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

Ten out-patients with primary Type IIa hyperlipoproteinemia and a further 10 with Types IIb, IV, and V were administered with DL-alpha-methyl-thyroxine ethyl ester (etiroxate) (20 mg twice daily) for an average of 308 days. The aim of the study was to determine the effects of the drug on the cholesterol and triglyceride levels, tolerance and side-effects, particularly in coronary patients. The T4 values rose in all but one patient and fell again when the drug was discontinued. In Type IIa patients cholesterol fell by an average of 75.5 mg/100 ml (20.6%) as compared with the period before treatment and normal triglyceride levels dropped by 17 mg/100 ml (12.6%). In Type IIb, IV and V patients cholesterol levels decreased by 69.1 mg/100 ml (21%) during treatment. Serum triglycerides, which in some patients were extremely high before treatment were only slightly affected, falling by an average of 165.3 mg/100 ml (22.8%). For the whole group of patients the fall in cholesterol during treatment was highly significant in comparison with the period before and after therapy, whereas the changes in the triglycerides were not significant. Only one patient had an increase in the frequency of angina pectoris attacks; another showed temporary restlessness and slies, were not observed. Red and white cell counts, differential blood count, thrombocytes, the transaminases SGOT, SGPT, alkaline phosphatase, bilirubin, urinalysis and erythrocyte sedimentation rate did not change during treatment. There was no lasting increase in pulse rate in any patient and no significant changes in systolic-diastolic blood pressure. ECG showed no rhythm disorders nor any other changes which were not present before treatment was initiated.
Atherosclerosis
PMID:Reduction of serum lipids by means of etiroxate (Liponorm). 121 78

Conventional risk factors predict only about 30-50% of incidental cases in cardiovascular diseases, which are still the leading cause of death in western societies. During the last decade, the importance of thrombosis as an essential mechanism in acute myocardial infarction (AMI) and stroke has been established. The introduction of thrombolysis has led to an impressive reduction in AMI case fatality and possibly also to a substantial amelioration of its prognosis. Evidence from experimental, clinical and epidemiological studies suggest, that several hemostatic and hemorheological factors (e.g., fibrinogen, Factor VII, plasma viscosity, hematocrit, red blood cell aggregation, total white cell count) might not only play an important role in the evolution of acute thrombotic events, but may also take part in the pathophysiology of atherosclerosis. An increasing number of studies reports altered hemostatic and hemorheological parameters to be associated with smoking, hyperlipoproteinemia, and high blood pressure, as well as with adverse dietary habits and other life-style factors. To date, their way of interaction with the atherosclerotic process is poorly understood. Hemorheological or hemostatic mechanisms that might promote thromboatherogenesis include the predisposition to thrombosis via a hypercoagulable state, the enhancement of atherosclerosis by fibrinogen and its metabolites, and finally the reduction of blood flow through various rheological effects (e.g., increase in plasma viscosity and red cell aggregation, or leukocyte activation). Future research should focus in more detail on the interrelationship between accepted risk factors and the hemostatic system as well as hemorheological parameters. Deeper insight into the mechanisms involved might lead to new preventive strategies as well as to therapeutic procedures in the management of atherosclerosis and associated thrombotic events.
Atherosclerosis 1992 Jun
PMID:The possible role of hemorheology in atherothrombogenesis. 163 76

The review examines the effects of smoking on blood parameters, concentrating on those seen as responses or reactions to the insult of smoking, and finds evidence that smoking causes chronic leucocytosis, macrocytosis and raised haematocrit, raised plasma fibrinogen concentration, reduction of the serum ratio of high to low density lipoprotein (HDL/LDL ratio), and platelet changes. Each of the changes resolved on "quitting", though for fibrinogen the evidence was indirect. Reports that elevations of the white cell count (WCC), and plasma fibrinogen and reduction of the HDL/LDL ratio each predict myocardial infarction, and that higher haematocrit increases the risk of cerebro-vascular incidents are reviewed, with reports of associations with other forms of arterial disease and COPD, and of their significance for the prognosis of established disease. After noting pathological mechanisms which implicate each of these factors, and platelets, in reactions likely to contribute to the development of atherosclerosis, infarction, arterial spasm, and/or lung damage, the author concludes that the evidence in man, backed up by experimental data, provides very strong support for the view that elevations of WCC, haematocrit, plasma fibrinogen and reduction of the HDL/LDL ratio represent (or are closely associated with) intermediate causal mechanisms through which smoking induces arterial disease and probably lung disease, and that experimental evidence indicates that platelet changes and macrocytosis also contribute. Differences in the extent of these responses to smoking could be valuable in differentiating the relative harmfulness of different types of cigarette (or of other inhaled pollutants) in terms of these diseases, and in predicting the susceptibility of individuals to these smoking-related diseases.
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PMID:Reactive changes in the blood of smokers and the development of arterial diseases and COPD, a review: evidence of associations between changes and subsequent disease with implications for the evaluation of harmful effects of cigarettes, and for susceptibility to the chronic effects of inhaled pollutants. 248 24

