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)

Chlamydia pneumoniae infection has been associated with coronary heart disease. To evaluate the mechanisms of this association, we studied whether chronic C. pneumoniae infection affects serum lipid values similarly to acute infections. Triglyceride, total and HDL cholesterol concentrations, and C. pneumoniae antibodies were measured from paired serum samples of 415 Finnish males taken 3 years apart. Chronic infection, defined as persistent IgG and IgA antibodies, was found in 20%, and the antibodies were negative (IgG < 32 and IgA < 16 in both samples) in 15% of the cases studied. The serum triglyceride and total cholesterol concentrations were higher in the subjects with a chronic C. pneumoniae infection than in the subjects with no antibodies (1.23 versus 1.03 mmol/L and 6.41 versus 6.31 mmol/L, respectively). The HDL cholesterol concentrations and the ratios of HDL cholesterol to total cholesterol were significantly decreased in the subjects with chronic infection (1.24 versus 1.36 mmol/L, P = .026; and 0.19 versus 0.22, P = .018, respectively). Chronic C. pneumoniae infection seems to be associated with a serum lipid profile considered to increase the risk of atherosclerosis. This finding supports the hypothesis that infections play a role in the pathogenesis of atherosclerosis.
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PMID:Chronic Chlamydia pneumoniae infection is associated with a serum lipid profile known to be a risk factor for atherosclerosis. 940 75

Autoantibodies against oxidatively modified low-density lipoproteins (oxLDL) and cardiolipin occur in patients with vascular diseases, including atherosclerosis. The ability of such antibodies to predict myocardial infarction (MI) was investigated in a prospective nested case-control study in which healthy 50-year-old men were followed up for 20 years. Raised levels of antibodies against oxLDL and cardiolipin at 50 years of age correlated positively with the incidence of MI and mortality related to MI 10 to 20 years later. IgG and IgA antibodies against cardiolipin were associated with MI between 50 to 60 years of age and IgG and IgA antibodies against oxLDL with MI at 60 to 70 years of age. Moreover, higher antibody levels were noted in those who died from acute MI in comparison to those who survived. The predictive power of IgA and IgG antibodies was strong and largely independent of that of other strong risk factors. In conclusion, raised levels of antibodies against oxLDL and cardiolipin may predict MI and MI-related death.
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PMID:Antibodies against cardiolipin and oxidatively modified LDL in 50-year-old men predict myocardial infarction. 940 6

To explore the relationship between human cytomegalovirus infection and atherosclerosis, we assayed the antibodies of human cytomegalovirus in the sera of 106 patients with coronary heart disease and 80 healthy people by indirect ELISA technique. The results showed that the positive rate of antibodies of HCMV IgG, HCMV IgM and HCMV IgA (95.3%, 12.3%, 13.2% respectively) is significantly higher than that in healthy people (85.0%, 2.5%, 3.8% respectively). Our findings indicated that HCMV infection is related to coronary heart disease. We consider that HCMV may be an etiological factor for human atherosclerosis. The periodical activation of latent HCMV may play a role in atherogenesis.
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PMID:[The detection of the antibodies of human cytomegalovirus in the sera of patients with coronary heart disease]. 959 40

The association of Chlamydia pneumoniae with atherosclerosis of coronary and carotid arteries and the aorta has been demonstrated by seroepidemiology and by detection of the organism in atheromata. We investigated the frequency of C. pneumoniae seropositivity in patients with acute myocardial infarction (AMI). C. pneumoniae-specific antibodies were measured by the microimmunofluorescence test in 160 AMI patients and 160 control subjects matched for age and gender. The odds ratios (ORs) were 2.2 (95% confidence interval (CI), 1.2 to 3.9) for immunoglobulin (Ig)G and 2.7 (95% CI, 1.7 to 4.3) for IgA. After adjustment for other cardiovascular risk factors of age, gender, hypertension, diabetes, cigarette smoking and serum cholesterol, the ORs were essentially unchanged. This study confirmed that the observations of an association between antibody against C. pneumoniae and coronary heart disease in Western nations is also present in Japan. Our results are comparable to the previous seroepidemiological studies reporting ORs of 2.0 or greater.
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PMID:Association of chronic infection of Chlamydia pneumoniae and coronary heart disease in the Japanese. 986 50

