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)

The metabolism and in vivo kinetics of fibrinogen labelled with radioactive iodine was studied in children with cyanotic congenital heart disease. The patients had a significantly lowered plasma fibrinogen pool, shortened fibrinogen half-life and increased fractional catabolic rate of fibrinogen compared with healthy children. The average plasma fibrinogen and absolute catabolic rate of fibrinogen did not differ from control values. The shortened fibrinogen half-life together with the correcting effect of anticoagulation with heparin indicated that fibrinogen was consumed by chronic disseminated intravascular coagulation. Inhibition of the fibrinolytic system with epsilon-aminocaproic acid in three cyanotic patients had no influence on the fibrinogen half-life in two of them but resulted in its prolongation in one patient.
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PMID:Fibrinogen metabolism in cyanoti congenital heart disease. 61 88

One hundred and seven patients with congestive heart failure, myocardial infarction and arteriosclerotic heart disease were studied by adenosine diphosphate-induced platelet aggregation, fibrinogen levels and ethanol gelation test. Both increases and decreases in platelet aggregation were observed. A significantly high percentage of patients showed a decreased platelet aggregation which was especially marked in the more acute as opposed to the less acute phase. In addition, most patients exhibited a marked shift from abnormal to normal platelet aggregation or vise-versa within a short time period. This pattern of platelet aggregation suggests an active role of platelets in the states of hypercoagulability. The hypercoagulability of these patients was further substantiated by a high percentage of positive ethanol gelation tests and high fibrinogen levels.
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PMID:Adenosine diphosphate-induced platelet aggregation in the states of hypercoagulability. 85 49

In 339 patients with various diseases factor XIII (FSF) was determined with the specific amine incorporation method of Lorand et al (1969). Normal values were found in patients with renal (216 patients) or liver diseases (33 patients), in 39 patients with recurrent deep venous thrombosis and in 17 children with congenital cyanotic heart disease. Low levels were found in patients with various conditions, such as sepsis, multiple fractures and combustio complicated by an abnormal proteolytic activity (fibrinolysis and/or activation of the coagulation system with signs of disseminated coagulation). No correlation was found between the FSF and the fibrinogen values or the levels of fibrin/fibrinogen degradation products (FDP). Low FSF values were found in 4 patients with erosive gastritis, with gastrointestinal bleedings and a local fibrinolytic activity in the gastric juice. Although the FSF must be very low (smaller than 1%) if it is to cause bleedings, the low levels in these patients with many other coexisting disturbances in the coagulation system and/or an increased fibrinolytic activity most probably contribute to the increased bleeding tendency in such patients.
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PMID:Factor XIII in a clinical material. 107 63

Cardiac survey following administration of 131-1 autologous fibrinogen is a noninvasive technique for the detection of intracardiac thrombosis. Fibrinogen is isolated from plasma by a rapid salting-out method with ammonium sulfate and is iodinated with chloramine T. The purity of 131-fibrinogen, expressed as clottable radioactivity, is greater than 90%. Cardiac survey consisting of serial gamma camera imaging or rectilinear scanning after intravenous administration of 131-I fibrinogen was conducted in dogs with freshly induced thromobosis of the left atrial appendage. An accumulation of radioactivity was detectable in the area of the left atrium and confirmed in each of nine dogs sacrificed. Similarly, 20 patients with heart disease predisposing to intracardiac thrombosis were surveyed. Eight of nine patients with positive studies and 11 of 11 with negative studies were confirmed subsequently at surgery or autopsy. Cardiac survey with 131-I fibrinogen is a simple and noninvasive method of detecting intracardiac thrombosis.
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PMID:Noninvasive detection of intracardiac thrombosis: 131-I fibrinogen cardiac survey. 126 36

Heart disease, a major women's health issue, is responsible for 28% of mortality among US females. Combined oral contraceptives (OCs) have been shown to interfere with the 3 phenomena--lipid metabolism, carbohydrate metabolism, and the hemostatic system--most involved in the coronary heart disease process. Disturbances in these systems are believed to underlie the general risk markers of heart disease, although it is not known to what extent OC-induced changes in these systems increase the likelihood of disease. Also unknown is whether there is a residual risk of heart disease in past users of OCs. Both low density lipoprotein (LDL) and high density lipoprotein (HDL) levels are predictive of coronary heart disease in women. Impaired glucose tolerance and hyperinsulinemia are associated with other biochemical and physiological disturbances that increase the risk of heart disease, including changes in serum lipids and lipoproteins. High levels of fibrinogen and factor VII are additional important independent predictors of coronary heart disease. Depending on the sex hormone dose and the OC's composition, the pill has been shown to produce changes such as lowered HDL and HDL2 cholesterol levels, raised LDL cholesterol, impaired glucose tolerance, and increased insulin levels--metabolic disturbances common in those at increased risk of myocardial infarction. REcent studies have found that impaired glucose tolerance and hyperinsulinemia are associated with a set of biochemical and physiological disturbances--known as syndrome X--that occur regularly in OC users. The lowering of the estrogen and progestin dose in newer OCs, as well as the development of progestins intended to reduce metabolic effects, represent major advances. Continued evaluation of the various OCs in terms of risk markers is recommended, however.
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PMID:Oral contraceptives and coronary heart disease. 204 75

