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Query: UMLS:C0042373 (vascular disease)
17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The prevention of cardiovascular disease has up till now generally been limited to control of the classical risk factors. The primary problem of the risk factor model is, that although a statistically verified relationship exists between risk factors and vascular disease, an individual prognosis is presently impossible. Surveys that show a relation between risk factors and impaired blood fluidity support the conception that a change in blood fluidity could be considered an early detection screening of vascular diseases. Prospective studies have shown that the hematocrit is related to circulatory disturbances. The main aim of the present study was to determine the clinical relevance of rheological parameters (hematocrit, plasma viscosity, erythrocyte rigidity, thrombocyte aggregation, erythrocyte aggregation), and the importance of altered blood fluidity as a predictor of manifest cerebral, cardiac or peripheral vascular disturbance.
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PMID:[Predictor function of hemorheologic parameters with reference to the incidence of manifest circulatory disorders: Concept of the Aachen study]. 376 16

This review of atherosclerotic risk factors in cardiovascular disease concentrates on those aspects of lipid and carbohydrate metabolism that may be associated with atherogenesis and that may be altered by ingestion of oral contraceptive (OC) agents. Atherogenesis is facilitated by 1 or more of at least 3 conditions: elevated low-density lipoprotein (LDL) levels, elevated intermediate-density lipoprotein (IDL) levels (which are remnants of very-low-density lipoprotein level catabolism), and increased quantities of the breakdown products of chylomicron metabolism (chylomicron remnants) and decreased high-density lipoprotein (HDL) levels. Over the year, considerable evidence has linked atherosclerosis, particularly that occurring in the coronary vessels, to elevated levels of both dietary and blood cholesterol. Since LDL is the major carrier of cholesterol in the plasma, it comes as no surprise that there is a strong relationship between elevated plasma LDL levels and coronary vascular disease. Low levels of HDL also are predictive of coronary vascular disease. Moreover, low HDL levels are increasingly associated with atherosclerosis in the cerebral and peripheral blood vessels, while total and LDL cholesterol levels are not as predictive of such disease. It has been reasonably well established that lipid abnormalities are associated with atherogenesis in the laboratory and with clinical vascular disease in patients. It has been more difficult to demonstrate that atherosclerosis can be prevented or reversed by treatment of such disorders. Yet, considerable evidence supports that point of view. Many questions remain concerning the relationship of atherogenesis and abnormalities of lipoprotein metabolism. The relationship between diabetes and atherosclerosis is even less well understood. There is little question that diabetics are at increased risk of developing atherosclerosis. In fact, atherosclerosis may be more prominent in diabetic women. Regarding OCs, several general points need to be made before discussing the effects of OCs on atherosclerotic risk factors: OCs may have effects on other metabolic parameters that have not been identified as prominent risk facts in atherogenesis; in some cases OCs appear to enhance the effects of other risk factors in ways that are not totally understood; and OCs may profoundly affect the metabolism of lipoproteins and glucose in ways that enhance atherogenesis. Women who use OCs must be carefully counseled about the interplay of such agents and other atherosclerotic risk factors. The decision to place a woman with 1 or more prominent atherosclerotic risk factors on OCs should be a careful one. Risk factors, particularly levels of total and HDL cholesterol, blood glucose, blood pressure, and smoking status, should be ascertained before prescribing OCs, particularly in women with family histories of heart disease.
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PMID:Atherosclerotic risk factors in cardiovascular disease. 377 10

The mortality rate from cardiovascular diseases was analysed for Italy as a whole and for individual regions in a sample year (1975). A distinction was made between cardiac and vascular diseases in order to assess the real incidence of the latter. The absolute number of deaths, the percentage mortality and the specific mortality quotient were studied. Deaths were also divided into age groups. Cardiovascular diseases were found to be the primary cause of death, circulatory disease the second. Among the latter, diseases of the encephalic circulation took first place. The same parameters were applied to the 1965-1983 period. Mortality due to cardiovascular disease remained constant over the period since the decrease in deaths from cardiac conditions was offset by an increase in those due to vascular disease in the strict sense. Finally the specific standardised mortality quotients per age and sex were considered in the 1970-1979 period. Mortality trends in Italy and in the individual regions were identical to those described using non-standardised indices.
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PMID:[Epidemiology of vascular diseases in Italy]. 380 82

