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

In the last years, a considerable number of studies have been performed on the correlation between Helicobacter pylori infection and ischaemic heart disease. The reason is the supposed role of some chronic infections in the genesis and development of vessel wall injury and atheromatous plaque, as already reported for Chlamydia pneumoniae and herpes viruses. While this association may be theoretically conceivable, it still remains debated from a practical point of view. Epidemiological and animal studies as well as some eradicating trials gave conflicting results, while studies investigating the specific molecular mimicry mechanisms induced by H. pylori strongly support the association. Moreover, none of the studies performed so far did take into account the effect of the genetic susceptibility to develop ischaemic heart disease or to respond to H. pylori infection. In particular, while the exposure to some known risk factor for atherosclerosis should lead to develop ischaemic heart disease, no condition or exposure, either individual or in combination, completely explains the occurrence and the progression of the disease, as many patients develop ischaemic heart disease in the absence of any risk factor. Based on these concepts, can we state that H. pylori infection may cause the same effect in patients with ischaemic heart disease as in healthy subjects? Further studies are needed in order to clarify this issue.
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PMID:Helicobacter pylori infection and ischaemic heart disease: an overview of the general literature. 1584 77

This paper is concerned with intracellular infections such as herpes virus, cytomegalovirus and Chlamydia pneumonia which may be implicated in the pathogenesis of atherosclerosis. These viral and bacterial pathogens are regarded as potential causative factors in the pathogenesis of atherosclerosis. The authors support the hypothesis that these infections may induce endothelial injury. The paper reviews both direct and indirect immune system-mediated effect of the viruses indicated on the disease process and the potential role of killer cells in endothelial injury.
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PMID:[The role of the immune system in the pathogenesis of atherosclerosis]. 1603 97

Human cytomegalovirus (HCMV) serology is linked to several measures of endothelial dysfunction. There is substantial evidence for HCMV having an aetiological role in transplant arterial disease and accumulating evidence for HCMV in the origins of preeclampsia. However, whether HCMV is a clinically significant cause of atherosclerosis in the general, immunocompetent population remains to be seen.
Herpes 2005 Oct
PMID:Human cytomegalovirus, endothelial function and atherosclerosis. 1620 60

Accumulating evidence suggests that chronic infections, such as periodontitis, are associated with increased risk for cardiovascular diseases (CVD). The mechanisms behind the association are not known. Like herpes viruses and Chlamydia pneumoniae, periodontal pathogens cause atherosclerosis in experimental animals and have been found in human atherosclerotic lesions. Higher concentrations of total and low density lipoprotein (LDL) cholesterol and triglycerides and lower concentrations of high density lipoprotein (HDL) cholesterol have been observed in individuals with periodontitis before periodontal treatment. Periodontitis also induces a peripheral inflammatory and immune response, reflected in elevated concentrations of C-reactive protein (CRP) and IgA-class antibodies to periodontal pathogens. The prevalence of CVD seems to be highest in those individuals in whom periodontitis coexists with elevated CRP levels. This may indicate that periodontitis is a CVD risk factor in individuals who react to the infection with a systemic inflammatory and immune response. This may be due to genetic reasons and may also apply to other chronic low-grade infections.
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PMID:Dental infections and cardiovascular diseases: a review. 1627 80

Infections have long been recognized as a potential, if uncommon, cause of cerebrovascular disease. In recent years, with the growing recognition of the importance of inflammation in atherosclerosis, there has been renewed interest in the possibility that common infections may participate in the atherosclerotic process or lead to stroke through other mechanisms. Specific organisms that have been implicated include Chlamydia pneumoniae, herpes viruses, human immunodeficiency virus, Helicobacter pylori, and organisms associated with periodontal infections. This article outlines the epidemiological, pathological, and laboratory evidence that these infections may be associated with atherosclerosis and stroke. Although definitive proof of an association between a specific infection and stroke is generally lacking, the accumulating evidence does indicate that several types of infections may be among the modifiable risk factors that contribute to the risk of stroke.
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PMID:Do common infections cause stroke? 1647 47

