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

Infection, mainly related to vascular access, is one of the main causes of morbidity and a preventable cause of death in hemodialysis patients. From January 1994 to April 1998 we conducted a prospective study to assess the incidence and risk factors of catheter-related bacteremia. One hundred and twenty-nine tunneled dual-lumen hemodialysis catheters were inserted percutaneously into the internal jugular vein in 89 patients. Bacteremia (n = 56) occurred at least once with 37 (29%) of the catheters (an incidence of 1.1/1,000 catheter-days); local infection (n = 45, 1/1,000 catheter-days) was associated with bacteremia in 18 cases. Death in 1 case was directly related to Staphylococcus aureus (SA) septic shock, and septicemia contributed to deaths in 2 additional cases. Catheters were removed in 48% of the bacteremic episodes. Treatment comprised intravenous double antimicrobial therapy for 15-20 days. Bacteriological data of bacteremia showed 55% involvement of SA. Nasal carriage of SA was observed in 35% of the patients with catheters. Bacteremic catheters were more frequently observed in patients with diabetes mellitus (p = 0.03), peripheral atherosclerosis (p = 0.001), a previous history of bacteremia (p = 0.05), nasal carriage of SA (p = 0.0001), longer catheter survival time (p = 0.001), higher total intravenous iron dose (p = 0.001), more frequent urokinase catheter infusion (p < 0.01), and local infection (p < 0.001) compared with non-bacteremic catheters. Monovariate survival analysis showed that significant initial risk factors for bacteremia were nasal carriage of SA (p = 0.00001), previous bacteremia (p = 0.0001), peripheral atherosclerosis (p = 0.005), and diabetes (p = 0.04). This study confirms the relatively high incidence of bacteremia with tunneled double-lumen silicone catheters and its potential complications. Possible preventive actions are discussed according to the risk factors.
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PMID:Risk factor analysis for long-term tunneled dialysis catheter-related bacteremias. 1211 69

End-stage renal disease (ESRD) is characterized by an exceptional cardiovascular mortality rate. Although traditional risk factors are common in ESRD patients, they alone may not be sufficient to account for the high prevalence of cardiovascular disease (CVD). Recent evidence demonstrated that chronic inflammation, a non-traditional risk factor which is commonly observed in ESRD patients, may cause malnutrition and progressive atherosclerotic CVD by several pathogenetic mechanisms. Although both malnutrition and inflammation have been shown to be strong predictors of cardiovascular mortality in ESRD patients, it must be remembered that the majority of studies describing the presence of inflammation and malnutrition have been performed in Western and Asian industrialized countries. As it is evident that the prevalence of malnutrition and inflammation may differ markedly between different regions of the world and developing countries face a much higher prevalence of chronic infectious diseases, comparative inter-regional studies focusing on the etiology and prevalence of the malnutrition, inflammation and atherosclerosis syndrome are warranted.
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PMID:Inflammation, malnutrition and atherosclerosis in end-stage renal disease: a global perspective. 1220 91

The occurrence of infections in organ transplantation is one of the most significant determinants of transplant outcome, because it is the most common life-threatening complication of long-term immunosuppressive therapy. Recently, besides the well-known direct effect of infections, other relevant biochemical factors such as cytokines, chemokines and growth factors have been considered. Aim of this review is to deal with the infections by mainly considering the unusual consequences of several infectious diseases like malignancies, graft loss and atherosclerosis. The number of patients affected by malignancies is increasing in all registries. Viral pathogens play a pathophysiological role in the development of the most frequent malignancies after solid organ transplantation. In some cases viruses act by altering cell transformation. Moreover, some pathogens may contribute to global immunosuppression and work together to promote oncogenesis. The viral load surveillance is recommended in the prevention of malignancies. The BK virus nephropathy in renal transplant recipients is emerging as an unusual consequence of graft loss. In this paper we examine the risk factors, the clinical characteristics and especially the diagnostic tools and treatments actually available. The third unusual consequence is the transplant vascular sclerosis, a multifactorial late complication of solid organ transplantation. The transplant vascular sclerosis has emerged as an important limitation in long-term graft survival. Several epidemiological, clinical and therapeutic interventional studies have shown how several potential contributing etiologic factors, such as Chlamydia and CMV infection, have been identified as being definitely associated with the development of transplant vascular sclerosis.
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PMID:[Unusual infections in transplantation]. 1243 46

