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S M Bates

Publications and source records attributed to S M Bates.

At least 19 recordsLinked to original sources
PubMed2001

Clinical trials that have influenced the treatment of venous thromboembolism: a historical perspective.

In 1960, Barritt and Jordan performed the first randomized trial demonstrating the efficacy of anticoagulant therapy in the treatment of venous thromboembolism. Since then, important therapeutic advances have been made in the treatment of deep venous thrombosis and pulmonary embolism. This paper reviews the important clinical trials involving anticoagulant therapy and vena caval interruption. The studies are discussed from a historical perspective, and an attempt is made to analyze both the thought processes that prompted their design and the reasons why they changed practice.

Anticoagulants↗
PubMed2001

Use of a fixed activated partial thromboplastin time ratio to establish a therapeutic range for unfractionated heparin.

BACKGROUND: The commonly recommended therapeutic range for patients receiving unfractionated heparin of 1.5 to 2.5 times the control activated partial thromboplastin time (aPTT) is not universally applicable. It has been suggested that the therapeutic range for each aPTT reagent should be based on plasma heparin levels. We sought to identify an aPTT ratio that corresponds to therapeutic anti--factor Xa heparin levels for combinations of several reagents and coagulometers that are commonly used. METHODS: Citrated plasma was collected from 126 unselected patients receiving unfractionated heparin. Four automated coagulometers and 6 commercial aPTT reagents were used to measure the aPTT. Plasma anti--factor Xa levels were measured by means of a commercially available assay. The relationship between the aPTT results and anti-factor Xa heparin levels for each reagent-coagulometer combination was determined by linear regression analysis, and the aPTT results corresponding to therapeutic anti--factor Xa heparin levels were calculated. RESULTS: For all reagent-coagulometer combinations studied, an aPTT ratio of 1.5 resulted in anti--factor Xa heparin levels considerably below the lower limit of the therapeutic range. When the aPTT was performed on any of the coagulometers assessed with the use of Actin (Dade Diagnostics, Aguada, Puerto Rico) and IL Test (Instrumentation Laboratories, Fisher Scientific, Unionville, Ontario) reagents, aPTT ratios necessary to achieve therapeutic anti--factor Xa heparin levels approximated 2.0 to 3.5. CONCLUSION: For laboratories that cannot perform heparin levels, the use of less responsive reagents and any of the coagulometers studied, along with target aPTT ratio between 2.0 and 3.5, appears to be a reasonable alternative.

Antithrombin III↗
PubMed2001

A latex D-dimer reliably excludes venous thromboembolism.

BACKGROUND: D-Dimer, a cross-linked fibrin degradation product, has a high sensitivity in patients with suspected venous thrombosis. Traditional latex D-dimer assays, however, have not been sufficiently sensitive to exclude venous thromboembolism. METHODS: To determine the clinical utility of a latex D-dimer assay (MDA D-Dimer; Organon Teknika Corporation, Durham, NC) in patients with suspected venous thromboembolism, we conducted a retrospective cohort study involving 595 unselected patients at 4 tertiary care hospitals. Patients had blood drawn for performance of the D-dimer assay and underwent objective testing for venous thromboembolism. Pretest probability was determined using validated models in 571 patients. Patients were classified as venous thromboembolism positive or negative according to results of objective tests and 3-month follow-up. The sensitivities, specificities, predictive values, and negative likelihood ratios of the assay were calculated for all patients and for subgroups of patients with known cancer or a low, moderate, or high pretest probability of venous thromboembolism. RESULTS: The prevalence of venous thromboembolism was 19.0% (113/595). Of those who had a pretest probability assessment, 35.9% had a low pretest probability, 49.7% a moderate pretest probability, and 14.4% a high pretest probability. Using a discriminant value of 0.50 microg fibrinogen equivalent units per milliliter, the assay showed an overall sensitivity of 96%, a negative predictive value of 98%, a specificity of 45%, and a negative likelihood ratio of 0.09. In patients with a low or moderate pretest probability, the sensitivity, negative predictive value, and negative likelihood ratio were 97%, 99%, and 0.07, respectively. CONCLUSIONS: The MDA D-Dimer assay is the first latex agglutination assay with sufficient sensitivity to be clinically useful in the exclusion of venous thromboembolism. A negative result has the potential to be used as the sole test to exclude venous thromboembolism in patients with a low or moderate pretest probability of disease.

Female↗
PubMed2001

The prevalence of Chlamydia trachomatis infection in male undergraduates: a postal survey.