The quantitative analyses of the concentration and composition of main plasma lipoprotein fractions in diabetic patients have so far not revealed such abnormalities that they could explain any major part of the excess atherosclerotic vascular disease present in both insulin-dependent and noninsulin-dependent diabetes. In insulin-treated patients the characteristic lipoprotein profile with low VLDL, normal LDL and elevated HDL levels prevents atherosclerosis rather than promotes it. However, the pattern will change to more atherogenic direction in the presence of either poor diabetic control or obesity or renal disease. It is possible that the patients who develop manifest clinical cardiovascular disease are in fact derived from these subcategories. In noninsulin-dependent diabetic patients the most common lipoprotein abnormality is an increase of VLDL and of total triglyceride, neither of which are currently held as strong risk factors. HDL is often at low side and may contribute to atherosclerosis, but may also represent a special hypercatabolic form of hypo-HDL-emia which is less atherogenic than the usual HDL deficiency.
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PMID:Are plasma lipoproteins responsible for the excess atherosclerosis in diabetes? 386 24

The relationship between parental history of vascular disease (heart attack, stroke, diabetes mellitus, and hypertension) and risk factor variables for cardiovascular disease was assessed in 3,312 offspring aged 5-17 years during the 1981-1982 school year in the biracial community of Bogalusa, Louisiana. Risk factors studied included systolic blood pressure, diastolic blood pressure, serum total cholesterol, triglycerides, and individual lipoprotein cholesterol (beta-, low density lipoprotein (LDL) cholesterol; pre-beta, very low density lipoprotein (VLDL) cholesterol; and alpha-, high density lipoprotein (HDL) cholesterol). Risk factors were adjusted for age, race, sex, and height (blood pressure only) prior to testing parental history effects. Univariate comparisons between risk factors in children and vascular disease in parents resulted in statistically significant increases in systolic and diastolic pressures associated with the presence of maternal or paternal hypertension (p less than 0.001). Paternal heart attack was also associated with elevations in diastolic pressure (p less than 0.01) of children. Maternal diabetes mellitus was associated with an increase in serum total cholesterol (p less than 0.05). Paternal diabetes mellitus and maternal heart attack (for female progeny only) were associated with increases in mean triglyceride levels of children. VLDL cholesterol results were similar to those for triglycerides. For HDL cholesterol, paternal diabetes mellitus was associated with a small decrease in mean levels (p less than 0.05). Dramatic increases to the highest decile of risk were found in association with the following parental disease combinations: paternal heart attack-paternal diabetes for serum total cholesterol (p less than 0.0001), maternal heart attack-paternal diabetes (p less than 0.001) and paternal stroke-maternal diabetes (p less than 0.0001) for LDL cholesterol. Multivariate analysis detected no significant effects of single parental vascular disease. However, paternal heart attack in combination with either diabetes mellitus or hypertension was statistically significant in their relationship to the risk factors overall.
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PMID:The relationship between parental history of vascular disease and cardiovascular disease risk factors in children: the Bogalusa Heart Study. 387 62

Diabetes mellitus affects almost 5.5 million Americans each year. An estimated additional 5 million individuals may have diabetes, but remain undetected. Individuals with diabetes are at high risk for the development of micro- and macrovascular disease, diabetic coma and adverse outcome of pregnancy. The rate at which these complications develop are now partially identifiable for the United States. For 5 potentially preventable complications (retinopathy, adverse outcome of pregnancy, vascular disease, nephropathy and diabetic coma) the morbidity and mortality rates can now be calculated. There exist 50,000 cases of blindness due to diabetes with an additional 5800 new cases each year. Adverse outcome of diabetic pregnancy occurs in over 18,000 births each year, with as many as 4500 related perinatal deaths. Each year 40,000 diabetics are required to have a lower extremity amputation. Of the already 70,000 diabetics who have had an amputation, 25,000 will die this year. End stage renal disease affects 4000 diabetics each year. During the same time period, of the 7500 existing cases of end stage renal disease, 2000 will result in mortality cases. Diabetic coma (DKA and HHNK) accounts for 67,400 hospitalizations and results in 3600 deaths each year. Together these complications and those associated with cardiovascular disease account for 323,000 deaths with diabetes as the underlying or contributing cause in the United States.
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PMID:An epidemiological model for diabetes mellitus in the United States: five major complications. 393 16

Twenty seven patients were operated on by perineo-sacral route for anal or rectal cancer. This technique used between 1965-1982 at the Institut Curie was selected because the patients were very old and/or presented with major visceral disease, where the abdomino-perineal resection was not indicated. There was no post-operative death. The margin were free of disease in every patients. 6/27 died within the 6 post-operative months mainly from cardiovascular disease. While most patients were irradiated pre operatively perineal healing was obtained within 6 months in 18/21 cases. 5 patients died of cancer during the two years following surgery. 16/21 are NED with a follow up 1-12 years. Perineo-sacral route is a good alternative from APR in old patients with cardio-vascular disease.
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PMID:[Amputation of the rectum by the perineosacral approach for anorectal cancer. Indications, results. Apropos of 27 cases]. 408 22

