Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibrinogen Matsumoto I is a novel hereditary dysfibrinogen identified in a 1-year-old boy with Down's syndrome. Though he showed no apparent bleeding or thrombotic tendency, he had a congenital heart disease. Preoperative coagulation tests of his plasma revealed a prolonged thrombin time and the fibrinogen level determined by the thrombin time method was markedly decreased. Molecular weight of fibrinogen chains showed apparently normal A alpha-, B beta-, and gamma-chains. The rate of fibrinopeptide release was normal, whereas fibrin polymerization was delayed. Fibrinogen gamma-chain gene fragments from the propositus were amplified by polymerase chain reaction then sequenced. The triplet GAT, coding for the amino acid residue gamma 364, was replaced by CAT, resulting in the substitution of Asp-->His. This residue is adjacent to the Tyr-363 that is demonstrated to be the primary site for fibrin polymerization. Our results indicate that the residue gamma 364 Asp is essential for normal polymerization of fibrin monomer.
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PMID:Fibrinogen Matsumoto I: a gamma 364 Asp-->His (GAT-->CAT) substitution associated with defective fibrin polymerization. 882 81

The increasing use of oestrogen replacement therapy in women has focussed attention on the cardioprotective properties it has demonstrated. Historically, it has been shown that women enjoy a certain protection from heart disease, a phenomenon, however, which has not been studied extensively. Women at every age have less coronary artery disease (CAD) than men, even when various risk factors are accounted for, although the presence of diabetes carries equal mortality for both sexes. However, women who do develop CAD have a greater risk of mortality than men with CAD. Other gender differences include a later age of onset of CAD for women, and a difference in the type of atherosclerotic lesions developed. Most striking is the fact that, in women, high-density lipoprotein (HDL) seems to be a more potent predictor of major cardiovascular events than low-density lipoprotein (LDL), or total cholesterol. The Postmenopausal Oestrogen and Progesterone Interventions (PEPI) Trial looked at changes in HDL, fibrinogen, blood pressure and serum insulin resulting from oestrogen use. Four regimens were compared against placebo in 875 women. The results showed that HDL was increased significantly, LDL decreased significantly, fibrinogen levels decreased significantly, and blood pressure and serum insulin levels were essentially unaffected by oestrogen and oestrogen/progestin interactions. The Heart and Oestrogen/Progestin Replacement (HERS) Study, currently underway, is a secondary prevention trial testing the protective effect of hormone therapy in women with documented CAD. This trial may definitively answer the question of whether hormones protect against CAD. After HERS, it may be unethical to continue conducting placebo-controlled trials in a therapy that has such documented cardioprotective benefit.
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PMID:Evidence for primary and secondary prevention of coronary artery disease in women taking oestrogen replacement therapy. 886 76

Individuals with a family history of coronary heart disease (CHD) may be predisposed to atherothrombosis. To investigate this hypothesis, a family CHD risk score was computed for approximately 13,000 men and women aged 45 to 64; hemostatic variables (fibrinogen, factor VIIc, factor VIIIc, von Willebrand factor, antithrombin III. protein C) were also measured in plasma. After adjustment for age and ethnicity, there was a statistically significant, positive association between the family risk score and four of the six hemostatic variables (fibrinogen, factor VIIc, factor VIIIc, von Willebrand factor) in women and all six hemostatic variables in men. In general, these associations were weak and substantially attenuated after adjustment for constitutional, lifestyle, and biochemical covariates. These results indicate that mean levels of selected hemostatic variables, like traditional CHD risk factors, are higher in individuals with a family history of heart disease.
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PMID:Family history of coronary heart disease and hemostatic variables in middle-aged adults. Atherosclerosis Risk in Communities Investigators and Family Heart Study Research Group. 903 55

Fibrinogen is an important risk factor for atherosclerosis, stroke and cardiovascular heart disease (CHD). This risk is increased when associated with a high serum cholesterol. Furthermore, it is also believed that not only fibrinogen concentration, but also the quality of fibrin networks may be an important risk factor for the development of CHD. CHD and stroke as a result of atherosclerosis, plus the related problems of hyperinsulinaemia, hyperlipidaemia and hypertension are strongly related to diet. The "western" diet, defined by low fibre and high fat, sucrose and animal protein intakes, appears to be a major factor leading to death. It has been established that the water-soluble dietary fibre, pectin, significantly decrease the concentration of serum cholesterol levels. Evidence is also accumulating that a diet rich in fibre may protect against diseases associated with raised clotting factors. This investigation studied the possible effects of pectin on fibrinogen levels and fibrin network architecture. Two groups of 10 male hyperlipidaemic volunteers each, received a pectin supplement (15 g/day) or placebo (15 g/day) for 4 weeks. Lipid and fibrin network structure variables were measured at baseline and the end of supplementation. Pectin supplementation caused significant decreases in total cholesterol, low-density lipoprotein cholesterol, apolipoprotein A & B and lipoprotein (a). Significant changes in the characteristics of fibrin networks developed in the plasma of the pectin supplemented group indicated that networks were more permeable and had lower tensile strength. These network structures are believed to be less atherogenic. It is suspected that pectin modified network characteristics by a combination of its effects on metabolism and altered fibrin conversion. This confirms the therapeutic possibilities of dietary intervention. Furthermore, this study also showed that changes in plasma fibrinogen need not be present to induce alterations in fibrin network architecture.
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PMID:Dietary pectin influences fibrin network structure in hypercholesterolaemic subjects. 917 40

