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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on the findings presented in this study, we propose the hypothesis that calcium could be a mediator for the development of atherosclerosis. Figure 8 shows a schematic illustration of the hypothesis. The presence of risk factors such as hypertension, hyperlipidemia, and smoking may increase the influx of calcium into vascular ECs. We have shown that reactive oxygen species, which are considered to be a risk factor for the development of atherosclerosis, actually increase [Ca++]i in vascular ECs. Increased intracellular calcium may damage the function of ECs, resulting in platelet aggregation at the damaged site. Increased intracellular calcium may also increase uptake of macromolecules in plasma such as fibrinogen and LDL, eventually forming atherosclerotic plaque. We have also shown that the influx of calcium into vascular ECs is associated with LDL transport across vascular ECs. The pretreatment by nifedipine inhibited both the increase in [Ca++]i and the increase in LDL transport, suggesting that intracellular calcium modulates LDL transport across ECs. Growth factors released from platelets may provoke migration and proliferation of medial SMCs in the aterial intima. It has been reported that migration of SMCs from arterial media to intima is enhanced by the presence of calcium, and can be inhibited by the pretreatment of calcium antagonist. As demonstrated in this study, calcium also plays an important role in the proliferation of SMCs provoked by some kinds of growth factors such as EGF. On the other hand, we found that an increased amount of dietary Mg suppressed the development of atherosclerotic lesions in the aorta of cholesterol-fed rabbits without affecting plasma total cholesterol and HDL-cholesterol concentrations. The mechanism of action might also be related to the calcium entry blocking action. The clinical and nutritional implications of these phenomena should be investigated further. The evidences presented in this study, however, would not be sufficient to fully explain the etiological role of calcium in atherogenesis. Further studies are required to elucidate the mechanism of the contribution of calcium to atherogenesis. The efficacy of calcium antagonist for the prevention of atherosclerosis in humans should also be investigated further.
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PMID:The role of calcium and magnesium in the development of atherosclerosis. Experimental and clinical evidence. 224 57

Changes in coagulative and fibrinolytic activities were studied in rats with hyperlipidemia induced by Triton WR-1339 (T-WR). After intravenous injection of T-WR (150, 200 or 300 mg/kg) into S.D. rats, dose-related increases in plasma lipids (total cholesterol, triglyceride, free cholesterol and phospholipid) were observed. In hyperlipidemic rats that received 300 mg/kg of T-WR, decreases in red blood cell count and Hb value were found. Significant increases in the ma value of the thromboelastogram and the fibrinogen level were observed in these T-WR treated rats. The alpha 2-plasmin inhibitor activity was found to decrease dose-relatedly. These results indicate that T-WR induced hyperlipidemia in rats is accompanied with an increase in coagulative activity and an indirect enhancement of fibrinolytic activity.
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PMID:Changes in coagulative and fibrinolytic activities in Triton WR-1339-induced hyperlipidemia in rats. 231 41

Vascular risk, mainly thromboembolitic risk, attributed to oral contraceptives (OCs) since 1962, has been primarily linked to ethinyl estradiol (EE). OCs which combine estrogen and have been associated with cerebral vascular accidents. A 1977 study showed a 40% increase of mortality due to cardiovascular complications in women taking OCs. There were of both an arterial and a venous character. The risk of myocardial infarction was 3 times more frequent among OC users. Deep venous thrombosis and pulmonary embolism were more numerous. Some other risk factors include smoking, hypertension, diabetes, and age 35. The risk of heart attack vanishes a few years after stopping OC use. The reduction of EE (and similarly progesterone) dosage from 100-50 mcg also lower the risk of hypertension, cerebral vascular accidents, and venous thrombosis. Prolonged use of OCs causes disorders of hemostasis affecting the walls of blood vessels, modifying the viscosity of blood flow (increase of hematocrits, reduction of venous tonus), modifying plasmatic coagulation (increase of platelets, increase of factors VII and X and plasma fibrinogen, and decrease of antithrombin III activity), and increased fibrinolysis. These anomalies are exclusively associated with high doses of estrogens. 5% of women using OCs develop moderate hypertension of 5-10 mm Hg of systolic pressure 5 years later, but after cessation it is reversed. OCs stimulate the renin-angiotensin-aldosterone system causing accelerated production of angiotensin II with the resultant forceful vasotension. 3 months after quitting OC use, high blood pressure returns to normal. EE can provoke diabetes; it increases very low density lipoprotein (VLDL) and high density lipoprotein (HDL) production, but total cholesterol is hardly affected. The androgenic property of progestogens reduces HDL. Combined OCs are contraindicated for women with hypertension, hyperlipidemia, diabetes, and a family history of vascular accidents.
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PMID:[Oral contraception and the vascular risk]. 251 20