Helicobacter pylori causes a chronic gastric infection, which has been associated with coronary heart disease. To evaluate the mechanisms of this association, we studied whether the infection affects serum lipid levels as previously shown in acute infections. We analysed the serum samples of 880 males who participated in a reindeer herders' health survey in Northern Finland in 1989. H. pylori IgG and IgA antibodies were measured by enzyme-linked immunosorbent assay and triglyceride, total cholesterol and high-density lipoprotein cholesterol concentrations by routine enzymatic methods. A total of 52% of the subjects were positive for both H. pylori specific IgG and IgA and 31% were antibody-negative. The serum triglyceride and total cholesterol concentrations were significantly higher in the males with positive IgG and IgA antibody titres for H. pylori than in the males with no signs of infection (1.20 vs. 1.03 mmol/l, P < 0.001 and 6.59 vs. 6.11 mmol/l, P < 0.001, respectively). The associations remained statistically significant in non-smokers after the adjustment for age, body mass index (BMI) and social class. The finding supports the hypothesis that chronic infections may modify the serum lipid profile in a way that increases the risk of atherosclerosis.
Atherosclerosis 1999 Jan
PMID:Association of Helicobacter pylori infection with elevated serum lipids. 1057 83

The aim of this study was to assess the presence of Chlamydia pneumoniae antibodies in patients with angiographically verified atherosclerotic coronary artery disease. A total of 114 consecutive patients were investigated between April 1995 and June 1996. Patients were divided into two groups: 72 patients with acute myocardial infarction (AMI; 53 men, 19 women, mean age 62.27 +/- 10.1 years), and 42 patients with chronic ischemic heart disease (CAD; 37 men, 5 women, mean age 62.75 +/- 9.2 years). A control group of 50 normal subjects matched for age (mean 62 +/- 9 years), sex, social status and geographical area was used. Identification of Chlamydia pneumoniae was carried out with the microimmunofluorescence method, on two serum samples taken from patients on admission and after 15 days. The IgM, IgG and IgA anti-Chlamydia pneumoniae titers were assessed, values > or = 1:16, > or = 1:32 and > or = 1:8 being respectively considered positive. Acute (IgM > or = 16 or four fold rise of IgG titer) and chronic (IgG > or = 128 e IgA > or = 32 or only elevated IgA titer) infections were analyzed. IgM antibodies were not found in AMI, CAD and control groups. IgG positivity (IgG > or = 32) was found in 38% of the control group, in 58.3% of the AMI group (p < 0.05) and 42.8% of the CAD group (p < 0.01). IgA positivity > or = 8) was found in 22% of the control group, in 31.9% of the AMI group (NS) and in 33.3% of the CAD group (p < or = 0.05). Acute infection was observed in 5.5% of AMI patients and in 12% of CAD patients (NS), whereas no subject of the control group showed these values. Chronic infection was observed in 9.7% of AMI patients and in 16.6% of CAD patients (NS) whereas nobody of the control group showed these values. In conclusion, our results suggest that Chlamydia pneumoniae infection is present only in the AMI and CAD groups. It is possible to suppose that this infection may be linked to atherosclerosis through an endothelial damage or a systemic endogenous procoagulant and inflammatory activity.
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PMID:[Chlamydia pneumoniae infection and cardiac ischemic syndromes]. 992 69

Antiphospholipid Syndrome (APS) was first described by Hughes and sometimes called as Hughes syndrome. Recent studies revealed that the antigen to anticardiolipin antibody (aCL) is not cardiolipin itself but co-factor beta 2-GPI which expresses its epitope when it combines cardiolipin or gets oxidized. Lupus Anticoagulant is now possibly considered as anti-prothrombin antibody. Livedo including Snedden syndrome, pulmonary hypertension and skin ulcer became considered as the part of symptoms of this disease. In ISAPA 1998, it is reported from several laboratories that IgA aCL is also pathogenic to thrombosis as well as IgG aCL. Atherosclerosis is also accelerated by aCL. Catastrophic APS is rare but fatal, reported 3 cases in Japan and 50 cases in the world.
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PMID:[Antiphospholipid syndrome]. 1007 9

