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

It was established that viral particles, like low-density lipoproteins (LDLP), when subjected to some modification changes, lost their ability to be internalized by tissue somatic cells and acquired tropism to macrophage cells. The data, obtained by us by using the polymerase chain reaction (PCR) method, made it possible to assert that atherosclerotic plaques, isolated from vessels of patients with ischemic heart disease (IHD) who underwent coronary bypass, contained RNA of the A(HINI) and AH3N3) influenza viruses. Whereas, the vessel portions, undamaged by atherosclerosis, did not contain any genetic substances of influenza viruses. It was for the first time that an experimentally supported understanding was expressed on that the atherosclerotic plaques serve as a "reservoir" for influenza viruses. It is also suggested that the mentioned plaques can be the carriers of influenza viruses for a long time, thus, prolonging the persistent form of influenza infection in the human body.
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PMID:[Influenza viruses and atherosclerosis: the role of atherosclerotic plaques in prolonging the persistent form of influenza infection]. 1274 53

On a variety of fronts, chronic infection has been found to be significantly associated with the development of atherosclerosis and the clinical complications of unstable angina, myocardial infarction, and stroke. For the most part, these relationships are still just associations. Failure to confirm initial reports of serologic associations also has been common. Specific causative relationships on par with that determined between H pylori and peptic ulcer disease have not yet been established. Potential mechanisms whereby chronic infections may play a role in atherogenesis are myriad. In the case of C pneumoniae, the effect may result from direct vessel wall colonization that may damage the vessel either directly or indirectly by initiating immunologic responses. In other cases the effect may simply be that of enhancing the pre-existing chronic inflammatory response of the body to standard risk factors such as hyperlipidemia. Even though the infectious agent may not directly infect the vessel wall, it may perform its critical role from afar. Chronic infection might also influence pre-existing plaque by enhancing T-cell activation or other inflammatory responses that may participate in the destabilization of the intimal cap. Hence chronic infection may play a role either in the initiation, progression, or the destabilization of atherosclerotic plaques. The infectious agents with the most evidence to support an etiologic role in atherosclerosis include C pneumoniae and cytomegalovirus. Evidence is mounting for a variety of other potential agents including other herpes viruses, influenza, other specific bacteria (such as M pneumoniae), and chronic infections with common bacterial agents (periodontal disease, chronic bronchitis, and chronic urinary tract infection, among others) [191]. Future studies are expected to elucidate further the pathophysiologic relationship between chronic infection and atherosclerosis and to evaluate further the potential of a variety of treatment approaches, including antibiotics.
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PMID:Chronic infection and coronary artery disease. 1462 50

Stroke is a disease with well-defined modifiable risk factors such as arterial hypertension, smoking, diabetes, hyperlipidemia and atrial fibrillation. The need of new risk factors is based on the fact that only half the cardiovascular disease risk is explained by conventional risk factors. Inflammatory markers, infection, homocysteine and sleep-disordered breathing rank as the four most important new risk factors in cerebral atherosclerosis. C-reactive protein is the inflammatory marker that has been most thoroughly studied. Elevated concentrations of C-reactive protein increase the risk of heart disease and thromboembolic stroke in men and women. The role of Chlamydia pneumoniae is still controversial. Influenza vaccination is a simple and effective preventive measure against stroke. Despite the potential relationship between homocysteine and stroke, we should wait to the results of the ongoing trials to know if the reduction of homocysteine levels with vitamin therapy is of clinical benefit. Sleep-disordered breathing is a potential new risk factor with an effective therapy. Neurologists should not forget to look for sleep disorders in their stroke patients and probably manage them with breathing therapy from the acute phase.
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PMID:Cerebral ischemia: new risk factors. 1469 79

