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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over a period of 11 years, commencing in December 1967, 31 cardiac transplants, 10 orthotopic and 21 heterotopic, were performed at Groote Schuur Hospital. Two patients with orthotopic transplants have a long survival, 1 for 7 1/2 and 1 for 9 1/2 years, and 1 with a heterotopic transplant for 4 years. Eighteen patients have died, and autopsy was performed from 13 to 623 days postoperatively. Rejection of the donor heart was found in 61,1% and was the cause of death in 44,4% of cases. Infection, attributable to immunosuppression, was a common finding and consisted of extensive pneumonia, usually due to Klebsiella aerogenes and Pseudomonas aeruginosa (38,8%), herpesvirus infection (38,8%), cytomegalic virus infection (37,5%), aspergillosis and other opportunistic infections. A combination of cardiac rejection and infection accounted for most of the deaths. The cardinal microscopic features of acute rejection were interstitial lymphocytic infiltration and myocytolysis, while chronic rejection was typified by obliterative myo-intimal proliferation of coronary arteries, with concurrent lipid deposition in the major coronary arteries. These lesions resembled atherosclerosis and caused graft failure due to myocardial ischaemia. Ultrastructurally, severe myofibre damage was reflected in extensive loss of cytoplasmic myofilaments. The advantages of heterotopic over orthotopic transplantation are discussed.
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PMID:The pathology of human cardiac transplantation: an assessment after 11 years' experience at Groote Schuur Hospital. 39 Jul 37

Several pieces of evidence suggest that vascular endothelium may be a site of latent herpetic viral infection, and that activation of such infection might cause or aggravate atherosclerosis. The present studies which utilized HSV-1 infection of cultured endothelial monolayers, provide insights into two phenomena seemingly relevant in considerations of atherosclerosis. Thus, mechanisms are reported by which infected endothelium may be damaged by marginated inflammatory cells, and be transformed from an anticoagulant to a procoagulant tissue. First, granulocytes are attracted to, and avidly bind, endothelium infected for very brief periods. This interaction is associated with denudation of intact cells as well as actual cytolysis through release of PMN proteases and toxic oxygen species. Second, several potentially additive abnormalities of HSV-infected endothelium would seem to foster coagulation. These include: a) its loss of surface heparans and thrombomodulin; b) its inability to synthesize prostacyclin with associated incapacity to deter platelet adhesion; c) its disordered membrane lipid conformation which is likely associated with excessive surface thrombin generation; and d) its unique ability to generate and release tissue factor. We speculate that mechanical abrasion may reactivate latent herpes (HSV or CMV) infection in endothelial cells particularly those exposed to high shear forces--for instance, at vessel bifurcations. This may underlie the endothelial damage, clotting and atheroma formation commonly found at these sites.
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PMID:Herpes virus infection of endothelium: new insights into atherosclerosis. 132 3

It has been reported that atherosclerotic lesions contain genomic material belonging to members of the herpes family. This suggests that latent viral infection may be one of the atherogenic triggers. In this study we show that early infection of endothelial cell monolayers with Herpes Simplex virus type 1 (HSV-1) or Cytomegalovirus (CMV) results in an increased monocyte (MC) and polymorphonuclear leukocyte (PMN) adherence, but not in an increased platelet adhesion. Further, is demonstrated that MC and PMN respond differently to virus infected endothelial cell monolayers: PMN adhesion to CMV infected cells is approximately 430% of the control adherence, while the MC adherence is increased to 160%. Also, a difference in virus acting is observed: the adherence of MC or PMN to HSV-1 infected endothelial cells is caused by a secreted adherence promoting factor, while the adherence of MC or PMN to CMV infected endothelial cells seems to be a cell-bound phenomenon. In addition, it was demonstrated that the augmentation of MC or PMN adherence to virus infected endothelial cells is sensitive to tunicamycin, suggesting that both virus infections induce the expression of glycoproteins on the endothelial cell membrane, which is responsible for the MC and PMN adhesion. Thus, HSV-1 and CMV infection of endothelium results in an increased adherence of leukocytes which is suggested, irrespective of the precise nature of the mechanism of virus induced atherosclerosis, to be the earliest event associated with endothelium cell damage.
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PMID:The effect of virus infection on the adherence of leukocytes or platelets to endothelial cells. 165 7