Fish intake has long been recognized to play an important role in human health, for example, in reduction of the incidence of heart disease and some cancers and as immunosuppressors. In this study, we examined the effect of dietary supplementation with fish oils (FO) on monocytic procoagulant activity (PCA) in dogs. Six mongrel dogs were fed daily chow containing FO concentrate (MaxEPA, 0.5 g/kg body wt/day) for 8 weeks. Blood samples were drawn during a 20-week experimental period [i.e., before, during (weekly), and after (biweekly) MaxEPA supplementation] to measure monocytic PCA, PCA activation induced by endotoxin [lipopolysaccharide (LPS)], and plasma levels of total cholesterol, triglyceride, and fibrinogen (FBG). PCA was generally stimulated drastically by approximately 19-fold on incubation of whole blood with LPS (1 microg/ml) in vitro for 2 hr. The basal PCA remained essentially unchanged over the entire experimental period irrespective of MaxEPA supplementation; however, LPS-induced PCA activation was reduced by 50% (P < 0.05) 3 weeks after MaxEPA was introduced. This inhibition remained significant up to Week 10 and reached 75% at Week 12. Thereafter, PCA activation gradually returned to the level before supplementation. The plasma levels of total cholesterol, triglyceride, and fibrinogen were determined to be 178.8 +/- 6.0, 46.7 +/- 3.9, and 61.3 +/- 5.5 mg/dl, respectively. These plasma contents were neither correlated with LPS-induced PCA activation nor affected significantly by MaxEPA supplementation. Following a similar protocol, we also showed that MaxEPA supplementation resulted in a profound depression (-80%) of LPS-induced PCA activation in a rabbit, and PCA activation was eventually restored after removal of MaxEPA from the diet. Our results suggest a beneficial potential of MaxEPA supplementation in the management of atherothrombotic diseases in response to LPS infection.
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PMID:Daily supplementation with MaxEPA suppresses endotoxin-inducible monocytic procoagulation in dogs. 927 Dec 84

Cigarette smoking is firmly established as a risk factor for coronary heart disease, stroke and peripheral vascular disease, and is associated with increased cardiovascular mortality. A possible explanation for this relation is that smoking increases the development of atherosclerosis. Indeed, tobacco smoking has been associated with modified lipids levels, decreased fibrinolysis, increased fibrinogen levels and changes in endothelial and platelet functions for instance, which are themselves either known risk factors for or early features of atherosclerosis. Passive smoking, defined as the the involuntary exposure of non-smokers to tobacco combustion products in the indoor environment is now convincingly linked to heart disease mortality and morbidity. Stopping smoking works, decreasing cardiovascular mortality and morbidity within 5 years, whatever the age and sex of the previous smoker.
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PMID:[Tobacco smoking and cardiovascular risk]. 936 21

Plasma fibrinogen is a consistent predictor of ischemic heart disease (IHD) in prospective studies, but there are fewer data relating other hemostatic variables to IHD and also to stroke. We therefore studied the relationships of plasma fibrinogen, von Willebrand factor antigen, tissue plasminogen activator (TPA) antigen, factor VII, and fibrin D-dimer to incidence of IHD and stroke and determined whether any associations could be explained by conventional risk factors and baseline heart disease. In the Edinburgh Artery study, 1592 men and women aged 55 to 74 years, randomly sampled from the general population, were followed prospectively over 5 years to detect fatal and nonfatal IHD and stroke events. During the 5 years, 268 new vascular events were identified. Baseline plasma fibrinogen was independently related to risk of stroke in multivariate analysis that adjusted for cigarette smoking, LDL-cholesterol, systolic blood pressure, and preexisting IHD (relative risk [RR] 1.52, 95% confidence interval [CI] 1.17, 1.98). TPA antigen, and fibrin D-dimer were also independently associated with risk of stroke (RR 1.69,95% CI 1.22,2.35 and RR 1.96, 95% CI 1.12,3.41, respectively). Significant relationships were found between TPA antigen and myocardial infarction (P < or = .05). In older men and women, increased coagulation activity and disturbed fibrinolysis are predictors of future vascular events (both IHD and stroke).
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PMID:Hemostatic factors as predictors of ischemic heart disease and stroke in the Edinburgh Artery Study. 940 28

