Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a randomised, double-blind study 5,000 IU heparin-dihydroergotamine mesylate (Dihydergot) or placebo were administered over 14 days to 107 patients with recent ischaemic cerebrovascular accident. The patients were studied daily for recent venous thrombosis in the legs by means of the 125I-fibrinogen test. Thirteen patients died before venous thrombosis had been demonstrated, 13 others were excluded by other causes. Of the 41 patients in the placebo group 23 developed venous thrombosis, but only 11 of the 40 drug-treated patients. Bilateral venous thrombosis occurred in six patients on the placebo and one patient on the drug. Univariate analysis indicated that heart failure, reduction of muscle tone, muscular power and level of consciousness favoured thrombosis. Multivariate analysis further indicated that both bed-rest of several days before start of the prophylactic treatment and extreme obesity favoured thrombosis. The relative thrombosis risk increased by a factor of 15.2 when prophylactic measures were omitted. Death rate in the treated group ws 17.4%, in the placebo group 28.0%. These results indicate that a prophylactic regimen of the type described is a practicable and effective measure after recent ischaemic cerebrovascular accident.
 ...
PMID:[Prevention of venous thrombosis in recent ischaemic cerebrovascular accident: double-blind study with heparin-dihydroergotamine (author's transl)]. 734 84

Patients with acute myocardial infarction of less than 48 hours duration were randomized into three groups. The "fully anticoagulated" group received heparin by intravenous infusion and warfarin sodium to maintain a whole blood clotting time of 30 to 90 minutes and a prothrombin index of 10% to 35%. The "low dose" heparin group received 500 units by intravenous infusion every 12 hours. The control group received no anticoagulants. The radioactive fibrinogen test was used to diagnose the presence of leg vein thromboses. The control group had an incidence of venous thrombosis of 29.7% compared with 13.9% in the low dose group and 11.3% in the fully anticoagulated group. Patients in the control group who had cardiac failure had a significantly higher incidence of venous thromboses (71.4%) when compared with patients not in failure (20.0%). In the two treatment groups no significant difference was observed in patients with and without cardiac failure. Patients with cardiac failure complicating an acute myocardial infarction have a high incidence of venous thromboses. Anticoagulants significantly reduce this incidence and low dose intravenous heparin is as efficacious as full anticoagulation.
 ...
PMID:Low dose heparin in the prevention of deep-vein thromboses in patients with acute myocardial infarction. 736 96

This study was designed to evaluate major fibrinolytic parameters in relation to parameters of inflammation associated with different kinds of pleural effusion. Sixty patients with pleural effusion were studied. The underlying aetiology was empyema in 10 cases, tuberculosis in 9, cancer in 31, cardiac failure in 7, and undetermined in 3. Plasminogen, plasminogen activator inhibitor 1 (PAI-1) and 2 (PAI-2), tissue type plasminogen activator (t-PA), urokinase (u-PA) and D-dimers (D-D) were quantified in plasma samples and pleural effusion specimens. These data were then correlated with inflammatory or infectious parameters, i.e. fibrinogen, von Willebrand factor (vWF), erythrocyte sedimentation rate (ESR), protein concentration, and white blood cell count. D-D levels were higher in pleural fluid than in plasma. D-D levels were not correlated with either plasminogen activator or plasminogen activator inhibitor levels, suggesting the presence of other fibrinolytic pathways. PAI levels (PAI activity, PAI-1 antigenicity, PAI-2 antigenicity) and vWF levels were significantly higher in patients with tuberculosis and empyema than in patients with cancer or cardiac failure. Regression analysis between inflammatory and fibrinolytic parameters showed that pleural PAI levels were significantly correlated with pleural neutrophil count, vWF levels, and plasma fibrinogen levels. D-D levels were correlated with blood ESR. No significant difference in pleural t-PA, u-PA and D-D levels was observed between aetiologies. The highest pleural t-PA and u-PA values were noted in patients with cancer, especially lymphoma. Plasma t-PA levels were higher inpatients with pleural effusion secondary to congestive heart failure, but this difference did not reach statistical significance.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Fibrinolytic and inflammatory processes in pleural effusions. 748 3