Human atherosclerotic plaques contain two type of leucocytes: 1. Monocytes/macrophages comprise almost two thirds of the cells in the center of the lesion (lipid core), and a quarter of the cells in its periphery (fibrous cap); 2. T lymphocytes comprise 10 to 15% of the plaque cells. Polymorphonuclear granulocytes are only present in very small number. The abundance of leucocytes, together with sclerosis and proliferation of mesenchymatous cells (arterial smooth muscle cells), confer to atherosclerosis the aspect of a chronic inflammatory reaction, a fact which has been recognised for a long time. Monocytes/macrophages may contribute to the development of atherosclerosis in several ways: stimulation of the fibro-muscular reaction, endothelial injury, accumulation of intimal lipids. The role of T lymphocytes is still poorly understood. According to some observations, they might be involved in an immunological reaction of the arterial wall which could be determinant in the evolution of the lesion. Arterial leucocytes have somewhat complicated, but also widened our pathogenic hypotheses of atherosclerosis. A major issue now is to identify the nature of the arterial aggressions which provoke the involvement of leucocytes, and the reasons why the defences they oppose are overwhelmed to result eventually in severe thrombo-occlusive events. Recent evidence has strengthened the possibility that viral infection plays a role in atherosclerosis. Beyond their pathogenic interest, these acquisitions might soon provide interesting therapeutic approaches.
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PMID:[Leukocytes and arteriosclerosis]. 179 22

The authors used a myocarditic coxsackievirus B3 infection in Balb/c mice to investigate cardiovascular lipid accumulation and whether a cholesterol-enriched diet influences the development of the myocardial inflammatory reaction. It was found that, seven days after CB3 infection, the accumulation of 14C-cholesterol increased by 75% (P less than 0.001) in the heart and by 92% (P less than 0.001) in the aorta. This infection also caused extensive inflammatory lesions (4.5% of tissue section area) and lipid accumulation in the myocardium seven days after inoculation. Seven weeks on a 1% cholesterol-enriched diet did not affect the myocardial area damaged (3.9%), the lethality, or immune cell activity (T, B, and natural killer [NK] cells). The response pattern of myocardial lymphocyte subpopulations was studied with an immune histochemical staining technique. The number of Mac 2+ (macrophages), class II expressing cells, or the T cytotoxic, suppressor/T helper cell ratio was not changed by the cholesterol diet. The number of class II cells tended to increase (38%) with cholesterol and was positively correlated (P less than 0.001) with the Mac 2 expression regardless of the cholesterol diet. Although moderate diet-induced hypercholesterolemia did not alter host response to viral infection, these results support the idea that virus and immune cells may cooperate and play a role in arterial and myocardial lipid accumulation, possibly acting as initiating factors for atherosclerosis.
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PMID:Cardiovascular lipid accumulation with Coxsackie B virus infection in mice. 215 46

To clarify whether some viruses could influence the different functions and membrane permeability of the aortic cells, we have examined in a model experiment the in vitro effect of the measles virus on the aortic endothelial and smooth muscle cells. The aortic cells infected with the virus failed to reveal gross cytopathic effect. Occasionally, however, syncytium formation and nuclear inclusions were observed. In infected endothelial cells lysosome containing viral nucleocapsids were seen. The early phase of measles virus replication inhibited the proliferation of endothelial cells of all species tested, while uniformly stimulated the replication of the smooth muscle cells relative to the control. In bovine aortic endothelial and smooth muscle cells the protein synthesis had been suppressed by the 4th to 6th hours postinfection. The results indicate that measles virus infection may be among the risk factors of atherosclerosis. It may damage endothelial cells by altering the cell membrane permeability and could induce proliferation of aortic smooth muscle cells.
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PMID:Influence of the measles virus on the proliferation and protein synthesis of aortic endothelial and smooth muscle cells. 227 Jul 38