Infection with Chlamydia pneumoniae has been implicated as a potential risk factor for atherosclerosis. This study was designed to investigate the mechanisms of the anti-chlamydial activity of aspirin. A reporter gene assay for NF-kappa B activity, immunoblot analysis for cyclo-oxygenase (COX)-2 and radioimmunoassay for prostaglandin E(2) (PGE(2)) were performed. Following infection of HEp-2 cells with C. pneumoniae, NF-kappa B was activated, COX-2 was induced and PGE(2) was elevated. Aspirin inhibited NF-kappa B activation at a concentration of 0.1 mM, partially inhibited COX-2 induction and blocked PGE(2) synthesis completely. In addition, high doses of aspirin (1 and 2 mM) inhibited chlamydial growth in HEp-2 cells, decreasing the number and size of inclusion bodies; this effect could be overcome by adding tryptophan to the culture. Indomethacin also blocked the synthesis of PGE(2), but had no effect on COX-2 expression or chlamydial growth. These results indicate that aspirin not only has an anti-inflammatory activity through prevention of NF-kappa B activation but also has anti-chlamydial activity at high doses, possibly through depletion of tryptophan in HEp-2 cells.
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PMID:Aspirin inhibits Chlamydia pneumoniae-induced NF-kappa B activation, cyclo-oxygenase-2 expression and prostaglandin E2 synthesis and attenuates chlamydial growth. 1272 17

Atherosclerosis has long been recognised as having an inflammatory component, and this has a particularly important bearing on to its clinical complications as it may result in plaque instability. Results of recent epidemiological studies have reinforced the potential importance of this aspect of the disease. Positive associations have been reported between exposure to several specific pathogens, and future risk of coronary heart disease (CHD). Whilst it is possible that each individual organism contributes to this susceptibility by a different mechanism, it is more likely that one or more common mechanism(s) exist. One possible hypothesis is that an immune response mounted against antigens on pathogenic organisms cross-react with homologous host proteins in a form of 'molecular mimicry'. A group of protein candidates that may be implicated in this process are the stress-induced proteins collectively known as heat shock proteins (HSP). HSPs are expressed and/or secreted by several pathogens, principally Chlamydia pneumoniae and Helicobacter pylori, but are also elaborated by mammalian vascular cells exposed to the stress associated with reperfusion injury or acute hypertension. The HSPs are also expressed by cells within atherosclerotic plaques. Serum titres of anti-HSP antibodies have been reported to be positively related to future risk of CHD. In addition, purified anti-HSP antibodies recognise and mediate the lysis of stressed human endothelial cells and macrophages in vitro. Furthermore, immunisation with HSP exacerbates atherosclerosis in experimental animal models. Some human vaccines, such as BCG, contain HSPs, hence although vaccination programmes are vital for maintaining 'herd' immunity and the prevention of serious infectious disease, they may leave a legacy of increased susceptibility to atherosclerosis. Development of HSP-free vaccines could satisfy the twin goals of protection from infection and reduced incidence of coronary disease.
Atherosclerosis 2003 Apr
PMID:Molecular mimicry in atherosclerosis: a role for heat shock proteins in immunisation. 1470 75

As people get older, their immune systems falter. The elderly are more susceptible to infections than youngsters are, and hyperactive inflammatory responses appear to contribute to some age-associated illnesses, including Alzheimer's disease and atherosclerosis. Investigating the effect of aging on the immune system was once a scientific stepchild, but card-carrying immunologists are now tackling the problem head-on. Despite the immune system's complexity, researchers have started to make sense of how its components change with age. As the research progresses, scientists hope to bolster elderly people's response to infectious diseases and quiet the inflammation that can make aging a painful experience.
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PMID:Immunity challenge. 1284 25

Infiltration of tissues by monocyte-derived macrophages is a prominent component of a wide-range of diseases, including atherosclerosis, glomerulonephritis, encephalitis, infectious diseases, and virtually all syndromes characterized by chronic inflammation. The molecular signals responsible for this directed migration are incompletely understood, but members of the chemokine family, especially the monocyte chemoattractant proteins (MCPs) (MCP-1 to MCP-5) are emerging as key players. Cells that respond to the MCPs do so because they express chemokine receptor 2 (CCR2), the cognate receptor. This review will summarize evidence supporting a key role for CCR2 in the pathogenesis of atherosclerosis, infections with intracellular pathogens, and regulation of the type I adaptive immune response.
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PMID:Chemokine receptor 2 (CCR2) in atherosclerosis, infectious diseases, and regulation of T-cell polarization. 1285 43

