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)

Infections, such as by Chlamydophilia pneumoniae, cytomegalovirus, herpes simplex virus, and Helicobacter pylori, have been shown to be involved in atherogenesis. Herpes simplex virus I (HSV-1) could infect vascular endothelial cells, and it has been shown that, when endothelial cells were activated with oxidized LDL (oxLDL), a number of cellular events are occurred, leading to endothelial cell dysfunction. Since LOX-1 is a major receptor for oxLDL on endothelial cells and its expression was increased in atherosclerosis, we investigated whether HSV1 infection can lead to the increase expression of LOX-1 in endothelial cells. LOX-1 mRNA expression determined by RT-PCR and LOX-1 promoter activity measured by luciferase assay were increased in endothelial cells following HSV-1 infection. This suggests that one of the mechanisms by which HSV-1 is involved in atherogenesis maybe the enhanced uptake of oxLDL via the increased expression of LOX-1 in endothelial cells.
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PMID:Herpes simplex virus 1 induced LOX-1 expression in an endothelial cell line, ECV 304. 1527 8

Herpes simplex virus type 2 (HSV-2), which has been recognized as a potential cardiovascular pathogen and implicated in carotid atherosclerosis and coronary artery disease, is independently associated with the future risk of cardiovascular death. Investigations have demonstrated that hypertension may be related to inflammation, and inflammation is one of the symptoms of HSV-2 infection. This cross-sectional study investigated the correlation between HSV-2 infection and essential hypertension. One thousand two hundred and forty four inpatients (488 patients with essential hypertension and 756 normotensives) were investigated serologically for the specific immunoglobulin G (IgG) to HSV-2 by enzyme-linked immunosorbent assay. Patients diagnosed with pheochromocytoma, primary aldosteronism, aorto-arteritis or renal artery stenosis were excluded. The prevalence of HSV-2 IgG seropositivity was significantly higher in the hypertensive group than in the normotensive group (38.3% vs. 29.8%, p =0.002). After adjustment for confounding factors, an association of HSV-2 IgG seropositivity with essential hypertension was found on binary logistic regression analysis. The adjusted odds ratio of essential hypertension was 1.4 (95% confidence intervals, 1.1 to 1.8; p =0.005) for HSV-2 infection; the adjusted covariates included age, male sex, smoking, body mass index, dyslipidemia, diabetes and coronary artery disease. The results of this study indicated that HSV-2 infection might be an independent risk factor for essential hypertension.
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PMID:Herpes simplex virus type 2 infection is a risk factor for hypertension. 1549 72

Low levels of high-density lipoprotein cholesterol (HDL-C) show a consistent relationship with the development of atherosclerosis. The underlying mechanisms are not well understood, but recent studies in subjects with primary hypoalphalipoproteinemia suggest that this could represent a proinflammatory condition. To better assess the link between HDL-C levels and C-reactive protein levels and the possible role of chronic infections as putative mediators of this relationship, we studied a population sample with nonselected causes of hypoalphalipoproteinemia. Eighty-six consecutive patients with HDL-C levels below 40 mg/dL who attend our lipid clinic and 86 control subjects with normal concentrations matched for gender, age, smoking habit, and weight were included in the study. Mean HDL-C levels were 34 +/- 3.9 and 55.4 +/- 8.8 mg/dL for subjects with hypoalphalipoproteinemia and control subjects, respectively. C-reactive protein concentrations were increased in case patients as compared with control subjects (2.13 +/- 2.0 vs 1.52 +/- 1.8 mg/L; P = .025). The prevalence of herpes simplex virus type 1, cytomegalovirus, Chlamydia pneumoniae , and Helicobacter pylori infections did not differ between the 2 groups. Although a possible confounding variable could be a degree of insulin resistance within the group of patients with low HDL-C levels, our results indicate that C-reactive protein levels are increased in subjects with nonselected hypoalphalipoproteinemia and that chronic infections do not appear to mediate this relationship.
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PMID:C-reactive protein levels and prevalence of chronic infections in subjects with hypoalphalipoproteinemia. 1612 40

