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

Researchers have found that oral contraceptives (OCs) change carbohydrate and lipoprotein metabolism and these changes are like those linked with increased risk of cardiovascular (CV) disease, especially myocardial infarction and stroke. Since CV disease is the major cause of death in US women, it is important that OCs not induce changes in carbohydrate and lipoprotein metabolism. A new progestin, norgestimate, has an advantage over other progestins in that it tends not to induce male traits. This is beneficial because androgenicity is related to atherosclerosis which increases the risk of myocardial infarction. Further studies show that the new combined OC (250 mcg norgestimate/35 mcg ethinyl estradiol) does not influence serum glucose tolerance levels. It also does not affect the physiologic regulating system of prostacyclin, the inhibitor of platelet aggregation, by high density lipoprotein (HDL). In addition, it increases prostacyclin metabolites and HDL which may indeed decrease the risk of occlusive thrombotic vascular diseases. Moreover a study in Germany demonstrates that it causes no changes in fibrinopeptide A,m the anticoagulation factors antithrombin III and protein C, or coagulation promoting factors fibrinogen, factor VII, and the components of VIII. In women, it is absorbed well and metabolized extensively before the body eliminates it. Moreover this new combined OC has an overall Pearl index of 0.25. Studies to data indicate that norgestimate/ethinyl estradiol may be more advantageous than other OC formulations. Yet only long term epidemiologic studies can determine if it can indeed decrease the risk of CV diseases linked with older OCs.
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PMID:Norgestimate: a clinical overview of a new progestin. 160 87

In this paper are reported the basal results of a multidisciplinary, multicenter study designed to explore in a population with ischemic disease the relation between hemostatic variables, conventional risk factors and atherothrombotic sequelae. 953 patients less than or equal to 69 yrs with documented coronary, cerebral or peripheral atherosclerotic disease were studied and followed-up for 24 months. Examinations included hemostatic and lipid laboratory assays, arterial Doppler examination, cerebral computerized tomography and nuclear magnetic resonance, exercise electrocardiogram and coronary angiography. Fibrinogen (301.4 +/- 71.52 mg/dl) correlated positively with antithrombin III (r = 0.27) and leukocytes (r = 0.25), negatively with HDL-cholesterol (r = 0.18) and tended to increase with smoking. Heavy smokers had higher leukocyte counts than non-smokers (8.0 +/- 2.0 vs. 7.2 +/- 2.1 x 10(3)/microliters), higher triglycerides (1.87 +/- 1.12 vs. 1.53 +/- 1.35 mmol/l) and lower HDL-cholesterol (0.93 +/- 0.27 vs. 1.00 +/- 0.25 mmol/l). FVII correlated positively with triglycerides (r = 0.16) and protein C (r = 0.45). vWF:Ag (145.4 +/- 70.58%) ad FVII:C (139.7 +/- 59.10%) were positively correlated (r = 0.44). FVIII:C correlated positively with fibrinogen (r = 0.21). Myocardial infarction survivors with associated cerebral and peripheral vascular lesions had higher FVIII:C, FVII, fibronogen and vWF:Ag. These findings suggest that hemostatic factors may enhance and/or mediate the effects of conventional risk factors in atherothrombotic ischemic events.
Atherosclerosis 1991 Oct
PMID:The PLAT Study: a multidisciplinary study of hemostatic function and conventional risk factors in vascular disease patients. 159 Aug 30

The influence of coffee and caffeine consumption on hemostatic factors was studied in 2 randomized trials. Both studies were conducted in young, healthy adults. In the first study, 107 participants were randomly allocated to one or 3 intervention groups, drinking filtered coffee, boiled coffee or no coffee at all, respectively, for a period of 9 weeks. In the second study, 69 subjects received either 4-6 tablets containing 75 mg caffeine or the same amount of placebo tablets, while using decaffeinated coffee. In this double-blind study caffeine intake from any other source was not allowed. Blood samples for hemostatic factors were obtained at baseline and after 9 weeks of intervention. The findings indicate no effect of coffee consumption on fibrinogen, clotting factor VII activity, factor VIII antigen, protein C and protein S and also no effect of caffeine consumption on fibrinogen and factor VII activity.
Atherosclerosis 1990 Aug
PMID:Coffee, caffeine and hemostasis: results from two randomized studies. 214 67