Relative rates of proportionate mortality from cancer of six sites based on total cancer deaths and the proportions expected in all towns, and from four types of cardiovascular disease based on total deaths from all causes, have been related in the 80 county boroughs of England and Wales to the sources of water supply and to the average hardness of water in the towns. The sources of water, from upland surfaces, artesian wells and rivers, were classified in eight groups, and significant associations were found for cancers of the stomach, oesophagus, prostate, male bladder and female breast, and for hypertensive and chronic rheumatic heart disease. No associations were apparent with intestinal cancer, vascular disease of the nervous system or arteriosclerotic heart disease. Hardness or softness of the water was classified in seven groups and significant associations were found for the same diseases as for source of water, none being evident for coronary disease.
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PMID:Mortality from cancer and cardiovascular diseases in the county boroughs of England and Wales classified according to the sources and hardness of their water supplies, 1958-1967. 451 76

The scientific basis for the statement that cigarette smoking increases the risk of serious cardiovascular side effects from oral contraceptive (OC) use is reviewed. The published literature and the new statistical analyses of the data are examined. Attention is directed to 3 broad categories of relevant vascular disease--deep vein thrombosis and pulmonary embolism, stroke--both occlusive and hemorrhagic, and ischemic heart disease. Within each category, the epidemiologic relationship of cigarette smoking alone, of OC use, and of a combination of the 2 is addressed. This review of smoking and OC use as risk factors for major classes of cardiovascular disease reveals little convincing evidence for an interaction of the smoking and OC use. Essentially all of the data have been interpreted to indicate that OC use is a risk factor for cardiovascular disorders derive from retrospective case-control studies, which continue to be a subject of controversy. The role of smoking as a risk factor appears to be little questioned in the case of myocardial infarction, and the evidence suggests that it may also be a factor in hemorrhagic stroke. There is little evidence to implicate smoking in the pathogenesis of thrombotic stroke in young women, and several publications suggest that it has a protective effect for deep vein thrombosis. In sum, evidence for an interaction of smoking and OC use has been reported but is deemed to be weak. A major existing difficulty is the methodological problems that are inherent in epidemiologic investigations, both retrospective and prospective. While conservatism could thus withhold needed and effective contraception, the recommendation is for the OC user to forego smoking.
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PMID:Smoking, oral contraceptives, and thromboembolic disease. 612 53

The recent introduction of the determinations of platelet factor 4 (PF4) and beta-thromboglobulin (beta TG) by radioimmunoassay provided a new tool to obtain knowledge of in vivo platelet activation. We evaluated the plasma level of PF4 and beta TG in 14 normal subjects (mean PF4 7.7 ng/ml; beta TG 28.8 ng/ml), in 29 patients with chronic stable cardiovascular disorders (mean PF4 9.8 ng/ml; beta TG 32.6 ng/ml) and in 15 diabetics with vascular disease (mean PF4 14.5 ng/ml; beta TG 41.8 ng/ml). The great majority had normal values and no statistical differences were noted among the three groups (p greater than 0.05). Fifteen days of treatment with 150 mg daily of dipyridamole produced a significant reduction in the levels of both proteins (p less than 0.01), in contrast of the daily administration of 650 mg of aspirin, which failed to produce any significant change (p greater than 0.5). The patients and the normal subjects were also administered 3,000 USP units intravenously of porcine heparin. The values of the heparin released-platelet factor 4 (HR-PF4), evaluated 5 minutes after the injection, showed a good correlation between platelet concentration and HR-PF4 levels (z = 2.37, p less than 0.02) in the patients. The determination of standard residual following linear regression analysis of HR-PF4 indicated the presence of two distinct patient populations. One group, including the vast majority of patients, did not differ from the control (patients mean HR-PF4 111.1 ng/ml; controls: mean HF-PF4 136 ng/ml). The other group, with severe cardiovascular disease, but with normal levels of PF4 and beta TG in almost all patients and similar platelet concentrations, showed a significantly higher HR-PF4 (219 ng/ml). Neither aspirin nor dipyridamole had any effect on the level of HR-PF4. This HR-PF4 could represent a possible marker of the interaction of platelets with a seriously damaged atherosclerotic vessel wall.
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PMID:Platelet factor 4 (PF4) and heparin-released platelet factor 4 (HR-PF4) in patients with cardiovascular disorders. 622 5


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