Clinical data on the contributory role of heart failure to thromboembolic risk does not differentiate between systolic and diastolic left ventricular dysfunction. We therefore conducted a population-controlled cross-sectional study to determine levels of plasma fibrinogen (associated with thromboembolism), fibrin D-dimer (a marker of fibrin turnover) and von Willebrand factor (a marker of endothelial dysfunction) in patients with ischaemic heart disease (a common cause of diastolic dysfunction) in whom left ventricular diastolic function was defined by echocardiography. We studied 106 patients: those with normal left ventricular function (n = 42, Group 1); those with left ventricular dysfunction but without aneurysms (n = 34, Group 2); and those with left ventricular aneurysm formation (n = 30, Group 3). Each of these groups was subdivided into those with (a) and without (b) diastolic dysfunction. Diastolic dysfunction was present in over 60% of patients, irrespective of left ventricular systolic impairment. There were no significant differences in median levels of plasma fibrinogen, fibrin D-dimer or von Willebrand factor in each group of patients with ischaemic heart disease, whether or not left ventricular diastolic dysfunction was present (Mann-Whitney test; P = N.S.). Systolic (rather than diastolic) dysfunction was the main correlate of these (analysis of variance, general linear model--ANOVA-GLM--P < 0.05) and the greatest abnormalities of fibrinogen, endothelial dysfunction and intravascular fibrin turnover were seen in patients with left ventricular aneurysms whether or not diastolic dysfunction was present. This study demonstrates that there is no evidence of a significant additional contribution to thrombotic risk (as assessed by plasma fibrinogen, von Willebrand factor and fibrin D-dimer) for patients with left ventricular diastolic dysfunction. A relationship is noted between some prothrombotic factors and Doppler indices of flow, which suggests a possible association between cardiac haemodynamics and thrombogenesis.
 ...
PMID:Is diastolic dysfunction associated with thrombogenesis? A study of circulating markers of a prothrombotic state in patients with coronary artery disease. 755 62

To assess hemostatic risk factors for sudden death in patients with stable angina, 323 consecutive patients were recruited prospectively. Patients with clinical heart failure or recent myocardial infarction were excluded. The following clinical variables were recorded: age, gender, smoking habits, hypertension, previous myocardial infarction, left ventricular hypertrophy, and severe ventricular arrhythmia. Angiographic variables included coronary extent, assessed from Jenkins' and mean atherosclerotic scores, and left ventricular ejection fraction. Lipid variables included total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and apolipoproteins A-I and B. Hemostatic factors included fibrinogen, fibrinopeptide A, antithrombin III, factor VIII antigen, factor VIII coagulant, protein C, plasminogen, alpha 2 antiplasmin, euglobulin clot lysis time, tissue plasminogen activator before and after venous occlusion, and plasminogen activator inhibitor. There were 34 deaths, 19 of which were sudden during the follow-up period (60 +/- 17 months). The association between each variable and the risk of sudden death was assessed by calculating the relative risk with the Cox univariate model. All significant predictors from the univariate analysis were then incorporated in a Cox multivariate model to select the independent predictors of sudden death. The independent predictors of sudden death were left ventricular hypertrophy (p < 0.04), lower left ventricular ejection fraction (p < 0.04), and shorter euglobulin clot lysis time after venous occlusion (p < 0.02), whereas fibrinogen (p < 0.07) and Jenkins' score (p < 0.08) were borderline. Determination of hemostatic variables, especially those pertaining to dynamic fibrinolysis, may thus be of value in assessing risk of sudden death.
 ...
PMID:Predictive value of hemostatic factors for sudden death in patients with stable angina pectoris. 761 16

Hypertension is a major contributor to cardiovascular disease, which imparts a threefold increased risk over that of normotensive persons the same age. It accelerates atherogenesis-promoting premature coronary disease, now its most common sequela. The effect of elevated blood pressure on cardiovascular disease morbidity and mortality in general and on coronary disease incidence in particular is independent of the influence of other predisposing atherogenic cofactors but is greatly affected by them. Elevated blood pressure is more often than usual associated with hyperlipidemia, hyperglycemia, hyperuricemia, excessive weight, elevated fibrinogen, and electrocardiogram (ECG) abnormalities, which enhance its impact. Hypertensive coronary candidates usually have an increased low-density lipoprotein/high-density lipoprotein (LDL/HDL) cholesterol ratio, impaired glucose tolerance. ECG abnormalities, or a cigarette smoking habit. These coexisting risk factors exert a greater influence than the character of the blood pressure elevation. Those at risk for hypertensive stroke have left ventricular hypertrophy (LVH), atrial fibrillation, cardiac failure, coronary disease, diabetes, or a cigarette habit. Cardiovascular risk ratios for hypertension diminish with advancing age, but this is offset by a higher absolute risk, making hypertension an important precursor of cardiovascular disease in the elderly.
 ...
PMID:Hypertension as a risk factor for cardiac events--epidemiologic results of long-term studies. 769 48