Experimental and clinical researches were done for the purpose of that to treat the hyperlipemia with Dahuang Zhechong Wan (DHZCW). The patients of primary hyperlipemia were divided into two groups. One group was treated with DHZCW, the other with inositol nicotinate as control. DHZCW could reduce the serum total cholesterol (0.05 less than P less than 0.2), triglyceride (P less than 0.05), the blood viscosity (P less than 0.01), reductive viscosity (P less than 0.001) and fibrinogen (0.05 less than P less than 0.2). No significant change of the other item of hemorheology, HDL-c and the subfraction were observed. No significant differential effect between those two groups. The experimental hyperlipidemic model was made by feeding cholesterol and axungia on rabbits. The results showed that DHZCW could reduce the serum total cholesterol (P less than 0.05), triglyceride (P less than 0.05), beta-LP (P less than 0.01), the blood viscosity (P less than 0.05) and plasma viscosity (P less than 0.05), but no significant effect on HDL-c and its subfraction, ESR, index of erythrocytic deformation and hematocrit. DHZCW could change the viscosity of blood of hyperlipemia and reduce the total cholesterol, triglyceride and fibrinogen of the blood. It might have some beneficial effects on atherosclerosis and prevent ischemic cardiovascular and cerebrovascular diseases.
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PMID:[Experimental and clinical studies of the effect of dahuang zhechong wan on hyperlipemia]. 260 35

An evaluation of the hemorheologic parameters and an ultrasonographic study of the extracranial carotid tract were performed on 48 patients, age range: sixty to seventy-five years, affected by acute stroke, 23 of whom had hypertension, while 27 were smokers. None of them was suffering from hyperlipidemia, diabetes mellitus, or symptomatic coronary heart or peripheral artery disease. The echotomographic analysis, using B-mode real-time echotomography revealed atherosclerotic lesions in 26 patients. The hemorheologic pattern (hematocrit, fibrinogen, whole blood filterability, whole blood and plasma viscosity) was determined in all the patients three months after the clinical event. Statistical analysis of the results indicates a possible link between atherosclerotic lesions of the extracranial carotid tract and age, fibrinogen levels, and whole blood filterability.
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PMID:Correlation between hemorheologic parameters and carotid atherosclerosis in stroke. 265 May 79

Smoking is one of the three major cardiovascular risk factors, the other two being hyperlipidaemia and hypertension. Cardiovascular diseases contribute in Austria, as well as in other industrialized countries, more than 50% to total mortality. Unlike in other industrialized countries ischaemic heart diseases in Austria have an unfavourable mortality trend, with a substantial relative increase. The atherogenicity of smoking is partly caused by interaction with other risk factors, especially hyperlipidaemia, hypertension and a high fibrinogen level. 30% of the Austrian population are smokers. The percentage has increased over the past few years, especially in young women. Other cardiovascular risk factors are very common too and, hence, a large proportion of the Austrian population is at risk due to a combination of risk factors. Smoking and the use of oral contraceptives is associated with significant risk of both myocardial infarction and stroke. The Austrian trend of cigarette smoking among young women points to a substantial increase in the number of women at risk by this combination of risk factors. Strategies to control the smoking epidemic have been internationally tested. An integrated approach is set out in a document provided by the International Union Against Cancer (1983). In a country like Austria with a tobacco monopoly the conditions for implementing smoking control measures should theoretically be better than in other countries.
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PMID:[Smoking and atherosclerosis]. 268 75

Blood coagulation in a strain of rabbits designated as Watanabe heritable hyperlipidemic (WHHL) rabbits was examined. The activities of vitamin K-dependent clotting factors, contact factors and clotting factor VIII (F VIII) and the fibrinogen level were significantly higher in WHHL rabbits than in normolipidemic rabbits (all age groups). Values for vitamin K-dependent clotting factor were already higher at 2 months of age. Contact factors and fibrinogen levels increased age after 5 to 8 months. F VIII increased between 5 and 8 months and then decreased. At 2 months of age, WHHL rabbits were divided into two groups. Group A was fed standard rabbit chow and group B standard rabbit chow containing 1% probucol. Probucol prevented the progression of atherosclerosis in group B in the absence of a significant reduction in plasma cholesterol level. F VIII and fibrinogen levels were statistically decreased in all rabbits at all ages in group B (P less than 0.05). These differences in clotting factors between the two groups were most obvious at 8 months (P less than 0.02). We conclude that vitamin K-dependent clotting factors may increase with hyperlipemia and that increases in F VIII and fibrinogen may be closely related to the progression of thromboatherosclerosis.
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PMID:Hypercoagulable state in the Watanabe heritable hyperlipidemic rabbit, an animal model for the progression of atherosclerosis. Effect of probucol on coagulation. 274 87

