Gene/Protein Disease Symptom Drug Enzyme Compound
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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

Findings from 44 autopsy examinations of cardiac transplant patients during a 10-year period were reviewed. The autopsy rate was 85%. One half of the autopsy patients underwent original transplantation for ischemic heart disease and 34% for cardiomyopathy. Survival after transplantation ranged from 0 (intraoperative) to 91 months. Rejection (including hyperacute rejection) was responsible for 41% of deaths, followed by infection (25%), and intraoperative deaths at first transplantation (9%). Most of the remaining complications were related to surgery or artificial heart support, accelerated allograft atherosclerosis, and lymphoma. Infections were not only responsible for a substantial percentage of deaths but were also a co-morbid finding in a number of patients who died primarily of other causes. Pulmonary infections represented the most common anatomic site. Twenty-five percent of the autopsy patients had gastrointestinal and/or pancreatic abnormalities, principally mucosal inflammation, erosions or hemorrhage, and pancreatitis. Review of premortem rejection history indicated that 64% of patients who died of or with rejection at autopsy had had an episode of rejection 3 weeks after transplantation and/or at least one episode of severe rejection.
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PMID:Autopsy findings in cardiac transplant patients. A 10-year experience. 154 52

Cardiac allograft vasculopathy (accelerated transplant atherosclerosis) is considered by most to involve a chronic allogeneic immune response to one or more constituents in the coronary vascular wall. Recent evidence suggests that there is an association between cytomegalovirus infection and the development of cardiac allograft vasculopathy (CAV). To determine whether CMV directly infects and/or potentially influences immunogenicity of vascular tissue, human umbilical vein (HU-VECs) or human aortic (HAECs) endothelial cells and human aortic smooth muscle cells (HASMCs) were isolated, cultured, and infected with CMV strain AD 169. Infection was detected using an immunoperoxidase-labeled monoclonal antibody to CMV immediate-early antigen (L-14). The presence and relative quantity of MHC class I and II antigens were determined flow cytometrically using monoclonal antibodies to monomorphic class I and class II HLA determinants. Gamma interferon was used as a positive control stimulant for the upregulation of MHC determinants. Both pooled HUVECs as well as 2 cell lines of HAECs served as targets for CMV infection though less than 10% of the cells were infected despite inocula of 10 pfu/cell. Infection of the pooled HUVECs resulted in no significant changes in the cell surface density of either MHC class I or II determinants. In contrast, HASMCs were excellent targets for CMV infection with virtually 100% of cells infected. CMV infection of 2 distinct HASMC cultures resulted in an increase of 254 +/- 158 relative fluorescence units (RFUs) in MHC class I antigen expression, as assessed by fluorescence intensity, in a variable portion of the HASMCs. A second population of cells exhibited a decrease of 73 +/- 16 RFUs in MHC class I antigen expression. No significant change in MHC class II antigen expression was noted. These results demonstrate that while HUVECs and HAECs are targets of CMV infection, human aortic smooth muscle cells can more readily be infected by CMV. Furthermore, CMV can regulate smooth muscle cell MHC class I expression, hence potentially altering immunogenicity. A pathophysiologic link between cardiac allograft vasculopathy and CMV disease can therefore be hypothesized.
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PMID:Cytomegalovirus-induced regulation of major histocompatibility complex class I antigen expression in human aortic smooth muscle cells. 165 93

To elucidate the long-term effects of cyclosporine, we retrospectively studied 310 consecutive patients who have undergone cardiac transplantation at our institution since December 1980 and in whom immunosuppression has been maintained with cyclosporine. The ages of recipients ranged from 1 month to 64 years and of donors from 1 month to 48 years. The actuarial survival rates for cyclosporine-treated patients were 80.7% at 1 year and 59.7% at 5 years and were significantly greater than those for previous patients not treated with cyclosporine (p less than 0.005). Their actuarial prevalence of rejection was 60.0% at 1 month and 86.9% at 1 year; 206 patients are living. The actuarial prevalence of lymphoma development was 4.6% at 5 years but has been significantly lower with the current immunosuppression protocol of lower doses of cyclosporine, and OKT3 in place of rabbit anti-thymocyte globulin (p less than 0.005). Infection remains the most common cause of death. Recipients less than 50 years of age had a significantly higher actuarial survival than older recipients (p less than 0.01). Male and female recipients had similar overall prevalence of survival and rejection, but men died of graft atherosclerosis significantly more frequently (p less than 0.005). Rehabilitation has been successful in 85% of patients surviving 1 year after transplantation. Of those surviving 1 year, 96.5% were in New York Heart Association class I. Thus the results of orthotopic cardiac transplantation have improved since the introduction of cyclosporine and have allowed measured liberalization of the criteria for recipient selection.
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PMID:Eight-year results of cyclosporine-treated patients with cardiac transplants. 230 68

During infection the vascular endothelial cell (EC) undergoes important immunologic alterations leading to increased leukocyte-EC adherence and initiation of a host inflammatory response. ECs express class 2 immune response genes and the interleukin 1 gene to a greater degree during infection and thus may be capable of amplifying the lymphocytic proliferative process. Lymphokines generated from stimulated lymphocytes, notably interferon-gamma, may in turn further enhance EC-leukocyte adherence and class 2 antigenic presentation by ECs. The ECs of different organ systems appear variable in terms of their immunologic capabilities. Infection of the endothelium has been demonstrated for an array of human pathogens, and even subclinical infection of ECs may ultimately assume importance in disease processes such as atherosclerosis. A potential role of the EC in the pathogenesis of newer infectious diseases, such as AIDS, is becoming evident and warrants further attention.
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PMID:Vascular endothelium in immunology and infectious disease. 249 65