Hypercholesterolemia (HC = hypercholesterolemia or hypercholesterolemic) was produced in rabbits by feeding them diets supplemented with cholesterol and peanut oil. Platelet counts and volumes, white cell counts, reticulocyte counts, and hematocrits were determined at intervals for 8-12 weeks in blood from HC animals and controls on a normal rabbit diet. Microthrombocytosis was a consistent occurrence in the presence of HC, developing as early as 2 weeks into the diet. Microthrombocytosis was generally associated with normal platelet counts, but mild thrombocytosis occurred late in the diet at the time of the highest levels of serum cholesterol (greater than 1300 mg/dl). Platelets from HC rabbits were morphologically normal by transmission electron microscopy. Survivals of 51Cr-labeled platelets from HC and non-HC rabbits were measured in HC and non-HC recipients. The results identified an intrinsic defect in the ability of HC platelets to survive in the circulation. They also confirmed previous findings of an environmental defect in HC that causes shortened platelet survival.
Atherosclerosis 1988 Nov
PMID:Morphological and kinetic abnormalities of platelets in hypercholesterolemic rabbits. 321 78

Smokers differ in terms of blood rheology from non-smokers. Ex-smokers differ from smokers but not from non-smokers. When investigated while abstaining from nicotine for 8 weeks, chronic cigarette smokers show a gradual normalization of blood and plasma viscosities, haematocrit, blood cell filterability, plasma fibrinogen levels as well as total white cell count. Those smokers who did not manage to abstain, reveal no such changes. The findings suggest that haemorheological alterations caused by smoking are reversible. This might play a role in the reduction of cardiovascular risk and in the elevation of tissue perfusion.
Atherosclerosis 1987 Mar
PMID:Abstention from chronic cigarette smoking normalizes blood rheology. 359 64

Delayed skin hypersensitivity and serum immunoglobulins were studied in relation to the severity of ischemic heart disease in 18 male monozygotic and 13 male dizygotic twin pairs, aged 55-78 years. The twin pairs were selected from the Swedish Twin Registry. Low IgG was seen in patients with myocardial infarction and definitive angina pectoris. No correlation between skin anergy and the severity of ischemic heart disease was found. These findings may support the possibility that immunological mechanisms play a part in the pathogenesis of ischemic heart disease. Significant F-ratios for IgA and differential white cell count support a genetic determination of these variables.
Atherosclerosis 1980 Jun
PMID:Immunologic evaluation of patients with ischemic heart disease. Genetic determination and relation to disease. 699 92

15-Lipoxygenase (15-LO) catalyzes hydroperoxidation of fatty acids, a reaction of potential relevance to inflammation, membrane remodeling, and atherosclerosis. In human leukocytes, 15-lipoxygenation of arachidonic acid produces 15-(S)-hydroxyeicosatetraenoic acid and lipoxin A4, which suppress white cell chemotaxis, adherence, and activation, and antagonize proinflammatory leukotrienes. Interleukin (IL)-13, produced by T-helper subset 2 (TH-2) lymphocytes, specifically and potently induced 15-LO gene expression and enzyme activity in human monocytes. Among other TH-2 lymphokines, this induction of 15-LO is shared by IL-4 but not by IL-10. Interferon-gamma, a product of TH-1 lymphocytes, blocked IL-13-mediated induction of 15-LO. The induction of the anti-inflammatory 15-LO pathway by IL-13 reveals a new facet of IL-13 biology that supports its role as a cytokine with potential to down-regulate inflammatory pathways. The contrasting effects of interferon-gamma and IL-13 on 15-LO induction demonstrate mechanisms by which T-lymphocyte subsets may modulate macrophage/monocyte function in inflammation or atherosclerosis.
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PMID:Induction of 15-lipoxygenase by interleukin-13 in human blood monocytes. 796 80

Twelve patients with Type II diabetes mellitus, insufficiently controlled with oral hypoglycemic agents, were studied before, after 2 months, and after 4 months on insulin therapy. For comparison the same variables were also studied in 10 healthy subjects. From the start, in the diabetic group, the authors found alterations in the hemorheologic parameters indicated by increased values for whole blood viscosity, plasma viscosity, red cell transit time (RCTT), and decreased values for white cell initial relative filtration rate (IrFR). In hematologic parameters they found increased values for mean corpuscular volume (MCV), leukocyte count, counts of neutrophils and monocytes, and a decreased count of lymphocytes. They also found increased values in the lipid parameters P-triglycerides and Apo B/Apo A-I ratio, risk factors of coronary atherosclerosis. After 4 months of insulin treatment whole blood and plasma viscosity were still increased, but there was a partial improvement of lipoprotein abnormalities. Red and white cell filterability, however, tended to normalize. These results indicate that changes in blood cell filterability do not necessarily influence in vitro measurements of blood viscosity. The change in RCTT during the insulin treatment was associated with a decreased MCV and the change in white cell IrFR with a decrease in the number of monocytes. This change of white cell filterability during insulin therapy, probably due to a reduced number of monocytes, may be of interest in the study of atherosclerosis and circulatory disease in diabetics.
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PMID:Reduced number of circulating monocytes after institution of insulin therapy--relevance for development of atherosclerosis in diabetics? 963 87