Metabolic and hemostatic effects of 2 low dose oral contraceptives (OCs), a triphasic (ethinylestradiol + (-)-norgestrel) and a monophasic (ethinylestradiol + desogestrel) preparation, were compared in a cross-over trial in fertile women over 35 years of age. Both combinations moderately affected plasma lipids, with 17-24% increases of total triglyceridemia. Triglycerides accumulate in low density lipoproteins, thus suggesting the possible formation of an atherogenic lipoprotein particle. Only the monophasic preparation increased high density lipoprotein (HDL)-cholesterol levels significantly, with a rise in HDL3 mass and cholesterol. OC treatment led to slight changes in HDL2 and HDL3 structure, with a rise of the cholesteryl ester and triglyceride contents, indicative of a stimulated cholesterol esterification and reverse transport. Changes in the hemostatic indexes (fibrinogen, antithrombin III and protein C) were negligible. The new low dose OCs, even when prescribed to relatively older women, affect to a relatively small extent lipid/lipoprotein metabolism, with the exception of changes in the low density lipoprotein composition.
Atherosclerosis 1990 Oct
PMID:Comparison of the lipoprotein and hemostatic changes after a triphasic and a monophasic low dose oral contraceptive in premenopausal middle-aged women. 214 69

Elevated blood levels of homocysteine are associated with atherosclerosis and thrombotic disease. We previously reported that treatment of cultured endothelial cells with homocysteine increased endogenous factor V activity by activation of the cofactor. Because endothelial cell-associated factor Va would be regulated by the protein C mechanism, the ability of homocysteine-treated arterial and venous endothelial cells to activate protein C was investigated. Both arterial and venous endothelial cells activated protein C; 0.6 mmol/L homocysteine reduced endothelial cell protein C activation by 12%. Maximal inhibition (90%) of protein C activation occurred with 7.5 to 10 mmol/L homocysteine after 6 to 9 hours of incubation. Metabolism of homocysteine was not accelerated by cultured endothelial cells. Investigation of the mechanism(s) by which homocysteine reduced protein C activation indicated that the metabolite did not induce an inhibitor to activated protein C, but in low concentrations acted as a competitive inhibitor to thrombin. These data suggest that perturbation of the vascular endothelial cell protein C mechanism by homocysteine may contribute to the thrombotic tendency seen in patients with elevated blood levels of this metabolite.
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PMID:Homocysteine, an atherogenic stimulus, reduces protein C activation by arterial and venous endothelial cells. 215 69

Latent infection of vascular cells with herpes-viruses may play a pathogenic role in the development of human atherosclerosis. In a previous study, we found that cultured human umbilical vein endothelial cells (HUVECs) infected with herpes simplex virus 1 (HSV-1) became procoagulant, exemplified both by their enhanced assembly of the prothrombinase complex and by their inability to reduce adhesion of platelets. We now report two further procoagulant consequences of endothelial HSV infection: loss of surface thrombomodulin (TM) activity and induction of synthesis of tissue factor. Within 4 hr of infection of HUVECs, TM activity measured by thrombin-dependent protein C activation declined 21 +/- 3% (P less than 0.05) and by 18 hr, 48 +/- 5% (P less than 0.001). Similar significant TM decrements accompanied infection of bovine aortic endothelial cells. Identical TM loss was induced with HSV-2 infection but not with adenovirus infection. Decreased surface expression of TM antigen (measured by the specific binding of a polyclonal antibody to bovine TM) closely paralleled the loss of TM activity. As examined by Northern blotting, these losses apparently reflected rapid onset (within 4 hr of HSV infection) loss of mRNA for TM. In contrast, HSV infection induced a viral-dose-dependent increase in synthesis of tissue factor protein, adding to the procoagulant state. The results indicate that loss of endothelial protein-synthetic capacity is not a universal effect of HSV infection. We suggest that the procoagulant state induced by reduction in TM activity and amplified tissue factor activity accompanying HSV infection of endothelium could contribute to deposition of thrombi on atherosclerotic plaques and to the "coagulant-necrosis" state that characterizes HSV-infected mucocutaneous lesions.
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PMID:Infection of vascular endothelial cells with herpes simplex virus enhances tissue factor activity and reduces thrombomodulin expression. 216 19