Although the metabolic syndrome together with insulin resistance and their consequences are probably basic factors in pathogenesis of atherosclerosis, inflammatory and infectious aspects of this process are unquestionable only in some of the patients. Endothelial dysfunction was identified both in the experiment and in patients after herpes virus simplex 1 infection, cytomegaloviral infection, Chlamydia pneumoniae infection, or Helicobacter pylori infection. However, it is not clear whether it is always caused by direct specific activity of a given pathogen or whether it is a result of inflammatory cytokines activity, heat shock protein activity, or CRP activity. In recent years secondary antibiotic prevention in patients after myocardial infarction has been discussed. Lower mortality rate from acute myocardial infarction and cerebral vascular accidents were found in several observations of patients vaccinated against influenza. In patients with non-stable angina pectoris we have found significantly more frequent occurrence of IgG antibodies against Chlamydia pneumoniae. This occurrence was more frequent in diabetics compared to non-diabetics. Endothelia exposed to cyto-megaloviral infection exprimed adhesive molecules on their surfaces. After an increase of the concentration of glucose in medium to 11.0 mmol/l and 16.5 mmol/l the expression of adhesive molecules after cyto-megaloviral infection increased. Relationship of infection, inflammation, and atherosclerosis has been a subject of intensive investigation in recent years. Discussion of possible consequences of these findings, especially from viewpoint of atherosclerosis prevention and its organ complications, is of the same intensity. Hypothesis about participation of infection and inflammation in pathogenesis of atherosclerosis seems to be very attractive. In spite of the fact that findings supporting this hypothesis cumulate final conclusion can't be made yet.
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PMID:[Infectious and inflammatory factors in the etiology and pathogenesis of atherosclerosis]. 1504 Jan 64

There is mounting evidence in support of a significant role for influenza infection in the development of atherosclerosis and the triggering of its complications. Here we review the biologic basis of this relationship, with special emphasis on the pro-inflammatory and pro-thrombotic effects of influenza infection. We also discuss the related epidemiologic findings and discuss in detail the possible causal relationship between influenza and cardiovascular disease. We appraise the relationship between influenza and coronary heart disease, on the basis of Bradford Hill's criteria of causality. We show that our proposed relationship meets the following criteria: strength of association, consistency, temporal sequence, coherence, biologic plausibility, experimental evidence, and analogy. Further studies are needed to assess whether it meets the criterion of biologic gradient. Specificity is not met, but meeting that criterion is of least importance in the study of multifactorial chronic diseases such as coronary heart disease. These criteria do not yield indisputable evidence for or against cause-and-effect, but they can help researchers appraise available evidence and determine the areas that need further research. The case for expanding the research on the effect of influenza on cardiovascular disease is a strong one, for most of Hill's criteria are met.
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PMID:Influenza and cardiovascular disease: is there a causal relationship? 1506 20

chlamdAs with other organ systems, the vulnerability of the nervous system to infectious agents increases with aging. Several different infectious agents can cause neurodegenerative conditions, with prominent examples being human immunodeficiency virus (HIV-1) dementia and prion disorders. Such infections of the central nervous system (CNS) typically have a relatively long incubation period and a chronic progressive course, and are therefore increasing in frequency as more people live longer. Infectious agents may enter the central nervous system in infected migratory macrophages, by transcytosis across blood-brain barrier cells or by intraneuronal transfer from peripheral nerves. Synapses and lipid rafts are important sites at which infectious agents may enter neurons and/or exert their cytotoxic effects. Recent findings suggest the possibility that infectious agents may increase the risk of common age-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and stroke. While scenarios can be envisioned whereby viruses such as Chlamydia pneumoniae, herpes simplex and influenza promote damage to neurons during aging, there is no conclusive evidence for a major role of these pathogens in neurodegenerative disorders. In the case of stroke, blood vessels may be adversely affected by bacteria or viruses resulting in atherosclerosis.
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PMID:Infectious agents and age-related neurodegenerative disorders. 1516 5