The Caerphilly and Speedwell studies have previously reported the predictive power of heat-precipitation, nephelometric, fibrinogen for 10-year incidence of ischaemic heart disease. A Clauss, clotting time, fibrinogen was also measured at baseline, but has not previously been reported. The predictive power of the two assays is compared. Both methods were employed on fasting blood samples from a total of 4391 men aged 45-63 years. Over the following 10 years 533 (12%) developed major ischaemic heart disease. Nephelometric fibrinogen was higher by 0.33 g/l among the men who developed disease; clottable fibrinogen was higher by 0.20 g/l. This difference is statistically significant (P=0.01). Relative odds of developing heart disease increased steadily to 3.53 (P<0.0001) in the 20% of men with the highest nephelometric fibrinogen; for clottable fibrinogen the corresponding relative odds increased to 2.24 (P<0.0001). When both measures of fibrinogen were included in logistic regression models together with age and smoking habit, the trend for incidence to increase with increasing nephelometric fibrinogen remained highly significant (P<0.0001), whereas for the Clauss fibrinogen the trend almost entirely disappeared (P = 0.37). We conclude that functional assays of clottable fibrinogen may not reflect all of the mechanisms which mediate the association between fibrinogen and cardiovascular disease and that assays of both 'heat precipitable' and 'clottable' fibrinogen should be included in all future prospective studies.
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PMID:The relative power of heat-precipitation nephelometric and clottable (Clauss) fibrinogen in the prediction of ischaemic heart disease: the Caerphilly and Speedwell studies. 950 45

Most people with diabetes die from thrombotic complications superimposed to degenerative arterial vascular lesions, mostly myocardial infarction. Diabetes is a risk factor per se for such complications, but often clusters with dyslipoproteinemia, hypertension and obesity. In NIDDM (Type-II) patients this is referred to as "metabolic syndrome" and often operates on a genetically programmed susceptibility which accelerates the pathogenesis of coronary artery disease in front of a much wider diabetes specific cardiopathy. From a pathophysiological point of view none of these associated risk factors explains the pathogenetic series of events leading to the precipitation of an occlusive thrombus at sites of complicated coronary plaques. In patients with diabetes the coagulation system is switched towards a prethrombotic state, involving increased plasmatic coagulation, diminished fibrinolysis, decreased endothelial thromboresistance and predominantly platelet hyperreactivity ("diabetic thrombocytopathy"). Some of these factors are associated with an increased coronary risk (e.g. fibrinogen, PAI-1, platelets), but are also directly linked to the pathogenesis of "atherothrombosis". Altered cardiac remodelling together with adhesion and coagulation mechanisms appears suitable to explain decreased functional performance of infarcted organs, decreased success of acute (reduced fibrinolytic response, reperfusion injury) and longterm intervention strategies (PTCA, CABG) in diabetes. Glucose adjustment alone will not adequately neutralize these complex mechanisms. Particularly in diabetes a multidimensional interventional repertoire is required including antihypertensive, antidyslipoproteinemic and antithrombotic drugs, customized according to the individual patients needs as assessed by early diagnostic measures ("early secondary prevention").
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PMID:Heart disease in diabetes mellitus: a challenge for early diagnosis and intervention. 951 54

The data gained from clinical studies in the past years have indicated that the thrombolytic therapy (TL) has favourable effect on patients with acute myocardial infarction (AMI). It is aimed at reperfusion in the ischaemic area, a decrease in the extent of infarction site and a decrease in mortality. TL administered within the initial hours after the onset of AMI leads to better results than when administered after several hours. Currently, TL is not limited by age. The patients who were given streptokinase (SK) or anistreplase (APSAC) prior to more than 4 days, if necessary, urokinase or alteplase (rt-PA) should be given. There are differences in the opinions as to the optimal selection of thrombolytic drugs. However, all currently used drugs lead to a significant decrease in mortality due to AMI. The preferential use of accelerated administration of rt-PA in contrast to SK is justified in younger patients with extensive AMI of the anterior wall, in whom the therapy has begun within 4 hours since its onset. The occurence of severe bleeding indicates that TL should be halted and coagulation factors should be replaces by freshly frozen plasma or fibrinogen concentrate, if necessary, transfusion of full blood should take place. If the severe bleeding occurs shortly after the administration of SK, the persisting plasminaemia can be arranged by antifibrinolytic drugs. An improvement in TL results can be achieved by adjuvant antithrombotic therapy. At the same time, in addition to acetylsalicylic acid, the patient treated with rt-PA should be given heparin. Heparin administration is not necessary in patients treated with SK or APSAC. However, heparin is indicated in patients at risk due to systemic embolization in congestive heart disease, extensive infarction or atrial fibrillation. (Tab. 1, Ref. 28).
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PMID:[In Process Citation] 966 37


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