Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thrombogenesis is increasingly recognised as an immediate cause of most major clinical episodes of ischaemic heart disease (IHD) and the haemostatic system makes a significant contribution to the development of atheroma. It is therefore important to consider how far concepts of increased thrombotic tendency and hypercoagulability can be demonstrated in reality. A number of general observations do suggest that characteristics of the circulating blood influence the course of events in IHD--for example, the occurrence of IHD or stroke in young women using oral contraceptives in whom advanced arterial wall changes are not a feature. Epidemiologically, the coagulation system has been more rewarding than the study of platelets. The Northwick Park Heart Study (NPHS) has demonstrated a strong relationship between the level of factor VII activity and the later incidence of IHD. Several biochemical characteristics of factor VII suggest that this relationship may well be one of cause and effect. There is growing evidence that high levels of factor VII activity lead to high levels of thrombin production. In addition to NPHS, three other prospective studies have shown an association between high levels of plasma fibrinogen and IHD incidence. Again, there are several reasons for believing that this association, too, is of pathogenetic significance. Dietary fat intake is a major determinant of the factor VII activity level, and smoking of the fibrinogen level. Hypercoagulability determining IHD is best defined, on present evidence, as over-activity of procoagulatory influences (whereas hypercoagulability leading to venous thrombosis is predominantly manifested as underactivity of natural defence mechanisms).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypercoagulability and ischaemic heart disease. 333 83

In five large-scale prospective studies the predictive value of hemostatic parameters indicating the occurrence of arterial thrombotic diseases has been estimated in healthy individuals. All the studies have consistently found a statistically significant association between hyperfibrinogenemia and arterial thrombotic diseases. In two studies, increased levels of factor VII were associated with an increased incidence of ischemic heart disease. The relationship between arterial occlusive diseases and plasma levels of fibrinogen or factor VII was closer than that for other well established risk factors such as plasma cholesterol. These data indicate the important pathogenetic role carried out by alterations of the clotting system in occlusive arterial diseases.
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PMID:Predictive value of coagulation tests in arterial thrombosis. 337 37

Associations of plasma testosterone and estradiol with some haemostatic factors (factor VII activity, fibrinogen, antithrombin III and alpha 2-antiplasmin) were cross-sectionally examined in 251 healthy, middle-aged men participating in the Paris Prospective Study II on risk factors for ischaemic heart disease. Testosterone levels were negatively correlated to factor VII activity and alpha 2-antiplasmin, the main inhibitor of fibrinolysis. No association was found either between testosterone levels and both fibrinogen and antithrombin III, or between estradiol levels and the set of haemostatic variables. The associations between testosterone and both factor VIIc and alpha 2-antiplasmin were independent of HDL-cholesterol, LDL-cholesterol, triglycerides, smoking, alcohol, body mass index and blood pressure. These results suggest that low circulating testosterone levels might be associated with a hypercoagulability state and therefore could contribute to an increased risk of IHD.
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PMID:Relationship between sex hormones and haemostatic factors in healthy middle-aged men. 337 81

High levels of factor VII are associated with an increased risk of death from cardiovascular disease, especially ischaemic heart disease (IHD). Theoretical considerations and experimental evidence, the latter including the results of clinical trials, suggest that the association may be one of cause and effect. The general epidemiology of factor VII also supports this view. Thus, characteristics such as increasing age, diabetes, obesity, the use of oral contraceptives and the occurrence of the menopause are each associated with raised factor VII levels as well as with an increased risk of IHD. Black ethnic group and vegetarianism, both apparently protective against IHD, are associated with low factor VII levels.
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PMID:Factor VII and ischaemic heart disease: epidemiological evidence. 635 Jan 23

There are approximately 20,000 excess deaths from cardiovascular disease each winter in England and Wales. The reasons for the excess have not been fully elucidated. For one year, we studied 96 men and women aged 65-74 living in their own homes in order to examine seasonal variation in plasma fibrinogen and factor VII clotting activity (FVIIc), and to investigate relationships with infection and other cardiovascular-disease risk factors. Both fibrinogen and FVIIc plasma values were greater in winter with estimated winter-summer differences (confidence intervals) of 0.13 (0.05-0.20) g/L for fibrinogen and 4.2 (1.2-7.1)% of standard for FVIIc. These differences could account for 15% and 9% increases in ischaemic heart disease risk in winter respectively. After adjustment for confounding by season, fibrinogen was strongly related to neutrophil count (p < 0.0001), C-reactive protein (p < 0.0001), alpha 1-antichymotrypsin (p < 0.0001), and self-reported cough (p < 0.0001) and coryza (p = 0.0004), but not to ambient temperature. Therefore, we suggest that seasonal variation in fibrinogen might be induced by winter respiratory infections via activation of the acute phase response. Seasonal variations in the cardiovascular risk factors fibrinogen and FVIIc provide further possible explanations for the marked seasonal variation in death from ischaemic heart disease and stroke in the elderly.
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PMID:Seasonal variations of plasma fibrinogen and factor VII activity in the elderly: winter infections and death from cardiovascular disease. 790 26

In the Northwick Park Heart Study, the coagulant activity of factor VII (FVII:C) has been identified as a risk marker of ischaemic heart disease. In the fasting state, the protein concentration of FVII (FVII:Ag) might be an even better risk marker, because of the low coefficient of variation of the antigen assay. Today, most analyses are performed in plasma samples, as it is unknown whether FVII, to some extent, is consumed during coagulation. In the present study, we have investigated, whether FVII:Ag can be measured equally well in plasma and serum. FVII:Ag was measured in 88 plasma and serum samples. Results were compared by means of linear regression, where y = 0.984 x +0.770, r = 0.96. No systematic variation existed between FVII:Ag in plasma and serum. The mean difference in FVII:Ag between plasma and serum was -1.17 (SD 11.92) arbitrary units, compared with a mean difference of 0.18 (SD 8.31) arbitrary units between duplicate measurements of the same plasma dilution. Our findings indicate that there is a good agreement between FVII:Ag in plasma and serum.
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PMID:The protein concentration of blood coagulation factor VII can be measured equally well in plasma and serum. 763 62

