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At least 19 recordsLinked to original sources
PubMed1978

Incidence of emboli with cloth-covered Starr-Edwards valve without anticoagulation and with varying forms of anticoagulation. Analysis of 183 patients followed for 3 1/2 years.

One hundred eighty-three patients with cloth-covered valves were studied from 1 1/2 to 8 years after operation, with an average follow-up time of 3 1/2 years. Over the total period, patients taking Coumadin sustained a 4 percent embolic incidence (1.2 per 100 patient-years); those taking aspirin had a 7 percent incidence (2.6 per 100 patient-years); and those taking Persantine had a 43 percent incidence (10 per 100 patient-years). Patients on no regimen of anticoagulation had a 16 percent embolic rate (four per 100 patient-years), whereas another group of patients who stopped anticoagulants after a year incurred a 13 percent embolic incidence in the subsequent 2 years (6.4 per 100 patient-years). These data showed a significantly lowered embolic rate with anticoagulation and suggest that all patients with cloth-covered valves should be taking anticoagulants. That these valves become epithelialized and do not form thrombus after a year was not borne out by this study. Persantine alone is not a satisfactory anticoagulant. Coumadin appears to be the superior anticoagulant, but if careful monitoring of its use is in question or if serious bleeding complications ensue, aspirin may provide satisfactory protection.

Anticoagulants↗
PubMed1977

Management of anticoagulation in outpatients: experience with an anticoagulation service in a municipal hospital setting.

In 66 months, a general hospital's outpatient Anticoagulation Service (ACS) monitored 263 patients who received 280 courses of warfarin sodium totalling 254 patient treatment years. Major hemorrhagic morbidity was 4% of courses and there was no mortality attributable to warfarin therapy. Major hemorrhage occurred in patients with increased anatomic risk of bleeding (diverticulosis, hemorrhoids, cystitis), and was not a function of patient age, sex, anticoagulation control, or medications administered concurrently with warfarin. Control of anticoagulation was not correlated with age or other medications, but was worsened significantly by the presence of congestive heart failure. We attribute a favorable experience with outpatient ACS to careful patient selection, patient education and monitoring, attention to duration of anticoagulation, and continuing communication with primary physicians who retained responsibility for medical care. An ACS offers safety, consistency, efficiency, and a unified approach to outpatient anticoagulation in the general hospital setting.

Aged↗
PubMed1979

Structural basis for the anticoagulant activity of heparin. 2. Relationship of anticoagulant activity to the thermodynamics and fluorescence fading kinetics of acridine orange-heparin complexes.

Complexing heparin or dermatan sulfate with the fluorescent probe acridine orange provides a means of studying electrostatic as well as static and dynamic conformational aspects of these glycosaminoglycans via the thermodynamic and photochemical (fluorescence fading) properties of these complexes. The cooperative binding constants (Kq), fluorescence fading rate parameters (r''), and anticoagulant activities of heparins fractionated according to anionic density all showed qualitatively the same dependence upon anionic density. When Kq and r'' were plotted against anticoagulant activity, empirical relationships were observed. Interestingly, the corresponding values for unfractionated dermatan sulfate fell on the lines defined by the heparin fractions. Temperature-dependence, studies demonstrated that differences in fading rate observed for heparins of different anionic densities are entropic in origin and reflect differences in the ability to assume a special configuration. Differences in activation entropy for fluorescence fading can be empirically correlated with anticoagulant activity. The latter correlation suggests a physical similarity in the roles played by anionic density in both fluorescence fading and anticoagulant activity.

Acridine Orange↗
PubMed1979

Anticoagulation and high dose liver radiation: a preliminary report.

Two groups of patients were observed for evidence of acute radiation hepatitis during "high dose" radiation to the liver. The first group of 18 patients with metastatic liver disease received an average of 4,050 rad to the whole liver. Half received anticoagulation with warfarin. One patient on anticoagulation developed evidence of acute radiation hepatitis while 2 patients did so without anticoagulation. Eleven patients with Hodgkin's disease received 4,000 rad to the left lobe of the liver during extended field radiation. Four of these 11 patients were anticoagulated to therapeutic range. Only one of the fully anticoagulated patients showed changes on liver scan consistent with radiation hepatitis whereas three did so without anticoagulation. No serious sequelae from anticoagulation occurred in either group. These preliminary data suggest that anticoagulation may be safely administered with high dose hepatic radiation and that further trials with anticoagulation are warranted.

Adult↗
PubMed1978

Anticoagulant therapy and central nervous system complications in patients with prosthetic valve endocarditis.