Nephrotic syndrome characterized by hypoalbuminemia and hyperlipidemia is associated with an increased incidence of thromboembolism and increased platelet hyperaggregability. Although plasma coagulation proteins are also abnormal, changes are too inconsistent to attribute thromboembolic complications to the coagulation cascade alone. Antithrombin III (ATIII) has been shown to be deficient in nephrotic syndrome. There is, however, an increase in alpha 2 macroglobulin. It is clear that platelet to platelet interactions require exposure of platelet fibrinogen receptors, the binding of fibrinogen to these receptors, platelet crossbridging, and subsequent platelet aggregation. Fibrinogen is consistently elevated in nephrotic syndrome. Hyperlipidemia and hypoalbuminemia in nephrotic syndrome increases the availability of thromboxane A2 (TxA2) by increasing the availability of TxA2 precursors and the removal of TxA2 inhibitors. Thromboxane A2 is a known inducer of platelet aggregation probably through the exposure of platelet fibrinogen receptors. Recently, fibronectins a group of adhesive proteins, were implicated in platelet to platelet interactions. Since thrombin increases the expression of platelet surface fibronectin, fibronectin may be involved in thrombus formation in nephrotic syndrome. Thromboembolic formation in nephrotic syndrome is a composite mechanism involving the coagulation cascade, platelet-platelet interactions, and platelet-surface interactions.
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PMID:Nephrotic syndrome: a platelet hyperaggregability state. 293 Sep 39

The results are reported of a clinical and laboratory evaluation of the use of a random-access centrifugal analyzer linked to a personal computer in the management of the routine workload of a hemostasis laboratory. Over a three-month period, prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin clotting time (TCT), and derived fibrinogen (Fib) were performed on a total of 929 samples. Included in the study were 448 samples from patients receiving anticoagulants (oral anticoagulants, 228; heparin, 166; heparin and warfarin, 130) and 351 samples from patients requiring coagulation screens (PT, APTT, TCT, Fib). Tests were done in parallel with tilt-tube manual techniques and the results correlated. The correlation coefficients were PT, 0.99; TCT, 0.72; APTT, 0.96; Fib, 0.97. Discrepancies were analyzed and were due to hypofibrinogenemia and hyperlipidemia. The poorer correlation coefficient of TCT was attributable both to lower reproducibility of the manual test and the effect of dysfibrinogenemia or FDPs in liver disease. In no case was an abnormality or diagnosis missed using the centrifugal analyzer. In several cases the increased sensitivity of the analyzer improved the detection of the lupus anticoagulant. The use of automation was accompanied by a major reduction in workload and reagent costs. The machine has been used to assay a wide range of coagulation tests by clot based and chromogenic substrate methods. In conclusion, a programmed centrifugal analyzer is a safe, efficient, and flexible way of automating routine coagulation tests. It widens the reportoire of tests performed in the Hemostasis laboratory by using a machine capable of being used in other areas of pathology.
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PMID:Automation of routine coagulation testing using a random access centrifugal analyzer. 334 69

Blood coagulation and fibrinolysis in pregnancy with or without hyperlipidemia were studied. Blood samples were taken from 36 cases with early pregnancy, 59 cases with late pregnancy, and the relationship between the hemostatic changes and the concentrations of lipids was examined. The following results were obtained: 1. In early pregnancy, all cases were non-hyperlipidemic, but in 41% of late pregnancy cases, hyperlipidemia was found. 2. In late pregnancy without hyperlipidemia, shortening of prothrombin time and activated partial thromboplastin time, increases in platelet epinephrine, collagen aggregation, fibrinogen, and plasminogen, and a decrease in alpha 2-plasmin inhibitor were marked compared with those in early pregnancy without hyperlipidemia. 3. In late pregnancy with hyperlipidemia, the platelet count and fibrinogen were increased, and prothrombin and activated partial thromboplastin time were shortened compared with late pregnancy without hyperlipidemia. The platelet epinephrine aggregation was slightly decreased. Antithrombin III was increased and alpha 2-plasmin inhibitor was slightly decreased. 4. In the same subjects, the relationship between changes in blood coagulation and fibrinolysis in early and late pregnancies and total cholesterol was studied by the independent matched pair test. There were significant correlations (p less than 0.02, p less than 0.05) between activated partial thromboplastin time (r = -0.5998) and fibrinogen (r = 0.6230). From these results the author concluded that late pregnancy was a hypercoagulable state and this tendency was more obvious in late pregnancy with hyperlipidemia.
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PMID:[Hemostatic changes during pregnancy in reference to hyperlipidemia]. 339 35


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