Chronic congestive heart failure is one of the risk groups of acquired hypercoagulant and hyperviscous state. In a group of patients with medium and severe cardiac failure the administration of sulodexide led to an increased activation of the fibrinolytic potential--a drop of PAI-1 and fibrinogen, to an increased activation of anticoagulatory potential--an increase of AT III and reduced plasma viscosity. Global coagulation and biochemical screening parameters were not affected by treatment. Administration of the preparation did not exert important undesirable effects and was well tolerated.
 ...
PMID:[Hemocoagulation and hemorheology in heart failure and the possible effects of glycosaminoglycans]. 771 90

Plasma DNA increases where cell death occurs in vivo. To investigate its significance in elderly patients, plasma DNA was assayed in 79 institutionalized patients over 68 years of age. The patients were divided into two groups: group I comprises 39 patients suffering from various acute or chronic illnesses; group II comprises 40 patients without chronic disease, and free of any clinical or biological symptoms of any infectious or inflammatory process. Plasma DNA was higher in group I than in group II (p < 0.0001) and in group II than in a control group of middle-aged subjects (p < 0.05). In group I, increase in plasma DNA concentration was found in various pathological situations associated with cell death phenomena, including infections, cancers with metastasis, hepatitis, irreversible cardiac failure, severe respiratory insufficiency and thrombophlebitis. Plasma DNA concentrations were not correlated with erythrocyte sedimentation rate, fibrinogen concentration, hemoglobin concentration or leukocyte count. In group I, as well as in the overall population, survival after 1 month was significantly reduced in patients with increased concentrations of plasma DNA. In conclusion, plasma DNA as a marker of cell death phenomena occurring in vivo, could be helpful for follow-up and management of elderly patients.
 ...
PMID:Plasma DNA as cell death marker in elderly patients. 824 49

Fibrinogen and factor VII have been identified as independent risk factors in cardiovascular morbidity. A relationship between factor VII coagulant activity (VII:C) and prognostically different manifestations of acute coronary heart disease (aCHD) has recently been suggested. In order to validate and to extend these observations, we prospectively studied patients admitted for aCHD (n = 76) and a control group without aCHD (CG, n = 27). According to their clinical evolution, the aCHD cases were subdivided into unstable angina (UA, n = 26), myocardial infarction without (M-I, n = 23) and with heart failure (M-II, n = 27). Before treatment blood was collected for the following assays: fibrinogen, factor VII procoagulant activity (VII:C), amidolytic test (VII:am), immunological (VII:Ag), protein C functional (PCf) and immunological (PC:Ag). We found no statistically significant difference between control and aCHD cases and between their subgroups for any assay of fibrinogen, factor VII and protein C. The VII:C/VII:Ag ratio was higher for UA, M-I, M-II and the entire aCHD group compared with the CG. However, it was not possible to separate the prognostically different aCHD subgroups from each other by ratios of measured values. Therefore, determinations of factor VII, protein C and fibrinogen in aCHD have no prognostic relevance.
 ...
PMID:[Factor VII and protein-C markers are no prognostic indicators in acute coronary heart disease]. 842 52

Ischaemic hepatitis, a condition to be distinguished from cardiac liver or stasis cirrhosis, can occur as an acute episode in patients with advanced stage congestive heart failure. The mechanism is massive necrosis in the central lobules resulting from acute hypoxia when low cardiac output reduces oxygen supply further aggravating the underlying condition of congestion due to poor venous outflow. We report 4 cases which illustrate the difficulties in diagnosis and treatment. All four patients (age range 79-86 years) were seen in an emergency situation caused by an acute drop in cardiac output aggravating their underlying heart failure. Clinical signs included jaundice, oligouria, abdominal pain and cardiovascular shock. The first element suggesting the diagnosis of ischaemic hepatitis was a sudden and massive peak in transaminase levels (> 20 times normal) which rapidly returned to normal. Prothrombin and fibrinogen levels fell rapidly and functional renal failure was present in all cases. Viral serology was negative and no hepatotoxic drugs could be incriminated. Despite symptomatic intensive care one patient died on day 15 due to cardiovascular shock. Enzyme movements, together with the lack of evidence for another cause, is the key to diagnosis of acute ischaemic hepatitis which thus is often established after the emergency situation has been controlled. Initially, viral hepatitis or drug-induced hepatotoxicity may be suspected, especially if the episode of low cardiac output goes unrecognized. Cases with signs of encephalopathy may also be difficult to distinguish from fulminating hepatitis and would be the only indication for needle biopsy in this acute situation. Outcome is generally unfavourable with mortality at 6 months estimated at 50%.
 ...
PMID:[Acute ischemic liver]. 854 28


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>