Among 52 cases of prosthetic valve endocarditis, adequate anticoagulant therapy was administered in 38 and discontinued or given in subtherapeutic dosage in 14. Our data suggest that anticoagulant therapy does not appreciably increase morbidity or mortality in patients with prosthetic valve endocarditis. On the contrary, in our patients the incidence of major clinical CNS (central nervous system) complications was increased and the mortality was higher if anticoagulant therapy was discontinued. CNS complications occurred in 10 of the 14 patients without adequate anticoagulant therapy and in three of the 38 with adequate anticoagulant therapy. Mortality was 57% among those treated without adequate anticoagulation and 47% among those with adequate anticoagulation. At autopsy, CNS complications were thought to be the primary cause of five of the eight deaths in cases without adequate anticoagulation.

Adolescent↗
PubMed1976

[Subdural hematoma and anticoagulant therapy].

The authors report a series of 22 cases of subdural hematomas in patients submitted to anticoagulant therapy. A review of the literature finds 150 cases. Subdural hematomas occurs in about one third of the patients presenting hemorrhage of central nervous system related to anticoagulant therapy. Among subdural hematomas of any cause, the possible role of a previous anticoagulant therapy is stressed in 4,8 to 14% of cases. In most cases, long term anticoagulants were indicated for arterial or heart (ischemic) lesions (16/22 cases). In 6 cases, anticoagulants were indicated for prevention or treatment of pulmonary embolies. In 18 cases, anticoagulant drug is from the group of dicoumarol or phenylindanedione. In 3 cases, the only anticoagulant given to patient was heparin. Pathogenic study suggests that hypocoagulability might not always be the only factor of bleeding: high blood pressure, other drugs and head trauma (10 cases) are often associated. Clinical features, in our series, are similar to those encountered in cases of subdural hematoma of any cause. According to the existence of a cranial injury and to the chronology of anticoagulant therapy, the authors divide their 22 patients into 3 groups. The use of protamin sulfate or human plasma fraction PPSB provides in few minutes a normal coagulability. Neurosurgical treatment in all our cases evacuated in 11 patients a chronic subdural hematoma, in 2 cases an acute, and in 9 cases a subacute hematoma. Results were fair in 19 patients with no sequelae. 3 patients died during the immediate post-operative period. The authors conclude by stressing several preventive measures.

Anticoagulants↗
PubMed1977

Oral anticoagulation in the treatment of a spontaneously metastasising murine tumour (3LL).

The effects of long-term anticoagulation with phenprocoumon on growth of the Lewis lung carcinoma (3LL) were studied. Oral anticoagulation initiated at the day of i.m. transplantation of the 3LL into C57BL mice significantly inhibited primary tumour growth and reduced the number of spontaneous metastases to the lungs. Intermittent anticoagulation was without effect on metastasis formation but still retarded primary growth. There was no influence of anticoagulation on the mean survival time (MST) of tumour-bearing animals. Phenprocoumon appears to improve the results of cyclophosphamide of 5-fluorouracil treatment, but there were no statisticially significant differences. In contrast, bleomycin treatment in combination with adjuvant anticoagulation suggested a possible drug synergy. No significant influence of anticoagulation on the response of the primary tumour to irradiattion was found, though the MST of irradiated and anticoagulated animals was greater than in the solely irradiated controls. The present investigations suggest that coumarin derivatives have some direct tumour-inhibiting capacities, but exert their antimetastatic action via deceleration of the blood clotting mechanism.

4-Hydroxycoumarins↗
PubMed1979

Anticoagulation in myocardial infarction: modern approach to an old problem.

The role of routine anticogulation in acute myocardial infarction continues to be a source of controversy. There is currently strong evidence to suggest that conventional anticoagulation will prevent the formation of most deep vein thrombi and subsequent pulmonary embolization. Anticoagulant agents also appear to reduce the incidence of emboli from cardiac mural thrombi to peripheral arteries. Patients without a predisposition to bleeding are unlikely to have hemorrhagic complications in the hospital after usual doses of anticoagulant drugs. In patients with severe hypertension, prior gastrointestinal bleeding, carcinoma or advanced age, small dose heparin therapy appears to reduce the incidence of venous thrombosis and probably of pulmonary emboli as well. Its value in preventing peripheral arterial embolization has not been defined. Anticoagulation with standard "large" doses is an effective means of preventing the risks of pulmonary and peripheral emboli during the in-patient phase of acute myocardial infarction. Small dose heparin therapy provides an excellent alternative to conventional anticoagulation when there is more than a negligible risk of hemorrhage. There is little evidence at this time to support the use of long-term anticoagulation beyond the acute phase of myocardial infarction.

Acute Disease↗
PubMed1976

A phospholipase A2 with anticoagulant activity. II. Inhibition of the phospholiped activity in coagulation.