Factor VII is an independent risk factor for ischemic heart disease. We performed a prospective study to evaluate the effect of combined low-dose warfarin-aspirin on activated factor VII (factor VIIa) and to determine if abruptly stopping this treatment is associated with a rebound in the level of factor VIIa. Thirty-three patients with clinically stable coronary artery disease were treated with combined 3 mg warfarin and 80 mg aspirin daily for 8 weeks. The factor VIIa level was measured before treatment, weekly during treatment, and 2 weeks after stopping treatment. The mean percent of pretreatment levels of factor VIIa for weeks 1 through 8 of treatment were 60%, 60%, 72%, 70%, 71%, 70%, 74%, and 87%, respectively (P < .05 compared with pretreatment for weeks 1 through 7 inclusive); 2 weeks after stopping treatment, the level was 122% (95% confidence interval [CI]; 111% to 133%; P < .001 compared with pretreatment). The mean percent level of factor VIIa on-treatment was 74% (P < .001). Factor VIIa is reduced by 26% on average during treatment. This finding provides further rationale for the antithrombotic effect of low-dose warfarin. The results suggest a rebound in the factor VIIa level may occur after treatment is stopped. The potential rebound and its clinical importance should be evaluated by further studies.
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PMID:Effect of treatment with low-dose warfarin-aspirin on activated factor VII. 775 39

General recognition of the thrombotic component in ischaemic heart disease (IHD) is comparatively recent. Despite the obvious role of platelets, it has in many ways--and certainly epidemiologically--been work on the coagulation system that has been more rewarding in characterising those at high risk of IHD on account of haemostatic abnormalities. Raised plasma fibrinogen levels are clearly and independently associated with the onset of both clinically manifest IHD and stroke and probably with lower extremity arterial disease as well. High fibrinogen levels also increase recurrence rates and the progression of these conditions. High factor VII activity levels are associated with increased mortality from IHD but not with non-fatal episodes. Low fibrinolytic activity and raised factor VIII levels are also associated with increased IHD incidence. High fibrinogen levels predispose to thrombosis by effects on viscosity, platelet aggregability, fibrin deposition and the atherogenic process. There is increasing evidence that raised factor VII activity levels lead to increased thrombin production. Associations of several personal characteristics--notably smoking in the case of fibrinogen and dietary fat intake in the case of factor VII activity--influence the coagulation system in ways that are likely to predispose to thrombosis. Besides well known agents such as aspirin and anticoagulants, increasing attention ought now to be given to the antithrombotic potential of fibrinogen-lowering agents.
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PMID:Haemostatic function and arterial disease. 780 29

An increased risk of ischemic heart disease has been reported in men with the Lewis blood group phenotype Le(a-b-). We have investigated the relationship between Lewis phenotype and cardiovascular risk factors in 1714 participants in the Coronary Artery Risk Development in Young Adults Study, an ongoing investigation on life-styles and evolution of cardiovascular risk factors. No significant differences were observed among Lewis phenotypes for body mass index, blood lipid levels, blood pressure, or clotting factors VII and fibrinogen. However, in white men with blood groups A, B, or AB, and the Le(a-b-) phenotype, significantly higher levels of factor VIII (p < 0.01) and von Willebrand factor (p < 0.03) were observed than in those with other Lewis phenotypes (Le[a+b-] or Le[a-b+]). Two-way analysis of variance indicated a significant interaction between blood group and Lewis phenotype (p = 0.0053) in terms of relationship to factor VIII. A similar trend was observed in black men with blood type A, B, or AB, and phenotype Le(a-b-) for factor VII/von Willebrand factor and in women with blood type A, B, or AB, and phenotype Le(a-b-) for factor VIII. Our data suggest that the Le(a-b-) phenotype and blood groups A, B, and AB, by virtue of their association with raised levels of factor VIII and von Willebrand factor, may be risk markers for future atherothrombotic disease.
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PMID:Relationship among Lewis phenotype, clotting factors, and other cardiovascular risk factors in young adults. 859 91

The Northwick Park Heart Study suggested that factor VII activity might be more strongly related to fatal than non-fatal events of ischaemic heart disease. We used polychotomous logistic regression to model simultaneously the probabilities of fatal events, non-fatal myocardial infarction, dying of causes other than ischaemic heart disease and of events, non-fatal myocardial infarction, dying of causes other than ischaemic heart disease and of event-free survival. We followed 1459 white men aged 40-64 at recruitment for a mean period of 16.1 years. Of these, 92 died of ischaemic heart disease, 100 experienced non-fatal myocardial infarction, 173 died of other causes, and 1094 men were alive. Factor VII activity was strongly related to fatal events of ischaemic heart disease but not to non-fatal events (p = 0.008). A difference of 1 SD in factor VII activity was associated with a difference of nearly 50% in the probability of dying of ischaemic heart disease, but with no difference for non-fatal myocardial infarction. This contrast was not seen for smoking, cholesterol, blood pressure, fibrinogen or factor VIII activity. High levels of VII activity may influence outcome at the time of plaque rupture and tissue factor release by enhancing thrombin production and thus fibrin deposition and platelet aggregability. The apparently differential effect of factor VII activity on fatal and non-fatal ischaemic heart disease may have important screening and prophylactic implications.
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PMID:Factor-VII activity and ischaemic heart disease: fatal and non-fatal events. 792 91


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