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

A mortality cohort study was carried out on 11,224 men with pneumoconiosis diagnosed during the period 1970-1985. The cohort was selected from among subjects entered into the National Register of Occupational Diseases and included 7,065 coal miners, 924 employees of underground work enterprises, 1,796 workers of the metallurgical industry and iron and nonferrous foundries, as well as 1,439 refractory materials, china, ceramics, and quarry workers. The cohort was traced up to the end of 1991. The mortality of all groups enrolled in the study, as compared with that of general male population of Poland, showed a statistically significant excess of overall mortality (SMRs ranging from 105; 95% confidence interval [CI]: 100-110 to 136; CI: 121-153) as well as a great excess of deaths from diseases of the respiratory system (SMRs from 383; 95% CI: 345-424 to 588; 95% CI: 457-744). In workers of the metallurgical industry, foundries, and those from refractory materials, china, and ceramics manufacturing plants as well as quarries, a statistically significant excess of deaths from infectious diseases (mostly tuberculosis) was found (SMRs: 503; 95% CI: 364-677 and 286; 95% CI: 177-437, respectively). Mortality from lung cancer was significantly elevated only in the group of metallurgical industry and iron and nonferrous foundry workers (SMR: 159; 95% CI: 124-201). In the remaining subcohorts, no significant excess of deaths from lung cancer was noted. The study does not support the hypothesis on the role of exposure to crystalline silica in the induction of lung cancer. Significantly lower mortality was seen for diseases of the circulatory system (SMR: 89; 95% CI: 82-96), hypertensive disease (SMR: 63; 95% CI: 38-98), cerebrovascular disease (SMR: 79; 95% CI: 62-99), atherosclerosis (SMR: 79; 95% CI: 66-93), and injuries and poisonings (SMR: 50; 95% CI: 38-64) in coal miners. In addition, lower mortality was noted for cerebrovascular disease (SMR: 56; 95% CI: 32-91) and injuries and poisonings (SMR: 34; 95% CI: 17-61) in metallurgical industry and iron and nonferrous foundry workers.
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PMID:Mortality among different occupational groups of workers with pneumoconiosis: results from a register-based cohort study. 891 18

An advanced type of population studies is now epidemiological studies of non-infectious diseases. Population pathology allows studying the whole spectrum of the disease development (predisease, early preclinical and overt stages) and the disease risk factors. Epidemiological studies of atherosclerosis provided information on the disease evolution within 25-year period in male population of 9 cities, a peculiar type of fibrous plaque formation in the aorta and coronary arteries is described and some features of lipid spots in the aorta in various populations are observed.
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PMID:[Population pathology--a new trend in pathology research]. 896 35

Cerebrovascular indices (cerebrovascular reactivity, plethora of pulse, the degree of atherosclerotic damage of carotids) were evaluated in 445 patients with either transient disturbances of brain's circulation or ischemic stroke. The patients' age was 32-85 years. It was found that the alterations in the system of neurogenic regulation which were the consequences of some pathogenic factors' influence (infectious diseases, closed brain's trauma, latent intoxication), resulted in some cases in formation of lower level of cerebrovascular reactivity which in turn was one of the reasons of ischemic cerebral disorder development. Further influence of such factors as atherosclerosis, increase of blood coagulability, decrease of total arterial pressure may result in alterations in cerebrovascular system's stability and in development of cerebrovascular diseases at younger age.
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PMID:[Cerebrovascular reactivity in the pathogenesis of ischemic brain lesions in patients of different ages]. 901 48

Abnormal migration and proliferation of arterial smooth muscle cells may be a central event in inflammatory proliferative arterial diseases such as atherosclerosis and restenosis after angioplasty. The proto-oncogene c-H-ras is considered to be a key transducer in various growth-signaling events. We constructed an adenoviral vector (AdexCAHRasY57) expressing a potent dominant-negative mutated form of c-H-ras in which tyrosine replaces aspartic acid at residue 57. Infection of smooth muscle cells with AdexCAHRasY57 produced a large quantity of H-ras-p21, completely inhibited serum-stimulated activation of mitogen-activated protein kinase, and abolished the DNA synthesis in response to serum mitogens. However, a surge of intracellular Ca2+ concentration in response to platelet-derived growth factor was not affected, suggesting that some cellular functions were preserved. When we applied AdexCAHRasY57 into balloon-injured rat carotid arteries from inside the lumen, neointimal formation was significantly reduced (neointima/media ratio: 0.28) compared with that (1.50) in arteries treated with either injury alone or injury and infection with a control adenovirus, AdexCALacZ, expressing bacterial beta-galactosidase. Our results suggest that adenovirus-mediated arterial transfer of dominant-negative H-ras may be a practical form of effective molecular intervention for proliferative arterial diseases.
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PMID:Adenovirus-mediated transfer of a dominant-negative H-ras suppresses neointimal formation in balloon-injured arteries in vivo. 915 53

To investigate the possibility of adenovirus-mediated gene transfer in the treatment of vascular occlusive diseases, we constructed a replication-deficient recombinant adenovirus vector coding for human basic fibroblast growth factor (bFGF) and examined its effect on the proliferation and differentiation of vascular endothelial cells in vitro. Human umbilical vein endothelial cells (HUVECs) were successfully infected with high efficiency and expressed 18 kD protein which is immunoreactive to anti-bFGF monoclonal antibody. This protein was accumulated mainly in the nuclei of the cells, but was also detected in the culture medium although the complimentary DNA (cDNA) did not contain the classical secreting signal sequence. The proliferation assay of HUVECs infected with bFGF-expressing adenovirus revealed a significant increase in cell number over control. Infection with this virus also enhanced tubular formation of HUVECs on reconstituted basement membrane. Neovascularization and the formation of collateral vessels play important roles in minimizing tissue damage in ischemic disorders. These results imply that the use of bFGF-expressing recombinant adenovirus may be a suitable in vivo gene therapy for ischemic diseases.
Atherosclerosis 1997 Jul 25
PMID:Adenovirus-mediated gene transfer of basic fibroblast growth factor induces in vitro angiogenesis. 924 65