We report a case of sudden unexpected death in a 17-year-old male student showing similar clinical background and pathological findings to Reye's syndrome. He was found following cardio-pulmonary arrest in his bed, and was immediately transferred to a hospital. However, resuscitation was not successful. He had a history of high fever of 38.3 degrees C, general malaise, myalgia, and gastrointestinal discomfort for the 2 days prior to his death, and an injection of pylazolon and medication comprising anti-emetics had been administered the day before he died. His biochemical findings showed almost normal levels of transaminase, electrolytes and protein fractions at the emergency room, but blood from the heart at autopsy revealed a high titer of the influenza A virus. Macroscopically, in addition to considerable fatty metamorphosis of the liver, concentric hypertrophy of the left ventricle, muscular bridge of left anterior descending artery, moderate coronary atherosclerosis, and mild downward displacement of the septal leaflet of the tricuspid valve were noted in the heart. Although panlobular microvesicular fatty infiltration of the liver was seen, deposition of lipid droplets was detected only in hepatocytes by frozen section of several organs. Serial sectioning of the epicardial coronary arteries showed about 50% stenosis at the distal site of the left circumflex artery, and diffuse interstitial fibrosis was evident in the bilateral ventricle and this was relatively severe for his age. In addition, the atrioventricular (AV) node artery showed severe narrowing just before entering the AV node, and downward displacement of the AV node with longitudinal elongation was also remarkable. We consider that the cause of death was sudden cardiac death rather than Reye's syndrome (RS), and that an arrhythmogenic event due to some preceding unusual cardiac lesions may have become overt due to the influenza infection and/or some related disorders. The present case would seem to suggest that a postmortem diagnosis of RS should be determined very carefully in cases of sudden death, even if the general circumstances would seem to be consistent with RS.
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PMID:Sudden unexpected death of a 17-year-old male infected with the influenza virus. 1555 16

Chronic inflammatory stimulus seems to contribute to atherosclerotic process. Several studies have established a relationship between infective agents as Chlamydia pneumoniae, herpes virus and cytomegalovirus and atherosclerotic lesions. Aim of this study was to investigate the effects of influenza infective state on endothelial function of healthy young subjects, expressed as brachial flow-mediated vasodilation (FMV) and soluble form of intercellular adhesion molecule-1 (sICAM-1) and vascular cell adhesion molecule-1 (sVCAM-1). In 10 male subjects (mean age 35+/-14 years) exhibiting influenza symptoms for 3 days, we determined total cholesterol, high-density lipoproteins (HDL), low-density lipoproteins (LDL), triglycerides, sVCAM-1, sICAM-1 and brachial FMV. All subjects had an antibody pattern characteristic of influenza A or B virus infection. After 3 months brachial FMV was significantly increased (8.6+/-2.3% versus 11.5+/-3.2%; p<0.001), while HDL (46+/-10 mg/dL versus 49+/-9 mg/dL; p<0.05), sICAM-1 and sVCAM-1 were reduced (respectively: 488+/-105 ng/mL versus 340+/-127 ng/mL; p<0.001, 1710+/-80 ng/mL versus 1216+/-63 ng/mL; p<0.001). Univariate analysis showed a positive correlation between changes in CRP and sICAM-1 levels (r=0.95, p<0.001), a negative one between changes in sICAM-1 and brachial FMV (r=-0.65, p<0.05) and between CRP and brachial FMV (r=-0.64, p<0.05). This small study suggested that inflammatory state determined by viral agents may transitorily alter endothelial function in healthy subjects.
Atherosclerosis 2005 Feb
PMID:Acute inflammatory state during influenza infection and endothelial function. 1569 44

It has been observed during influenza epidemics and in a number of population and clinical trials that this prevalent viral infection was associated with increased death rates from cardiovascular diseases. The clinical and experimental data that may explain accelerated coronary atherosclerosis in influenza infection with implications involving autoimmune mechanisms are reviewed in this article. Both cellular and humoral autoimmune mode could be proposed to participate in the onset or progression of atheromatous lesions due to influenza infection.
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PMID:Influenza, autoimmunity and atherogenesis. 1572 56

It has been observed during influenza epidemics and in a number of population and clinical trials that this prevalent viral infection was associated with increased death rates from cardiovascular diseases. The clinical and experimental data that may explain accelerated coronary atherosclerosis in influenza infection with implications involving autoimmune mechanisms are analyzed in this article. Both cellular and humoral autoimmune modes could be proposed to participate in the onset or progression of atheromatous lesions due to influenza infection.
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PMID:Autoimmune nature of influenza atherogenicity. 1601 58


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