An anticoagulant factor with phospholipase A2 activity has been isolated from Vipera berus venom. Phospholipase activity was studied on platelet phospholipid and on brain cephalin. The venom factor showed a potent anticoagulant activity: 1 mug impaired the clotting of 1 ml of citrated recalcified platelet-poor plasma. The anticoagulant inhibited clotting by antagonism to phospholipid. The antagonism constant (Kan = 6.8-10(-9) M) demonstrated the high affinity of the inhibitor for phospholipid. As with other phospholipases A2, the venom factor was thermoresistant but very sensitive to photo-oxidation. Both activities (anticoagulant activity and phospholipase activity) were not markedly dissociated by either denaturation or neutralization processes. Slightly different curves of photo-oxidative inactivation of both activities suggested the presence, on the molecule, of two very close sites responsible for phospholipase and anticoagulant activities. The inhibitor effect on coagulation was independent of the hydrolysis process. In fact, lysoderivatives and fatty acids, resulting from complete hydrolysis with the venom factor, were as active as the native phospholipids. Moreover phospholipase A2 from other viperidae venom, which did not have anticoagulant activity, produced similarly active lysoderivatives. This showed that the cleavage of the beta-acyl bond does not interfere with the activity of phospholipid. A possible mechanism of clotting inhibition by the venom factor was proposed. Owing to its high affinity for phospholipid, the inhibitor would complex phospholipid at its protein binding site impairing the normal arrangement of coagulation protein factors and, consequently, their activation. The positive charges of the inhibitor (pI = 9.2) could bind with phosphoryl or carboxyl groups of phospholipid, making them unavailable for protein binding. The complex formation involves a loss of dissociating capacity of the enzyme towards its substrate. This required an additional interaction of the inhibitor with a coagulation protein factor. The inhibitor could be removed from the complex by specific antibodies, permitting recovery of normal phospholipid-protein interaction. The role of calcium in the complex has not yet been elucidated. This venom factor affords a useful tool for investigating the phospholipid-clotting protein interaction.

Anticoagulants↗
PubMedDate not supplied

Clinical pharmacokinetics of oral anticoagulants.

Warfarin is clinically the most widely used oral anticoagulant and its properties have been extensively studied. Assay method for these compounds have until recently been relatively nonspecific. The advent of chromatographically based techniques has enabled re-evaluation of the pharmacokinetics of oral anticoagulants, but most work continues to involve warfarin. The most important recent work has concerned the different anticoagulant potencies and metabolic pathways of the optical isomers of some of these drugs. The effects of age and some diseases on pharmacokinetics of warfarin have been examined but much remains to be done, especially with oral anticoagulants other than warfarin. There are several well established pharmacokinetic drug interactions with warfarin. There is a wide awareness of the drugs most likely to reduce anticoagulant effects by enzyme induction and alternative drugs can be used. Mechanisms of some interactions have been re-investigated. In vivo drug displacement interactions are complicated by the correlation between hepatic clearance of these drugs and the size of the unbound fraction in plasma. The interactions between phenylbutazone and warfarin and metronidazole and warfarin, resulting in potentiation of anticoagulant effect have been suggested to be due mainly to an inhibition of the metabolism of the more potent S isomer of warfarin.

Aged↗
PubMed1979

Interaction between anticoagulants and contraceptives: an unsuspected finding.

To assess the effects of oral contraceptives on anticoagulant treatment the prothrombin times of 12 patients were measured while they were taking both drugs simultaneously and while they were taking only anticoagulants. The mean prothrombin time ratio was significantly higher when patients were taking both drugs than when they were taking only anticoagulants and their doses of anticoagulant were significantly lower. During both periods most of the prothrombin values remained in the therapeutic range. These findings suggest that, contrary to the common belief that oral contraceptives diminish the effects of anticoagulants, contraceptives in fact potentiate the action of the anticoagulants.

Acenocoumarol↗
PubMed1979

Audit of anticoagulant therapy of pulmonary embolus, deep vein thrombosis and thrombophlebitis.

The use of heparin sodium and warfarin sodium in the treatment of pulmonary embolus (PE), deep vein thrombosis (DVT) and thrombophlebitis (TP) was studied by a hospital pharmacy department. During a four-month period, the charts of 26 patients were audited for anticoagulant dosages used; laboratory test monitoring of anticoagulant dosage used; laboratory test minitoring of anticoagulant therapy; complications of, contraindications to, and patient compliance with anticoagulant therapy. These variables were evaluated on the basis of compliance with a written anticoagulant protocol. Initial doses of heparin sodium and warfarin sodium were acceptable in 43% of patients. Maintenance dosing with heparin sodium was acceptable in 89% of patients. Activated partial thromboplastin times (APTT) were ordered correctly for 65% of patients. APTTs were within therapeutic ranges in 31% of patients. The duration of heparin-warfarin overlap was possibly to definitely acceptable in 71% of patients. Prothrombin times were properly monitored in 50% of patients. Complications of anticoagulant therapy were evident in only one patient. There were a number of potentially serious diversions from the protocol. The pharmacy department planned to issue bulletins designed to correct the problems.