There is much evidence to suggest the existence of racial differences between blacks and whites in the behaviour of endothelial function. Infective state, sustained by viral or bacterial agents, may injure the endothelial surface favouring the onset and progression of atherosclerotic process, mainly by an inflammatory mechanism. The aim of the study was to investigate endothelial function, expressed as brachial flow-mediated vasodilation (FMV), in black and white healthy subjects, along with antibody titer to cytomegalovirus, hepatitis virus (B, C), herpes virus-1 and 2, Epstein-Barr, Chlamydia pneumoniae and the expression of adhesion molecules. We enrolled 22 young (mean age 27+/-8 years) healthy subjects of black race (10 males) and 20 healthy young subjects (10 males, mean age 28+/-9 years) of white race. Total infectious burden (TIB) was defined as the number of serological positive infections. Black subjects have a reduced brachial FMV (6.9+/-3.5% versus 11.6+/-3.0%, p<0.01) and increased values of hsCRP (0.35+/-0.15 mg/dL versus 0.07+/-0.08 mg/dL, p<0.05), white cells (8578+/-1041/mmc versus 5833+/-998/mmc, p<0.01) and adhesion molecules (respectively: sVCAM-1 945+/-142 versus 779+/-93, sICAM-1 534+/-107 ng/mL versus 325+/-80 ng/mL; both p<0.01) in comparison to white subjects. The total infectious burden in black race was significantly higher than in white race (5+/-1 versus 2+/-1, p<0.01). At the univariate analysis, brachial FMV was significantly related to the levels of adhesion molecules (respectively: sVCAM-1 r=-0.49; sICAM-1 r=-0.50, both p<0.05), hsCRP (r=-0.47, p<0.05) and white blood cells (r=-0.43, p<0.05). TIB was associated with brachial FMV (r=-0.64, p<0.05), sVCAM-1 (r=0.55, p<0.05) and hsCRP (r=0.47, p<0.05). At the multivariate analysis the only predictive variables for brachial FMV were hsCRP, TIB and brachial diameter (respectively: beta=-0.49, -0.19, -0.54, all p<0.05). This study confirms that endothelial reactivity is impaired in young African black patients; moreover its behavior is strictly related to the inflammatory state and to the total infectious burden.
Atherosclerosis 2007 Mar
PMID:Racial difference in endothelial function: role of the infective burden. 1671 54

It is assumed that various infectious agents play direct or indirect roles in the pathogenesis of atherosclerosis which is accepted as a chronic inflammatory phenomenon. However, the data obtained from different studies are contradictory. The aim of this study was to investigate the roles of herpes virus group [Herpes simplex virus (HSV), Epstein-Barr virus (EBV), Cytomegalovirus (CMV)] and hepatitis A virus (HAV) which are debated in terms of their impact in the pathogenesis of coronary arterial diseases. For this purpose, atherome plaque samples collected from 28 patients (23 were male; age range: 43-74 years) with atherosclerotic heart disease and vein samples from 22 control patients (19 were male; age range: 37-85 years) who had vascular diseases other than atherosclerosis, were investigated by means of the presence of nucleic acids of the above mentioned viruses by real-time polymerase chain reaction (PCR). Besides, classical cardiovascular risk factors (hypertension, hyperlipidemia, hypercholestrolemia, diabetes mellitus, smoking habits, gender, age and familial background) were questioned in both patient and control groups. As a result, no positivity were detected for nucleic acids of HSV type 1 and 2, EBV and HAV, whereas CMV-DNA was found positive in three of 28 (10.7%) atheromateous plaques (viral loads were 21, 188 and 288 copies/mg). Amongst 22 vascular samples from controls, two (9.1%) yielded positive results for EBV-DNA (viral loads were 5 and 10 copies/mg), while the other samples were found negative for nucleic acids of HSV type 1 and 2, CMV and HAV. The evaluation of the known risk factors for atherosclerosis revealed that, the difference between the presence of hypertension and hyperlipidemia which are the major risk factors, was statistically important (p < 0.05) in patient group (64% and 50%, respectively) and control group (32% and 23%, respectively). In conclusion, the hypothesis concerning the possible relationship between these viral agents and the progression of atherosclerosis, have not been supported by our data which are similar to the results obtained from various other studies. Actually, further studies are needed to clarify such direct or indirect roles of infectious agents in the pathogenesis of coronary arterial diseases.
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PMID:[Investigation of herpes group and hepatitis A virus nucleic acids in the atherome plaque samples of patients with coronary arterial disease]. 1817 72