To investigate the presence of infectious agents in human atherosclerotic arterial tissues. Atherosclerotic plaques were removed from 128 patients undergoing carotid endarterectomy or other bypass procedures for occlusive disease, and from twenty normal arterial wall samples, obtained from transplant donors with no history of diabetes, hypertension, smoking, or hyperlipidemia. Using the polymerase chain reaction (PCR) or reverse transcription-PCR, these samples were analyzed for the presence of Chlamydia pneumoniae, cytomegalovirus, enterovirus, adenovirus, herpes simplex viruses types 1 and 2, and Epstein-Barr virus. The amplicons were then sequenced, and phylogenetic analyses were performed. Enteroviral RNA was found in 22 of 128 atherosclerotic vascular lesions (17.2%), and C. pneumoniae and cytomegalovirus were each found in 2 samples (1.6%). In contrast, adenovirus, herpes simplex viruses, and Epstein-Barr virus were not identified in any of the atherosclerotic samples. Enterovirus was detected in 6/24 (25.0%) aortas, 7/33 (21.2%) carotid arteries, 6/40 (15.0%) femoral arteries, and 3/31 (9.7%) radial arteries of patients with chronic renal failure. There were no infectious agents detected in any of the control specimens. Using phylogenetic analysis, the enterovirus isolates were clustered into 3 groups, arranged as echovirus 9 and coxsackieviruses B1 and B3. Enteroviral RNA was detected in 17.2% of atherosclerotic plaques, but was not observed in any of the control specimens. This suggests a connection between enteroviral infection and atherosclerosis. These findings differ from those of other studies, which found more frequent incidence of C. pneumoniae and cytomegalovirus infection in atherosclerotic plaques.
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PMID:Detection of enterovirus, cytomegalovirus, and Chlamydia pneumoniae in atheromas. 1565 Jun 86

We report an adolescent girl with a history of angiolymphoid hyperplasia with eosinophilia (ALHE) diagnosed at the age of 10 years. The patient also suffered from chronic persistent multiresistant herpes simplex virus infection. Atherosclerotic occlusive disease of the abdominal aorta and its major branches was observed at the age of 17 years, necessitating vascular surgical intervention 1 year later because of disease progression. Histological examination of the aorta disclosed widespread atherosclerosis and high levels of gene expression of both T-helper cell type (Th) 1- and Th2-derived cytokines. This suggests that a highly stimulated systemic immune response including increased production of both Th1- and Th2-derived cytokines such as interferon-gamma and interleukin-4 may result in severe atherosclerotic lesions at a very young age. In addition, the patient developed a peripheral T-cell lymphoma at the age of 18 years. Neither systemic atherosclerosis nor T-cell lymphoma has been reported in association with ALHE. It is suggested that a highly stimulated dysfunctional immune response may play a key role in persistent inflammatory disease and premature development of atherosclerosis as well as malignant transformation of T cells.
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PMID:Severe atherosclerosis of the aorta and development of peripheral T-cell lymphoma in an adolescent with angiolymphoid hyperplasia with eosinophilia. 1588 66

A group of patients with ischemic heart disease (IHD), who underwent surgical aorta-coronary vascular shunting, was examined in this investigation. Low titers of HSV-1 specific IgG were detected in all patients, the obtained values being consistent with similar data obtained in healthy subjects of the same age. Negative PCR of HSV-I DNA in blood and biopsy results were obtained. None of the patients demonstrated typical clinical pattern of infectious disease caused by herpes simplex virus. These data are evidence of the absence of the HSV-1 correlation with coronary atherosclerosis in patients with the IHD diagnosis. The significance of HCMV specific IgG titers and HCMV DNA detected in blood plasma in 87.7% cases is probably attributed to existence of connection of HCMV infection markers revealing in patient' blood with IHD diagnosis and coronary atherosclerosis. Besides, the HCMV DNA presence in biopsy taken from myocardium or vascular wall with lesion is revealed in 100% cases. The cytomegalovirus markers in tissue lesions with the help of specific antiserums marked to HSMV recombinant proteins are also revealed in 100% cases. This fact indicates the connection between pathological atherosclerotical process in IHD and cytomegalovirus infection.
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PMID:[The study of markers of herpes virus infections in myocardial ischemia]. 1633 25

The subjects of the study were 64 patients with coronary artery disease (CAD), and 38 healthy controls. The study included determination of Chlamydia pneumonia (CLPN), Toxoplasma gondii (TG), Herpes simplex virus (HSV) 1, 2, Epstein-Barr virus (EBV), and antibodies to these microorganisms. Diagnostically significant elevation of the serum levels of IgG antibodies to CLPN, HSV 1, 2, or TG was associated with CAD progression, and seropositivity to several of the agents strongly correlated with CAD progression. Moreover, the risk of future coronary events increased depending on the level of total pathogen burden. These results suggest that intracellular infectious agents are involved in the development of atherosclerosis and CAD.
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PMID:[Effect of respiratory infections on the clinical course of coronary artery disease]. 1640 34