BACKGROUND: The potential correlation between chronic infection with Chlamydia pneumoniae and the progression of small abdominal aortic aneurysms (AAAs) and lower limb atherosclerosis was studied. METHODS: Mass screening for AAA was carried out in outdoor clinics at all hospitals in the county. Some 139 men (aged 65-73 years) with a 3.0-4.9-cm AAA were followed prospectively for 1-3 (mean 2.7) years. Initially, an interview and examination was performed, and blood samples were taken. RESULTS: Some 62 per cent (53-71 per cent) had an immunoglobulin (Ig) A level of 40 or more, or an IgG level of 64 or above. Some 83 per cent (74-93 per cent) had an IgA level of 20 or more, or an IgG level of 32 or more. Men with an IgA level of 20 or more had 51 per cent greater AAA expansion and men with an IgA level of 40 or above had 24 per cent more expansion. An IgA level of 20 or more, or IgA of 40 or greater, were significant independent predictors of AAA expansion adjusted for age, smoking, initial AAA size, steroid treatment, diastolic blood pressure, pulmonary function and other plasma factors. The ankle blood pressure index (ABI) of the IgA-seropositive men decreased 11 per cent, while the ABI decreased by 5 per cent among IgA-seronegative men (P < 0.05). The significant difference persisted after adjusting for age, smoking, initial systolic ankle blood pressure, initial brachial systolic or diastolic blood pressure, but disappeared after adjusting for low-density lipoprotein (LDL) levels. CONCLUSION: A high proportion of men with a small AAA have signs of chronic C. pneumoniae infection. The progression of AAAs and lower limb atherosclerosis seems to be correlated to chronic infection with C. pneumoniae.
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PMID:Vascular surgical society of great britain and ireland: immunoglobulin A antibodies against chlamydia pneumoniae are associated with expansion of small abdominal aortic aneurysms and declining ankle blood pressure 1036 Dec 4

The presence of Chlamydia pneumoniae in atheromas has been demonstrated in several studies. Culture of the organism from arterial tissue has been difficult. We report the use of a reverse transcriptase polymerase chain reaction to detect viable Chlamydia pneumoniae in carotid atheromas. We analyzed 30 patients (14 females, mean age 69.6 +/- 8.8 years) who underwent surgery for the removal of atherosclerotic plaques from carotid arteries. During surgery, samples of lingual vein and superior thyroideal artery were also taken. We applied two molecular biology techniques to the carotid plaques on lingual vein or thyroideal artery samples: 1) polymerase chain reaction (PCR) and 2) reverse transcriptase-PCR (RT-PCR) for the detection of bacterial mRNA, employing PCR primers designed to detect a fragment of the 16S rRNA gene. Blood samples were obtained from the patients for determination of Chlamydia pneumoniae IgG, IgA, and IgM antibody titers by a microimmunofluorescence technique. The results of the present study confirmed the presence of viable Chlamydia pneumoniae in atheromas and support the hypothesis that the organism may be an active factor in the pathogenesis of atherosclerosis.
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PMID:Demonstration of viable Chlamydia pneumoniae in atherosclerotic plaques of carotid arteries by reverse transcriptase polymerase chain reaction. 1039 39

There are numerous studies that were able to find C. pneumoniae infections as a contributing factor in atherosclerosis pathogenesis. Positive serology for C. pneumoniae was found in most studies in patients with atherosclerosis (IgG, IgA, IgM). Most studies were able to correlate an elevated IgA antibody titer rather than the IgG titer to the risk for atherosclerosis. C. pneumoniae and its components (DNA, antigens) were detected in atherosclerotic plaques using immunohistochemistry, PCR, electron microscopy and cell cultures. C. pneumoniae has been located in endothelium, smooth muscle cells and macrophages of arterial wall with atherosclerosis but not in normal arteries. Cellular models have shown that C. pneumoniae is able to replicate in endothelium, macrophages and smooth muscle cells. A high C. pneumoniae antibody titer was found to correlate with high level of LDL and triglycerides and low level of HDL. C. pneumoniae infection increases platelet adhesion and adhesion molecules at the surface of endothelium. C. pneumoniae could be a cofactor for atherosclerosis combined with high level of lipids as shown in an animal model but not alone. Strong cellular and humoral immunity have been found in men with atherosclerosis and positive C. pneumoniae titers. This organism could be found in diverse arteries with atherosclerosis. One particular C. pneumoniae strain (AR 39) appears to be more frequently involved in atherosclerosis. Antibiotic treatment with azithromycin appears to be protective against atherosclerosis complications. However, there is as yet no conclusive evidence that C. pneumoniae causes atherosclerosis, but most likely it may enhance this process. Two large randomized clinical trials are currently underway evaluating azithromycin treatment in patients with atherosclerosis which will hopefully give us answers about the role of antibiotic treatment.
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PMID:Infection with Chlamydia pneumoniae and atherosclerosis: a review. 1047 18


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