The metabolic syndrome in association with obesity is a major clinical problem inducing hypertension, diabetes mellitus, and atherosclerosis. Leptin induces angiogenesis by its proliferative effects on endothelial cells (ECs) via OB receptor (OB-Rb) gene. We evaluated the growth of ECs and intracellular signalings in response to leptin in vitro and the angiogenic effects of leptin in the cornea in vivo with and without adenovirus-mediated transfer of the OB-Rb gene in Zucker fatty (ZF) rats as a model for the metabolic syndrome. Recombinant adenovirus vector encoding rat OB-Rb (Ad.OB-Rb) or Escherichia coli. LacZ (Ad.LacZ) was transfected into cultured ECs from Zucker lean (ZL) rats and ZF rats. Leptin increased DNA synthesis dose-dependently in ECs from ZL rats but not ZF rats. Infection with Ad.OB-Rb, but not with Ad.LacZ, improved the growth effects of leptin in ECs from ZF rats. Leptin induced phosphorylation of Janus kinase (JAK)2, signal transducer and activator of transcription (STAT)3, and extracellular signal-regulated kinase (ERK) in ECs from ZL rats but not ZF rats. Infection with Ad.OB-Rb restored phosphorylation of JAK2 and STAT3 in ECs from ZF rats. Leptin induced angiogenesis in cornea from ZL rats, but not from ZF rats. Coadministration of leptin and Ad.OB-Rb induced angiogenesis in cornea from ZF rats. Ad.LacZ did not influence the angiogenic effects of leptin. The impaired endothelial function with the leptin resistance may be one of causes of the atherosclerosis in the metabolic syndrome.
Atherosclerosis 2003 Aug
PMID:Effects of leptin on endothelial function with OB-Rb gene transfer in Zucker fatty rats. 1292 73

Atherosclerosis is a complex pathologic process initialed by the formation of cholesterol-rich plaque. Macrophages play a central role in the development of atherosclerosis, specifically in the initial accumulation of cholesterol in the arterial wall. It has been suggested that infection and chronic inflammatory conditions such as periodontitis may influence the atherosclerosis process. Porphyromonas gingivalis, one of the major pathogens involved in periodontitis, has been detected in human atheromas, suggesting that P. gingivalis infection may be associated with atherosclerosis. However, a causal relationship between this pathogen and the disease process has not yet been established. The purpose of the present investigation was to determine whether P. gingivalis could induce macrophages to form foam cells using the murine macrophage cell line (J774) as a model system. For inocula smaller than one bacterium per ten cells, P. gingivalis 381, as well as its lipopolysaccharide (LPS), induced foam cell formation of macrophages when cultured in the presence of human low-density lipoprotein (LDL). Infection of macrophages with increasing doses of P. gingivalis resulted in higher levels of foam cell formation. More than 70% of the cultured macrophages form cholesterol ester droplet-rich cells in the presence of 100 mug/ml of LDL when the inocula was more than 10 bacteria per cell. Low concentrations of P. gingivalis outer membrane vesicles also induced foam cell formation in the presence of LDL. In addition, it was demonstrated that P. gingivalis LPS alone was able to induce macrophage foam cell formation. P. gingivalis and its vesicles not only promoted LDL binding to macrophages but also induced macrophages to modify native LDL, which plays an important role in foam cell formation and the pathogenesis of atherosclerosis. Therefore, P. gingivalis cells or its vesicles released from periodontal lesions into the circulation may deliver virulence factor(s) such as LPS to the arterial wall to initiate or promote foam cell formation in macrophages and contribute to atheroma development.
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PMID:Porphyromonas gingivalis induces murine macrophage foam cell formation. 1458 Mar 89

The disease of cardiovascular system is one of the causes of invalidity and unfavorable outcomes. Together with such common diseases as rheumatism, hypertension, atherosclerosis that cause the development of cardiovascular insufficiency there are many other diseases including the infectious one that have rather unfavorable influence on the myocardium and vascular system. The disorders in cardiovascular functions at acute infectious diseases are noted frequently (80%) and closely connected with total pathogenesis of the disease. They influence the clinical course and outcomes of infectious process. Follow-up of the infectious patients and conduction of rational and especially intensive therapy require the wide functional control of cardiovascular state at different stages of the disease. The work shows our great experience in development of the problem of clinical-and-electrocardiographic investigations in infectious patients. The critical analysis of the problem condition today according to the literature data is presented. The material is based on the investigation of about 25 thousand patients treated in the clinic of infectious diseases of the Military Medical Academy for the last 30 years.
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PMID:[Cardiopathy in infectious diseases: clinical and pathogenetic aspects of diagnosis]. 1459 76


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