Eotaxin (CCL11) is a potent chemoattractant for eosinophils and lymphocytes. Apart from its functions in the eosinophilic system, eotaxin has been shown to be overexpressed in atherosclerosis. We therefore sought to determine whether chronic infection with Chlamydia pneumoniae or other infectious agents is correlated with concentrations of eotaxin or C-reactive protein since this mechanism could explain the finding that chronic infection stimulates smooth muscle cell migration and plaque development. Patients undergoing percutaneous coronary angioplasty (PCI) for acute coronary syndrome or stable angina were included in the study. Blood was drawn before PCI, at 6 weeks, and 6 and 12 months after coronary intervention. Eotaxin and C-reactive protein were determined by enzyme-linked immunosorbent assay (ELISA). Antibodies against Candida, C. pneumoniae, cytomegalovirus, Helicobacter pylori, and herpes simplex virus were measured by ELISA or immunofluorescence. Two hundred five consecutive patients undergoing PCI (stable angina, n = 136; acute coronary syndrome, n = 69) and 83 patients with normal coronary arteries were enrolled in the study. Eotaxin concentrations at inclusion were higher in patients with coronary artery disease than in control patients, p = .01, and comparable in patients with stable angina and those with acute coronary syndrome but did not correlate with C-reactive protein. Eotaxin concentrations at inclusion and during follow-up weakly correlated with concentrations of antibodies against C. pneumoniae, H. pylori, and herpes simplex virus but not with concentrations of antibodies against Candida or cytomegalovirus. Eotaxin concentrations and antibody titers against C. pneumoniae significantly increased following angioplasty and remained elevated thereafter. In conclusion, our data demonstrate that eotaxin concentrations are elevated independently from C-reactive protein in patients with coronary artery disease and correlate with antibodies against infectious agents known for chronic infection in humans.
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PMID:Association between eotaxin (CCL11), C-reactive protein, and antimicrobial antibodies in patients undergoing coronary angioplasty. 1716 68

In order to assess the real significance of some plasma and vascular indices in disorders of the stable course of coronary heart disease (CHD) in chronic bacterial- and viral infection-invasion, we determined the blood plasma lipid hydrogen peroxide (LHP) activity, a direct index of the lipid peroxidation degree, and measured the concentration of specific antibodies to Chlamydia pneumoniae (C. pneunoniae), herpes simplex virus type 1 (HSV-1), cytomegalovirus (CMV) and Epstein-Barr virus (EBV) by means of the enzyme-linked immunosorbent assay (ELISA). We examined a total of 70 patients presenting with CHD combined with a concomitant infection both with a stable course of the disease (Group One) and acute coronary syndrome (Group Two), as well as 50 infected people without verified signs of coronary atherosclerosis (Group Three). The comparison group consisted of patients with CHD, being seronegative for the causative agents referred to above. The condition of the major vessels was appropriately assessed by means of duplex ultrasonography (DU). Resulting from the findings of the carried out investigation, we singled out a triad of symptoms characteristic of the transformation of the chronic infectious process into the recurrent phase, which for the CHD patients with the presence of the conventional risk factors of atherosclerosis might become a cause of the disordered stable course of the disease and development of acute ischaemic attacks. The revealed alterations seemed to have been based upon an infectious-origin inflammatory lesion of the vessels, which was duly confirmed by duplex ultrasonography.
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PMID:[Chronic bacterial-and-viral vasculitis as a possible risk factor of disordered stability of the coronary atherosclerosis course]. 1764 12

Several infectious agents, such as Chlamydia pneumoniae, cytomegalovirus (CMV), herpes simplex virus (HSV), and Helicobacter pylori, have been implicated in the pathogenesis of atherosclerosis; however, but the contribution of infection may vary among races and geographic conditions. The present study investigates the association between the presence of these pathogens and carotid atherosclerosis and examines the relevance of an infectious burden during atherogenesis in Japanese patients undergoing carotid endarterectomy. We investigated a total of 50 carotid atherosclerotic plaques resected during carotid endarterectomy by polymerase chain reaction (PCR) for C. pneumoniae, CMV, HSV, and H. pylori and by immunocytochemistry (ICC) for C. pneumoniae. We also examined the presence of antibodies to IgG and/or IgA for each pathogen in blood samples. We detected HSV DNA in 2 specimens (4%) and positive ICC for C. pneumoniae in 8 (16%). The results of PCR, ICC, or serum antibodies, as well as the number of seropositive antibodies, did not correlate with severely stenotic, ulcerative, or symptomatic plaques. Our findings indicate that the detection rate of infectious agents within atherosclerotic plaques was significantly lower in our patients than that in other studies. Thus, an inflammatory mechanism might not correlate with the pathogenesis of carotid atherosclerosis among Japanese patients with severe carotid artery stenosis.
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PMID:Lack of association between infectious burden and carotid atherosclerosis in Japanese patients. 1768 10


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