A number of human and animal herpes viruses encode G-protein coupled receptors with seven transmembrane (7TM) segments-most of which are clearly related to human chemokine receptors. It appears, that these receptors are used by the virus for immune evasion, cellular transformation, tissue targeting, and possibly for cell entry. In addition, many virally-encoded chemokine 7TM receptors have been suggested to be causally involved in pathogenic phenotypes like Kaposi sarcoma, atherosclerosis, HIV-infection and tumour development. The role of these receptors during the viral life cycle and in viral pathogenesis is still poorly understood. Here we focus on the current knowledge of structure, function and trafficking patterns of virally encoded chemokine receptors and further address the putative roles of these receptors in virus survival and host -cell and/or -immune system modulation. Finally, we highlight the emerging impact of these receptor on virus-mediated diseases.
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PMID:Structure, function and physiological consequences of virally encoded chemokine seven transmembrane receptors. 1820 88

The XXth century is marked by the substantial increase in human life expectancy. Historically, main reasons for that are four achievements of medicine: (1) improvements in common hygiene, such as waste disposal and water purification which led to the significant reduction of communicable diseases; (2) common recognition of Pasteur's Germ Theory followed by improvements in occupational and personal hygiene as well as introduction of antiseptic and aseptic measures; (3) decrease in childhood mortality due to the discovery and widespread application of vaccination; and (4) the discovery and clinical application of antibiotics. An epidemiological transition took place, i.e. the shift from communicable infectious diseases, as a main cause of morbidity and mortality, to chronic degenerative diseases, mainly considered non-infectious. Experimental evidence has been accumulated on a significant number of microorganisms, including viruses (such as a group of herpes viruses, hepatitis viruses, etc.), bacteria (Chlamydia, Helicobacter, periodontal pathogens, etc.), fungi and parasites, as an underlying reason for many of diseases, such as atherosclerosis, various cancers, type 1 and 2 diabetes, neurodegenerative and some psychiatric diseases, osteoporosis, autoimmune diseases and others. On the other hand, most of these diseases have been traditionally associated with age, together with other "age-related" disorders, such as immune system suppression, thymus involution, pathologic calcification, etc. Taken together, these facts suggest that aging, among others, has infectious origins, and that burden of infections may lead to enhanced senescence and premature death. In fact, infections may serve as a trigger of senescence, presumably via the mechanisms of chronic oxidative stress, low-grade inflammation, telomere shortening, and autoimmune processes due to the molecular mimicry. We believe that next step in human longevity increase can be possible by common appreciation of the role of infections as the main trigger of age-related diseases and disorders, and by efforts to cure and/or eradicate these infections.
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PMID:[Fifth revolution in medicine: on the role of infections in pathogenesis of aging and chronic diseases]. 1882 37

Whereas C-reactive protein (CRP) is acknowledged as a cardiovascular risk marker, there is ongoing discussion about its role as a risk factor. Previous studies focused on the effects of CRP on ischaemic heart failure and atherosclerosis. In this study we investigated distribution of CRP, the Terminal Complement Complex (C5b-9) and macrophages (CD68) in the myocardium of patients suffering from non-ischaemic heart failure and their implication on clinical parameters. Endomyocardial biopsies were taken from 66 patients suffering from dilated cardiomyopathy (DCM). Biopsies were analysed by immunohistochemical and immunofluorescent staining for CRP, C5b-9 and CD68. Viral DNA/RNA for adenovirus, enterovirus, parvovirus B19 and human herpes virus 6 was detected by PCR and Southern blot analysis. Myocardial biopsy findings were correlated with plasma level of hsCRP and NT-proBNP as well as echocardiography, exercise test and NYHA class. In 18 (27%) patients, a positive staining for CRP and in 57 (86%) patients a positive staining for C5b-9 was detected. All patients showed myocardial infiltration with macrophages with an average of 39 cells/mm(2). CRP, C5b-9 and CD68 co-localised within the myocardium. No correlation was observed for inflammatory proteins and plasma level of hsCRP, NT-proBNP and clinical parameters. CRP is frequently present in the myocardium of patients suffering from DCM and co-localises with C5b-9 and macrophages. CRP may contribute to myocardial damage in DCM via activation of the complement system and chemotaxis of macrophages.
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PMID:Myocardial inflammation and non-ischaemic heart failure: is there a role for C-reactive protein? 1934 15


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