This paper evaluates the current information on the relationship between oral disease (specifically periodontitis) and atherosclerosis/coronary heart disease (CHD) to determine whether the information is sufficient to conclude that periodontitis is a risk factor for atherosclerosis/CHD. As background for this evaluation, the term "risk factor" is defined, and the 3 criteria used to establish exposures as risk factors are reviewed. In addition, epidemiologic criteria for defining an exposure as causal are presented. The available evidence then is evaluated according to the criteria for causality, which are extensions of the criteria for establishing a risk factor. This review is done in the context of the relationship between atherosclerosis/CHD and inflammation. A number of findings are briefly reviewed that link inflammation and atherosclerosis/CHD, such as: 1) prior flu-like symptoms were more common in cases of myocardial infarction than in concurrently sampled controls; 2) high levels of cytomegalovirus antibody titers were associated with elevated carotid intimal-medial wall thickness 18 years later; 3) prior infection with cytomegalovirus was a strong independent risk factor for restenosis after coronary atherectomy; 4) dental infections were more common in cases of cerebral infarction compared to community controls matched on age and sex; and 5) the gingival index was significantly correlated with fibrinogen and white cell counts in periodontal patients and controls, adjusted for age, smoking, and socioeconomic status. Three case-control studies and 5 longitudinal studies investigating the relationship between dental conditions and atherosclerosis/CHD are reviewed in terms of strength of associations, consistency of associations, specificity. of associations, time sequence between exposure and outcome, and degree of exposure and outcome. Related to the last criterion, new findings are presented which indicate that the extent of the periodontal infection, a measure reflecting microbial burden, also is related to onset of new CHD events. Our previously published model describing the potential biological mechanisms underlying the associations found is reviewed. This model places the associations into a context of an intrinsic or acquired hyperinflammatory monocyte trait that results in a more intense inflammatory response to lipopolysaccharide (LPS) challenges, such as periodontal infections. This hyperinflammatory response may promote atheroma formation and thromboembolic events. finally, new findings from ongoing animal studies are presented, indicating that high fat diets in atherosclerotic-susceptible mice induce greater inflammatory responses to Porphyromonas gingivalis challenges. We conclude that the available evidence does allow an interpretation of periodontitis being a risk factor for atherosclerosis/CHD. This conclusion, however. is made with some qualifications. While the associations found across a wide variety of subjects are remarkably consistent, for the most part they are represented by incidence odds ratios around 2.0. While this level of association would result in oral conditions contributing to a large number of CHD cases, it is possible that associations of this magnitude are due to bias in the study designs. In addition, some studies report that periodontitis is associated with all-cause mortality and low birth weight infants. These multiple associations detract from the credibility of periodontitis as a risk factor, as specificity of association is more often related to causality. However, all-cause mortality may largely be driven by mortality from cardiovascular events: and some exposures, such as smoking. are indeed risk factors for multiple conditions. On the other hand, current findings regarding the associations between oral conditions and atherosclerosis/CHD imply that the criteria for causality may be met in the not-too-distant future.
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PMID:Periodontitis: a risk factor for coronary heart disease? 972 97

In the Type 1 diabetes population, coronary heart disease (CHD) and lower-extremity arterial disease (LEAD) are the two common macrovascular complications leading to early mortality and morbidity. However, it is not clear if these two complications share the same risk factors. The Pittsburgh Epidemiology of Diabetes Complications (EDC) Study prospectively examined and compared the risk factors for LEAD and CHD (including CHD morbidity and mortality). EDC subjects (332 men and 325 women), all diagnosed at Children's Hospital of Pittsburgh between 1950 and 1980, were first examined at baseline (1986-1988), and then biennially, for diabetes complications and their risk factors. Data used in the current analysis were from the first 6 years of follow-up, 98% provided at least some follow-up data for these analyses. CHD was defined as the presence of angina (diagnosed by the EDC examining physician) or a history of confirmed myocardial infarction or CHD death. An ankle-to-arm ratio of less than 0.9 at rest was considered to be evidence of LEAD. Among 635 subjects without CHD at baseline, 57 developed CHD (1.69/100 person-years), and among 579 without LEAD at baseline, 70 developed LEAD (2.31/100 person-years). CHD incidence rate was slightly higher in males, while LEAD incidence rate was slightly higher in females. Compared to non-incident cases, subjects who developed either complication were older, had a longer diabetes duration, higher LDL and total cholesterol, and were more likely to be hypertensive. In multivariate analyses, hypertension, low HDL cholesterol level, high white cell count, depression, and nephropathy were the independent risk factors for CHD (including morbidity and mortality). For LEAD, higher HbA1 level, higher LDL cholesterol level and smoking were the important contributing factors. In conclusion, the risk factor patterns differ between the two vascular complications. Glycemic control does not predict CHD overall but does predict LEAD, while hypertension and inflammatory markers are more closely related to CHD than to LEAD.
Atherosclerosis 2000 Jan
PMID:Are predictors of coronary heart disease and lower-extremity arterial disease in type 1 diabetes the same? A prospective study. 1058 Jan 82


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