Adult↗
PubMed1978

Carotid and vertebral-basilar transient ischemic attacks: effect of anticoagulants, hypertension, and cardiac disorders on survival and stroke occurrence--a population study.

A population of 199 patients from Rochester, MN, was followed from the time of their first carotid or vertebral-basilar transient ischemic attack (TIA). Patients treated with anticoagulants had no significant difference in survival from untreated patients. Among patients with carotid TIA who received anticoagulants, the net probability of stroke was slightly but not significantly lower than in untreated patients. The difference favoring treated patients with vertebral-basilar TIA was significant starting at three months. The rate of intracranial hemorrhage was higher higher among all patients receiving anticoagulant treatment than among untreated patients and was significantly higher among those 55 to 74 years old. Almost all the hemorrhages occurred after a year or more of anticoagulant treatment and in patients more than 65 years old. Patients with high diastolic blood pressure had a significantly higher net probability of stroke than did patients with lower blood pressure and those receiving antihypertensive drugs. By implication, treatment of hypertension was effective in preventing stroke in patients with TIA. Linear discriminant analysis and actuarial analysis indicated that diastolic blood pressure and anticoagulant therapy were the only factors that influenced stroke occurrence. There was no suggestion that previous myocardial infarction, angina pectoris, valvular heart disease, cardiac arrhythmia, or congestive heart failure--individually or in combination--influenced the occurrence of stroke or survival.

Adult↗
PubMed1978

Purification and characterization of the anticoagulant principle of Trimeresurus mucrosquamatus venom.

By means of CM-Sephadex column chromatography, Trimeresurus mucrosquamatus venom was separated into 20 fractions. Fraction XX had the marked anticoagulant action. This fraction was refractionated three times on Sephadex G-75, and a single peak was obtained. The patterns of microzone and disc electrophoresis also showed a single band. A single, symmetrical boundary with a value of 1.61 S was obtained by ultracentrifugation. It was a single peptide chain with a molecular weight of 11 700. The isoelectric point was higher than pH 10. The anticoagulant principle possessed phospholipase A activity and was calcium ion dependent. It did not possess proteolytic, tosyl-L-arginine methyl ester esterase, phosphodiesterase and alkaline phosphomonoesterase activities of the crude venom. The phospholipase A activity was heat-labile at pH 7.4, but was heat-stable at pH 5.6. The anticoagulant activity was more resistant to heat treatment as compared with phospholipase A activity. The anitoagulant action of the purified principle was competitively inhibited by platelet phospholid, tissue thromboplastin and cephalin, and was neutralized by antiserum. The anticoagulant principle inhibited platelet aggregation induced by ADP. It did not destroy fibrinogen, Factor X, prothrombin and thrombin; nor did it induce fibrinolysis nor interfere with the interaction between thrombin and fibrinogen. It is concluded that the anticoagulant action of this phospholipase A was due to the inhibition of the activations of Factors X and II through the inactivation of the procoagulant activity of phospholipids mediated partly by phospholipid-binding activity of this venom enzyme and partly by its enzymatic hydrolysis of phospholipids.

Amino Acids↗
PubMed1979

Structural basis for the anticoagulant activity of heparin. 1. Relationship to the number of charged groups.

This study was undertaken to provide further information concerning the chemical heterogeneity of heparins and the relationships between the anticoagulant activity (USP assay) and the anionic density of the heparin. A sample of commercial heparin was fractionated into 13 fractions by sequential extraction in a two-phase system of 1-butanol-aqueous NaCl containing excess hexadecylpyridinium chloride. The anionic density distribution was characterized by the fractional distribution of uronate among the fractions. The fractions were characterized by several molar ratios of constituents, molecular weight, charge density, and anticoagulant activity in recalcified sheep plasma. The heparin was broadly distributed among the last 10 fractions; the first three contained impurities which were completely separated from the heparin fractions. The heparin fractions differ systematically in anionic density but are of substantially the same molecular weight. Anticoagulant activity increased markedly with anionic density, ranging from 81 units/mg for the heparin fraction with the lowest anionic density up to a high of 243 units/mg. The relationship between anticoagulant activity and either anionic density or its square is nonlinear. However, in the latter case an initial linear relationship was observed for anticoagulant activities of less than 200 units/mg.

Animals↗