Infection as a possible underlying cause of atherosclerosis has aroused increasing interest in recent years, Chlamydia pneumoniae being one of the organisms upon which attention has been focused. Newly published results of antibiotic treatment of vascular disease not only appear to provide further support for the infection hypothesis, but also suggest a quite different approach to the treatment of atheromatous cardiovascular disease. However, confirmatory clinical trials will be needed before antibiotic treatment can be considered in such cases.
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PMID:[Arteriosclerosis caused by infection? A possible link between Chlamydia pneumoniae and atherosclerosis]. 963 Aug

An increasing number of clinical and experimental studies point to a contribution of various infectious organisms like chlamydia pneumoniae or herpesviruses to atherosclerosis in man. Cytomegalovirus induces atherosclerotic lesions in animals. In vitro studies reveal functional changes of endothelial cells after infection with cytomegalovirus. Infection with this virus renders endothelial cells immunogenic for cellular and humoral immune reactions. In man a significant association of infections with herpesviruses and atherosclerosis could be established in several studies. Cytomegalovirus infection has been incriminated as an independent risk factor in restenosis after coronary angioplasty.
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PMID:[Cytomegalovirus and herpes simplex virus in pathogenesis and progression of native arteriosclerosis and recurrent stenosis after intervention]. 964 1

Powerful diagnostic technology, plus the realization that organisms of otherwise unimpressive virulence can produce slowly progressive chronic disease with a wide spectrum of clinical manifestations and disease outcomes, has resulted in the discovery of new infectious agents and new concepts of infectious diseases. The demonstration that final outcome of infection is as much determined by the genetic background of the patient as by the genetic makeup of the infecting agent is indicating that a number of chronic diseases of unknown etiology are caused by one or more infectious agents. One well-known example is the discovery that stomach ulcers are due to Helicobacter pylori. Mycoplasmas may cause chronic lung disease in newborns and chronic asthma in adults, and Chlamydia pneumoniae, a recently identified common cause of acute respiratory infection, has been associated with atherosclerosis. A number of infectious agents that cause or contribute to neoplastic diseases in humans have been documented in the past 6 years. The association and causal role of infectious agents in chronic inflammatory diseases and cancer have major implications for public health, treatment, and prevention.
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PMID:Infectious causes of chronic inflammatory diseases and cancer. 971 80

Atherosclerosis displays all the features of a chronic inflammatory process. Aggressions that ignite and fuel atherosclerotic inflammation warrant keen attention. Infection is a potential clue, implying microbes with certain discrete characteristics: a wide epidemiologic distribution, a tropism for the arterial wall, and an aptitude for persistence, latency and recurrence. The infectious theory has built up from the pioneering observations of Fabricant et al. (1978) on the arterial lesions provoked by Marek's disease herpesvirus in chicken. So far one virus (cytomegalovirus) and two bacteria (Chlamydia pneumoniae and Helicobacter pylori) have been implicated in human atherosclerosis, based upon experimental, sero-epidemiologic, or pathologic evidence. None of these potential contributions has yet been established beyond reasonable doubt. However, grounded on the suspicion about C. pneumoniae, provocative therapeutic evidence has added recently: according to two pilot studies, treatment with macrolide antibiotics appear to improve the prognosis of coronary artery disease in both its chronic and acute forms. If ongoing larger-scale studies confirm these preliminary results, a novel era will open in our capacity for explaining, treating and preventing atherosclerosis. An infectious aetiology of atherosclerosis is now to be considered earnestly, and is already being submitted to more intensive clinical and experimental investigation.
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PMID:[The infection theory in atherosclerosis]. 983 76

Peripheral arterial disease of the lower limbs is a manifestation of atherosclerosis, and may also affect other vascular territories such as the coronary and cerebral arteries. Progressive narrowing of the vessels up to total occlusion can present as intermittent claudication or pain at rest, with or without cutaneous lesions. Patients with intermittent claudication are at a low risk of amputation, and the symptom has to be regarded as a warning signal for myocardial infarction and stroke. Nevertheless, if the patient's walking distance is too limited to allow a near-normal life, symptomatic treatment to improve quality of life should be considered. Treatment may consist of walking exercise, surgical or interventional radiological revascularisation, or, in some cases, administration of vasoactive drugs. Antiplatelet agents should be administered in an attempt to limit disease progression and prevent cardiac and cerebrovascular complications, together with active measures to reduce established risk factors such as smoking, diabetes, hyperlipidaemia, and arterial hypertension. The presence of pain at rest indicates that a lower limb is jeopardised, especially when the criteria for critical ischaemia have also been met. These criteria include the presence of chronic (lasting for more than 2 weeks) symptoms of ischaemia at rest and a systolic blood pressure less than 50 mm Hg or 30 mm Hg at the ankle or big toe, respectively. In such a situation, revascularisation should be attempted whenever possible. If this is not possible or if the procedure has failed, prostacyclin administered intravenously for days or weeks is an alternative. After revascularisation, early reocclusion may be prevented by administering anticoagulants and late reocclusion by antiplatelet agents, in conjunction with eradication of risk factors. In all situations, therapeutic decision-making should be undertaken in a multidisciplinary setting and should include the following: specialists in angiology (an internist) and interventional radiology; a vascular surgeon; an orthopaedic surgeon, if necessary; and diabetes and infectious disease specialists.
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PMID:[Drug treatment strategies for peripheral obliterative arteriopathy]. 984 99


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