE, the appearances of which are variable and non-specific, ranging from necrotizing angiitis which is undistinguishable from periarteritis nodosa, to scarring lesions. Micro-angiitis is easily demonstrated in skin lesions and is also encountered to varying degrees in CNS, renal, cardiac, pulmonary and gastrointestinal localisations. Disease of large vessels is more rare and sometimes causes gangrene of the limbs. In SLE, vasculitis should be distinguished from thrombosis related to lupus anticoagulant and from atherosclerosis favoured by chronic steroid therapy but perhaps initiated by vascular deposits of immune complexes during the acute inflammatory stage. The treatment of lupic angiitis is mainly based on steroid therapy. The results are variable, probably due to the fibrous nature of some of the vascular lesions.
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PMID:[Lupus vasculitis]. 332 46

A case of aneurysms of saphenous vein coronary artery bypass (CAB) grafts is presented with CT and echocardiography findings. Aneurysms of the bypass graft are rare complications of CAB surgery but many occur due to atherosclerosis, infection, surgical technique, or vasculitis.
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PMID:Saphenous vein graft aneurysms demonstrated by computed tomography. 348 97


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