Experiments on rabbits have shown that state of T-immunodeficiency induced by persisting virus infection promotes atherogenesis. Correction of age immunodeficiency by transplantation of the autologous bone marrow taken in young age considerably retards the atherosclerosis development. Inhibition of atherogenesis is also achieved by introduction (to animals) of natural thymic vilosene preparation which compensates a decrease in the functional activity of the thymus gland occurring under conditions of experimental hyperlipidemia.
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PMID:[Relation of atherogenesis and T-immunodeficiency]. 259 81

Current theory suggests that life began in a prebiologic era, progressed to a ribonucleic-deoxyribonucleic cellular era, and finally entered an era characterized by multicellular organisms. If this progression is correct, it is not surprising that, as medicine studies living organisms with increasing sophistication, factors that are initially discovered to have systemic effects are, in many instances, later determined to have paracrine, autocrine or even intracellular ("intracrine") effects. This schema is potentially of value in analyzing the pathogenesis of cardiovascular disease and, in particular, the development of the sequelae of hypertension. A case is made for the idea that the actions of common peptide and nonpeptide factors at local tissue levels can play an important role in the development of atherosclerosis and left ventricular hypertrophy. In making this case, the potential roles of insulin, angiotensin II and other vasoactive factors are considered. In addition, it is argued that some peptide and nonpeptide factors with cardiovascular impact may operate in the intracellular environment, thus broadening prospects for study and intervention. Finally, genomic alterations either spontaneously occurring or resulting from chronic stimulation or viral infection are considered and their potential role is discussed.
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PMID:Emerging issues in the cellular biology of the cardiovascular system. 305 99

Endothelial injury is important in the pathogenesis of thrombosis, atherosclerosis, disseminated intravascular coagulation, and vasculitis. The ability of several common human viruses to infect cultures of endothelial cells obtained from human umbilical veins or bovine thoracic aorta was demonstrated. Indicators of infection included cytopathology, viral growth curves, and antigen detection by immunofluorescence. Herpes simplex virus type 1, adenovirus type 7, measles virus, and parainfluenza virus type 3 infected both human venous and bovine aorta endothelium. Mumps virus, poliovirus type 1, and echovirus type 9 grew only in human venous cells; coxsackievirus B4 infected only bovine arterial cultures; and cytomegalovirus, influenza A/Victoria/75 (H3N2) virus, and respiratory syncytial virus failed to grow in either cell culture. During replication some viruses caused acute lytic changes; some produced chronic, less destructive alterations; and other induced no apparent cytopathology. The results suggest that viral replication within endothelium may be important in the pathogenesis of viral disease of initiation of vessel-wall injury.
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PMID:Virus infection of endothelial cells. 626 Aug 74

175 patients with histological evidence of chronic diffuse liver disease, 67 patients with heart failure, diabetes and atherosclerosis, and 118 healthy adults under 30 years of age engaged in sports were studied for the prevalence of hepatitis A virus antibody (anti-HAV) by radioimmunoassay using a HAVAB (Abbott)-kit. Infection with hepatitis-A virus is highly prevalent in Hungary, anti-HAV having been demonstrated in a very high proportion of controls as well as of patients. Over the age of 40 the incidence is 100% in controls and 98% in patients with chronic liver disease. Infection with hepatitis-A virus must have been asymptomatic in the majority, since no more than 11.4% of the subjects had a history of acute hepatitis. The prevalence of acquired anti-HAV increases with age until it attains 100% in advanced age. The present results lend no support to the possibility that hepatitis-A virus infection might be involved in the production of chronic diffuse liver disease.
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PMID:Hepatitis a virus antibody in chronic diffuse liver disease. 666 44


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