The levels of plasminogen activator inhibitor (PAI), protein C (pC), total cholesterol (TC), high and low density lipoprotein cholesterols (HDLC and LDLC), apolipoproteins A1 (apoA1) and B (apoB) were measured in 45 patients with coronary heart disease angiographically documented and 10 healthy subjects without coronary heart disease and coronary atherosclerosis as evidenced by coronary angiography and provocative tests. Twenty three patients had primary angina (PA) with a duration of less than 3 months, twenty two patients presented with chronic coronary heart disease (CCHD) with a duration of more than 4 months. In general, a negative correlation between PAI and HDLC levels in the patients under study (r = -0.413; p = 0.02), it was higher in PA (r = -0.687; p = 0.02), but disappeared in CCHD (r = 0.027). The content of PAI correlated with the cholesterol index (r = 0.654; p less than 0.001 in the whole group), more greatly in PA (r = 0.865; p = 0.001) than in CCHD (r = 0.506, NS). There was a good correlation between the levels of pC and apoB in the whole group (r = 0.606; p less than 0.001) and in PA (r = 0.662; p = 0.001), but not in CCHD (r = 0.288, NS). The content of pC also correlated with a apoB/apoA1 ratio (r = 0.445; p = 0.002 in the whole group of patients). This correlation was significantly positive in PA (r = 0.455; p = 0.044), but not in CCHD (r = 0.022). Thus, higher levels of PAI coincided with atherogenic changes in those of HDLC, and an increase in the content of pC was in agreement with that of apoB. The interrelationships are particularly typical of early stages of CHD.
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PMID:[Plasminogen activator inhibitor and protein C: their relation to plasma lipids and lipo- and apoproteins in ischemic heart disease of different duration]. 239 63

In order to carry out a multicenter study aimed at understanding the association of hemostatic factors with atherosclerotic vascular disorders for the Atherosclerosis Risk In Communities (ARIC) Study, we compared a blood collection and processing system developed in our laboratory with the state-of-the-art-procedures. The salient features of our system included the use of a new phlebotomy set for venipuncture, the use of Millipore filters for removing platelet residues in the plasma and the use of a mixture of anticoagulants and antiplatelet agents for inhibiting the in vitro activation of platelets, coagulation and fibrinolytic system. The results derived from systematic evaluations indicate that this newly developed system yields the lowest values of plasma beta TG, PF 4 and FPA when compared with the reported values. The technique also gave reliable values of representative hemostatic measurements such as fibrinogen, factor VII, factor VIII, von Willebrand factor, antithrombin-III, protein C, tissue-type plasminogen activator, and serum thromboxane B2. Further experiments revealed that the samples withstood temporary storage at -70 degrees C and overnight "shipping" manipulations without significant changes in the hemostatic values. We conclude that the described blood collection and processing system may be a valuable asset for conducting multicenter cooperative clinical trials and epidemiologic studies involving blood collection by multiple field centers or clinics.
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PMID:ARIC hemostasis study--I. Development of a blood collection and processing system suitable for multicenter hemostatic studies. 252 84

We report a study of 61 cases of retinal vein occlusion, followed for 3-10 years. The oedematous form only were studied; 39 were branch vein occlusion (BVO) and 22 central retinal vein occlusion (CRVO). Of the CRVO's 5 were female, 17 were male, ages ranged from 5 to 75 years, averaging 58 years of the BVO's there were 19 females and 20 males with ages ranging from 27 to 79 years, averaging 61 years. High blood pressure and atherosclerosis were the most frequent causes. High intraocular pressures were mostly associated with CRVO (25%). Study of serum lipids and blood coagulation are most useful in CRVO in young patients. Platelet agreggation anomalies, protein C deficiency were seen in some cases. Visual prognosis is relatively good; bilateralisation was seen in 5% of BVO and in 9% of CRVO. Visual acuity better than 20/200 was observed in 87% of BVO and in 75% of CRVO.
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PMID:[Long-term follow-up and etiologic factors in edematous forms of central retinal vein obstruction]. 262 8

Significant advances have been made in our understanding of the role of the vascular endothelium in preventing thrombosis and in decreasing vascular spasm. The endothelium provides a surface receptor, thrombomodulin, that binds thrombin. In this form, thrombin loses its ability to clot fibrinogen or to aggregate platelets, but is able to activate protein C. In its activated state, protein C is able to act as an inhibitor of coagulation by virtue of its proteolytic destruction of Factors Va and VIIIa. Congenital deficiency of protein C is associated with early and recurrent thrombosis. The discovery that the endothelium is responsible for the production of a short-acting inhibitor of smooth-muscle contraction (EDRF) was a remarkable advance. One of the EDRF substances has been demonstrated to be NO, which has inhibitory effects on both smooth muscle and blood platelets. Activity of EDRF appears to be diminished or lost as a consequence of atherosclerosis, and stimuli that cause vasodilation via the EDRF pathway in normal vessels cause vasoconstriction in atherosclerotic arteries. Regression of atherosclerosis in experimental animals appears to be associated with restoration of EDRF activity.
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PMID:The endothelium, platelets, and coronary vasospasm. 264 64


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