OBJECTIVES: To determine the prevalence of Chlamydia trachomatis infection in male undergraduates and to investigate whether prevalence increases with time spent at university. To investigate the feasibility of screening men for C trachomatis by self sampling and posting of urine specimens. METHODS: The study design was a postal survey undertaken by the Department of Genito-Urinary Medicine (GUM) and Student University Health Service (SUHS) in SHEFFIELD: 2607 male undergraduates from the SUHS patient list were invited to participate in the study by providing a first void urine specimen and posting it to the laboratory. The main outcome measure was the detection of C trachomatis infection. RESULTS: 758 students participated in the study, a response rate of 29.1%. Nine students (1.2%) tested positive for C trachomatis. The prevalence of infection in the first, second, and third year of study was 0.7%, 1.5%, and 1.6% of participants respectively. There was no statistically significant difference in prevalence of infection between first and third year students (chi(2) test, p = 0.32). However, students with chlamydia had a higher median age (Mann-Whitney U test, p < or = 0.05). Contact tracing identified four further cases of C trachomatis infection. CONCLUSION: Screening for C trachomatis infection by postal survey is feasible. However, the response rate in this study was poor and the estimated sample size was not reached. Therefore, it has not been possible to determine the true prevalence of infection in this population or to accurately assess changes in prevalence with time spent at university.

Adolescent↗
PubMed2000

Criteria for evaluating evidence that laboratory abnormalities are associated with the development of venous thromboembolism.

The identification of conditions associated with an increased risk of venous thromboembolism may indicate the need for aggressive prophylaxis during periods of high risk, prolonged anticoagulant therapy after an initial venous thromboembolic episode, the investigation of asymptomatic family members and the avoidance of oral contraceptives. Advances in laboratory medicine have led to the identification and assessment of many proteins responsible for normal hemostasis, and associations between abnormalities in a number of these proteins and venous thromboembolism have been reported. Without the ability to appraise this information critically, physicians may be unable to determine whether or how they should modify their clinical practice. Criteria for determining whether specific laboratory abnormalities have a relationship with venous thromboembolism are proposed here, and one example of the application of these guidelines is provided.

Anticoagulants↗
PubMed2000

Beyond heparin and aspirin: new treatments for unstable angina and non-Q-wave myocardial infarction.

The goals of therapy for unstable angina and non-Q-wave myocardial infarction (MI) are to maintain myocardial perfusion by inhibiting platelet aggregation and fibrin deposition at sites of plaque rupture, thereby preventing ongoing or new myocardial ischemia and cardiac death. Although aspirin and heparin sodium are cornerstones in the management of unstable angina and non-Q-wave MI, both have significant limitations that have prompted the development of new agents. The thienopyridines, ticlopidine hydrochloride and clopidogrel, appear to be at least as effective as aspirin in the management of unstable angina. Glycoprotein IIb/IIIa receptor antagonists are a new class of platelet inhibitors that are more potent than aspirin, because they target the final common pathway of platelet aggregation. Low-molecular-weight heparins provide a more stable pharmacodynamic response and are more convenient to use than unfractionated heparin. Direct thrombin inhibitors show promise for inhibiting thrombin-mediated platelet aggregation and fibrin deposition. We focus on the opportunities presented by these agents, detailing mechanisms of action, advantages over aspirin and heparin, and performance in recent clinical trials.

Angina, Unstable↗
PubMed2000

The mechanism of action of thrombin inhibitors.

Although heparin is widely used to treat arterial thrombosis, it has limitations in this setting. These limitations reflect heparin's inability to inactivate fibrin-bound thrombin, a major stimulus for thrombus growth, and the fact that heparin is neutralized by platelet factor 4, large quantities of which are released from platelets at the site of plaque rupture. Heparin also has a propensity to bind non-specifically to other plasma proteins. Because plasma levels of these heparin-binding proteins vary from patient to patient, the anticoagulant response to heparin is unpredictable and careful laboratory monitoring is necessary to ensure that an adequate anticoagulant effect is achieved. Direct thrombin inhibitors, such as bivalirudin and hirudin, overcome many of the limitations of heparin. These agents inhibit fibrin-bound thrombin, as well as fluid-phase thrombin. Direct thrombin inhibitors also produce a more predictable anticoagulant response than heparin because they do not bind to plasma proteins and are not neutralized by platelet factor 4. Bivalirudin appears to have a wider therapeutic window than hirudin. Because this may permit administration of higher doses of bivalirudin, this agent may also have an efficacy advantage over hirudin. Differences observed between hirudin and bivalirudin demonstrate that not all direct thrombin inhibitors have the same risk-benefit profile.