Infection of normocholesterolemic, specific-pathogen-free chickens with Marek's disease herpesvirus (MDV) has been shown histologically to lead to chronic atherosclerosis like that in humans. The development of herpesvirus-induced atherosclerosis in vivo and the presence of specific Marek's antigen within aortic cells suggested that MDV infection may modify lipid metabolism and lead to significant lipid accumulation. Experiments reported herein were designed to determine the types and quantity of lipid present in aortas from MDV-infected and uninfected chickens between 2 and 8 months of age following infection and assess one possible mechanism of lipid accumulation by evaluating the effect of MDV infection on aortic cholesterol and cholesteryl ester (CE) metabolism. Chromatographic-fluorometric analyses indicated that at 4 and 8 months of age after MDV inoculation, MDV-infected animals had a significant (P less than 0.05) two-fold to threefold increase in total aortic lipid accumulation characterized by significant increases in cholesterol, CE, triacylglycerol, and phospholipid as compared with aortas from uninfected animals. At 8 months of age, similar increases in aortic lipid accumulation were observed in MDV-infected animals as compared with those animals vaccinated with turkey herpesvirus and later challenged with MDV. CE synthetic activity was increased significantly by 50% at 4 months of age in the MDV-infected group as compared with the uninfected group, which could explain the initial increase in CE accumulation. By 8 months of age, the authors also observed a twofold increase in CE synthetic activity and a 30% and 80% reduction in lysosomal and cytoplasmic CE hydrolytic activities, respectively, in aortas of MDV-infected chickens as compared to controls. Moreover, infection with MDV blocked the activation of cytoplasmic CE hydrolytic activity by dibutyryl cyclic AMP or exogenous cyclic AMP-dependent protein kinase. Taken together, these results suggest that lipid accretion in aortas of MDV-infected chickens results, in part, from alterations in cholesterol/CE metabolism during early stages of the disease. These findings support the hypothesis that human atherosclerosis may result from specific herpesvirus infection which can alter lipid metabolism and lead to lipid accretion.
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PMID:Virus-induced atherosclerosis. Herpesvirus infection alters aortic cholesterol metabolism and accumulation. 293 87

We describe herein the effects of Marek's disease herpesvirus (MDV) on cholesterol and cholesteryl ester metabolism in cultured chicken arterial smooth muscle cells. Infection of arterial smooth muscle cells from specific pathogen-free chickens with MDV, but not a virus control, herpesvirus of turkeys led to a 7-10-fold increase in the accumulation of free and esterified cholesterol and a 2-fold increase in phospholipids. The cellular lipid changes observed in the MDV-infected arterial smooth muscle cells resulted, in part, from the following: decreased low-density lipoprotein-cholesteryl ester hydrolysis due to decreased lysosomal (acid) cholesteryl ester hydrolytic activity; increased de novo synthesis of cholesterol; decreased excretion of free cholesterol; and, both increased cholesteryl ester synthetic activity and decreased cytoplasmic (neutral) cholesteryl ester hydrolytic activity which resulted in increased incorporation of oleic acid into cholesteryl ester. Other changes noted in the MDV-infected cells as compared to uninfected cells included a 2-fold increase in both total protein synthesis and lysosomal and microsomal marker enzyme activities. These alterations in lipid and protein metabolism in MDV-infected arterial smooth muscle cells may explain in part our in vivo findings that herpesvirus (MDV) infection of specific pathogen-free chickens fed a normocholesterolemic diet will induce arterial thickening and lipid accumulation resembling human atherosclerosis.
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PMID:Altered cholesteryl ester cycle is associated with lipid accumulation in herpesvirus-infected arterial smooth muscle cells. 399 16

The patient with diabetes represents to the surgeon a particular challenge in the management of acute abdominal problems. In addition to their ongoing and potential metabolic problems, diabetics have specific difficulty in their ability to handle infections and heal wounds. The present report reviews the general principles in the peri-operative management of diabetics and discusses the implications in the diabetic of several specific clinical problems. In view of the known accelerated atherosclerosis associated with diabetes, the risks of anesthesia and surgery must be assessed in the context of the coronary, cerebral, visceral, and peripheral vascular status. Infections in diabetics (potential or established) must be treated aggressively and promptly. Acidosis in the diabetic with abdominal pain must be considered both a metabolic problem and a possible secondary manifestation of an intra-abdominal process. In view of these challenges, the need for careful, anticipatory management of the diabetic patient facing major abdominal surgery is clear.
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PMID:Diabetes and abdominal surgery: the mutual risks. 642 50

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

Chlamydia pneumoniae is a common respiratory pathogen. Recent studies have demonstrated the presence of C. pneumoniae in coronary and aortic atherosclerotic lesions. To study the role of C. pneumoniae in atherosclerosis, we investigated the susceptibilities of three different cells of the human vascular wall to infection with C. pneumoniae AR-39. These cell types were endothelial cells, smooth muscle cells, and macrophages derived from peripheral blood monocytes. Infection was assessed by using a direct fluorescent antibody to assess inclusion counts. Duplicate cell samples were harvested 3 days postinfection and were passed in HL cells, a susceptible human epithelial cell line, to determine if infectious organisms were produced. Endothelial cells, smooth muscle cells, and macrophages were capable of supporting C. pneumoniae growth in vitro. These results showed that three different cell types known to be important in atherogenesis are susceptible to infection with C. pneumoniae.
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PMID:In vitro susceptibility of human vascular wall cells to infection with Chlamydia pneumoniae. 749 38


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