The effects of Ticlopidine on platelet function at rest and after exercise test in 12 patients with a history of myocardial infarction but no risk factors and/or residual angina, were investigated. The patients were treated with 500 mg per diem Ticlopidine or placebo for 15 days in a crossover double-blind study. Blood samples were taken before and 3 minutes after maximum effort exercise cycle tests. Blood samples from 25 healthy volunteers of comparable age and sex were used for control purposes. The parameters examined were: platelet aggregation induced by ADP (1 and 3 mumol/l), Arachidonic Acid (AA) (1.3 mmol/l) and collagen (2 micrograms/ml); the presence of circulating platelet aggregates and plasmatic fibrinogen levels. When compared with the controls, the patients showed higher levels of aggregation caused by ADP, AA and collagen as well as circulating aggregates. Exercise produced a statistically significant increase in platelet activation, while Ticlopidine significantly inhibited the platelet aggregation induced by ADP, AA and collagen as well as circulating aggregates both at rest and after the exercise test. Fibrinogen levels were higher in the heart attack patients than the controls especially after exercise, but not to a statistically significant degree. Treatment with Ticlopidine did not influence plasma fibrinogen levels. It is not known whether the patients with signs of effort-induced platelet aggregation run a higher risk of ischaemic cardiopathy or whether drug treatment could prevent this eventuality.
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PMID:[Effects of ticlopidine on platelet function at rest and after exercise in patients with previous myocardial infarct. An acute crossover double-blind study]. 217 69

In systemic sclerosis (SS), cardiovascular commitment was recorded in an autopsy series, in widely different percentages, from 12 to 81%. On the other hand, clinical diagnosis of cardiopathy is made in far fewer cases. In addition, the coexistence of renal and/or pulmonary commitment makes difficult separation between primary and secondary heart damage. In 22 patients (2 m, 20 f) aged between 34 and 75 (average 55 +/- 11) with SS, a study has been made of the a) prevalence of cardiovascular commitment; b) the significance of the classic risk factors; c) the erythrocyte filtration time or TF (index of microangiopathic damage). Metabolic stability, fibrinogen, haematocrit and TF (Reid et al. method) were assessed in each patient. Nine patients (40.9%) presented ischaemic cardiopathy (myocardial infarction in three and effort angina in six), one (4.5%) presented hypertensive cardiopathy. Conduction disturbances were observed in five patients (22.7%). Whereas a statistically significant increase in TF was observed in cardiopaths, no differences in plasma levels of glucose, cholesterol or fibrinogen were observed. The incidence of smoking and the familial factor were also insignificant.
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PMID:[Cardiovascular involvement and relative risk factors in systemic sclerosis. Personal contribution]. 223 76

Compared to non-smokers, chronic smokers are at increased risk of developing atherosclerotic vascular disease, myocardial infarction, unstable angina and sudden death. The acute systemic hemodynamic response to smoking includes an increase in the heart rate, arterial pressure, cardiac output and myocardial contractility. These acute effects are primarily mediated by activation of the sympathetic nervous system. In patients with heart disease, smoking may cause a deterioration in cardiac performance. In the coronary circulation, smoking induces coronary vasoconstriction which can be prevented by alpha-adrenergic blockade, nitrates and calcium channel blockers. Non-selective beta-adrenergic blockade potentiates both the systemic and coronary vasoconstrictor effect of smoking. Other adverse effects of smoking on the cardiovascular system include a reduction in high-density lipoprotein (HDL) cholesterol, an increase in platelet reactivity and an increase in fibrinogen concentrations. These effects on systemic and coronary hemodynamics, lipid metabolism and hemostasis may contribute to the long-term adverse consequences of smoking.
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PMID:Smoking and cardiovascular function. 228 53

We assessed the severity of carotid atherosclerosis in 412 men from eastern Finland aged 42, 48, 54 or 60 years at examination with B-mode ultrasonography in 1987 in the Kuopi ischaemic Heart Disease Risk Factor Study (KIHD). Thirty-seven per cent of participants had intimal-medial thickening, 10% had plaques and 2% had stenosis. Age (P less than 0.001), cigarette-years (P less than 0.001), serum LDL cholesterol (P = 0.005), low income (P = 0.020) and low alcohol consumption (P = 0.048) had significant partial associations with the severity of carotid atherosclerosis. A linear regression model including these variables and plasma fibrinogen (NS) and serum HDL-cholesterol (NS) accounted for 33% of the variation in atherosclerosis severity. Our data provide further evidence on the role of smoking and LDL-cholesterol in atherosclerosis.
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PMID:Risk factors for carotid atherosclerosis: the Kuopio Ischaemic Heart Disease Risk Factor Study. 266 52

Coagulation abnormalities with and without haemorrhagic manifestations have been frequently reported in newborn-infants affected by hypoxia. Particularly in postmature-infants and in those ones with acute asphyxia at birth, respiratory distress syndrome (RDS), intra-uterine growth retardation (IUGR) and cyanotic congenital heart disease (CCHD). A reduction of synthesis or a consumption of blood coagulation factors are the main causes of these abnormalities. The anomalies of platelet number and of their function, of haemostasis global tests, of coagulation factors and physiologic inhibitors levels, of fibrinogenesis and fibrinolysis are examined, including authors' studies and a review of literature too. The authors think platelet count, PT, PTT, fibrinogen, factor V and VIII, and PDF determinations are necessary laboratory investigations for newborn-infants with RDS or acute asphyxia for about the first week of life, because of the risk of consumption coagulopathy. In the other hypoxic newborns (IUGR, CCHD, postmature infants) platelets count, PT, PTT and serum PDF determinations could be enough in order to value any coagulation abnormalities presence.
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PMID:[Neonatal hypoxia and hemocoagulative changes]. 269 28


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