Angioplasty, Balloon, Coronary↗
PubMed1999

Prevention of activation of blood coagulation during acute coronary ischemic syndromes: beyond aspirin and heparin.

Many of the acute coronary ischemic syndromes are triggered by spontaneous or mechanical disruption of atherosclerotic plaques with resultant activation of platelets and coagulation. Given the central role of platelets and thrombin in arterial thrombosis, current strategies for its prevention and treatment focus on both inhibition of platelet aggregation and control of thrombin generation and activity. Although aspirin and unfractionated heparin are the cornerstones of current treatment strategies, both have limitations. This review will describe these limitations and discuss new antithrombotic agents developed for use in acute coronary ischemic syndromes and as adjuncts for percutaneous coronary revascularization procedures.

Anticoagulants↗
PubMed1999

Optimal management of pregnant women with acute venous thromboembolism.

Venous thromboembolism (VTE) is an important cause of obstetric morbidity and mortality. Its management during pregnancy is problematic because anticoagulants, the cornerstone of initial therapy for VTE, may have significant foetal as well as maternal side effects. Unfractionated heparin has been the anticoagulant of choice in pregnancy; however, there is growing clinical experience with low-molecular-weight heparin (LMWH) in this patient population. A recently published systematic review of the literature suggests that the use of LMWH during pregnancy is not associated with adverse foetal/infant outcomes. Moreover, its long-term use appears to be safe for the mother, as symptomatic osteoporosis, bleeding and heparin- induced thrombocytopenia occurred only infrequently. There are limited data regarding the efficacy of anticoagulant therapy in the treatment of VTE during pregnancy, and treatment recommendations have largely been extrapolated from data in non-pregnant patients and case series of pregnant patients. This paper will briefly review the challenges and areas of controversy associated with the use of anticoagulants in the treatment of pregnancy-associated VTE.

Female↗
PubMed1999

Anticoagulation in pregnancy.

The use of anticoagulants during pregnancy for prevention and treatment of venous thromboembolism and prevention of systemic embolism in patients with valvular heart disease presents several problems. This article discusses the complications associated with warfarin, unfractionated heparin, and low-molecular-weight heparin as well as the benefits of each. While a literature review turned up only limited data, the authors extrapolated from existing data recommendations for treatment during pregnancy, finding that oral warfarin should be replaced by heparin during pregnancy, especially from the 6th to the 12th week and near term. In addition, treatment recommendations are provided for different stages of pregnancy, delivery, and postpartum.

Anticoagulants↗
PubMed1998

Direct thrombin inhibitors for treatment of arterial thrombosis: potential differences between bivalirudin and hirudin.

Given the central role of thrombin in arterial thrombogenesis, most treatment strategies for acute coronary syndromes are aimed at inhibiting its generation or blocking its activity. Although heparin has been widely used, it has limitations in the setting of arterial thrombosis. These limitations reflect the inability of heparin to inactivate thrombin bound to fibrin, a major stimulus for thrombus growth. In addition, the anticoagulant response to heparin varies from patient to patient, and heparin is neutralized by platelet Factor IV, large quantities of which are released from platelets activated at sites of plaque rupture. Consequently, heparin requires careful laboratory monitoring to ensure an adequate anticoagulant effect. Direct thrombin inhibitors, such as hirudin and bivalirudin, overcome the limitations of heparin. These agents inhibit fibrin-bound thrombin, as well as fluid-phase thrombin, and produce a predictable anticoagulant response. Bivalirudin has both safety and potential efficacy advantages over hirudin. Bivalirudin appears to have a wider therapeutic window than hirudin, possibly because bivalirudin only transiently inhibits the active site of thrombin. The better safety profile of bivalirudin permits administration of higher doses, which may give it an efficacy advantage. Hirudin prevents thrombin from activating protein C, thereby suppressing this natural anticoagulant pathway. In contrast, bivalirudin may promote protein C activation by transiently inhibiting thrombin until it can be bound by thrombomodulin. Differences between bivalirudin and hirudin, as well as other direct thrombin inhibitors, highlight the pitfalls of considering all direct thrombin inhibitors to have equivalent risk-benefit profiles.

Acute Disease↗
PubMed1998

The new heparins.

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Clinical Trials as Topic↗