Academic literature on the topic 'Thrombosis; Anticoagulant drugs'
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Journal articles on the topic "Thrombosis; Anticoagulant drugs"
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Weitz, Jeffrey I., Saskia Middeldorp, William Geerts, and John A. Heit. "Thrombophilia and New Anticoagulant Drugs." Hematology 2004, no. 1 (January 1, 2004): 424–38. http://dx.doi.org/10.1182/asheducation-2004.1.424.
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Abstract Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, is the result of an imbalance among procoagulant, anticoagulant and profibrinolytic processes. This imbalance reflects a complex interplay between genetic and environmental or acquired risk factors. Genetic thrombophilic defects influence the risk of a first episode of thrombosis. How these defects influence the risk of recurrence in patients whose first episode of venous thromboembolism was unprovoked is less certain. Thus, when anticoagulants are stopped, patients with unprovoked venous thromboembolism have a risk of recurrence of at least 7% to 10% per year, even in the absence of an underlying thrombophilic defect. Consequently, there is a trend toward longer durations of anticoagulation therapy for these patients, which is problematic given the limitation of existing anticoagulants. This chapter provides an overview of the thrombophilic defects and how they influence the risk of venous thromboembolism. The chapter also details advances in anticoagulant therapy, focusing on new inhibitors of factor Xa and thrombin. In Section I, Dr. Saskia Middeldorp describes the various thrombophilic defects and reviews their relative importance in the pathogenesis of a first episode of venous thromboembolism. She then discusses the influence of these defects on the risk of recurrent thrombotic events in patients with unprovoked venous thromboembolism and in those whose thrombosis occurred in association with a known risk factor, such as surgery. In Section II, Dr. William Geerts reviews the pharmacology of new parenteral and oral factor Xa inhibitors and describes the results of the Phase II and III clinical trials with these agents. He then provides perspective on the potential advantages and drawbacks of these drugs for the prevention and treatment of venous thromboembolism. In Section III, Dr. John Heit focuses on direct thrombin inhibitors. He discusses their mechanism of action and compares and contrasts their pharmacological profiles prior to describing the results of Phase II and III clinical trials. Dr. Heit then provides perspective on the potential advantages and limitations of these drugs relative to existing anticoagulants.
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Kumano, Osamu, Kohei Akatsuchi, and Jean Amiral. "Updates on Anticoagulation and Laboratory Tools for Therapy Monitoring of Heparin, Vitamin K Antagonists and Direct Oral Anticoagulants." Biomedicines 9, no. 3 (March 7, 2021): 264. http://dx.doi.org/10.3390/biomedicines9030264.
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Anticoagulant drugs have been used to prevent and treat thrombosis. However, they are associated with risk of hemorrhage. Therefore, prior to their clinical use, it is important to assess the risk of bleeding and thrombosis. In case of older anticoagulant drugs like heparin and warfarin, dose adjustment is required owing to narrow therapeutic ranges. The established monitoring methods for heparin and warfarin are activated partial thromboplastin time (APTT)/anti-Xa assay and prothrombin time – international normalized ratio (PT-INR), respectively. Since 2008, new generation anticoagulant drugs, called direct oral anticoagulants (DOACs), have been widely prescribed to prevent and treat several thromboembolic diseases. Although the use of DOACs without routine monitoring and frequent dose adjustment has been shown to be safe and effective, there may be clinical circumstances in specific patients when measurement of the anticoagulant effects of DOACs is required. Recently, anticoagulation therapy has received attention when treating patients with coronavirus disease 2019 (COVID-19). In this review, we discuss the mechanisms of anticoagulant drugs—heparin, warfarin, and DOACs and describe the methods used for the measurement of their effects. In addition, we discuss the latest findings on thrombosis mechanism in patients with COVID-19 with respect to biological chemistry.
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Srinivasan, Divyamani, and Bree Watzak. "Anticoagulant Use in Real Time." Journal of Pharmacy Practice 26, no. 3 (November 25, 2012): 270–79. http://dx.doi.org/10.1177/0897190012465950.
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Venous thromboembolism (VTE) encompasses deep vein thrombosis (DVT) and pulmonary embolism (PE). Each year, VTE affects about 300 000 to 600 000 people in the United States, and death is the first manifestation in one-fourth of this population.1{Beckman, 2010 #79} Moreover, approximately 10% of the US population has genetic factors that increase their risk for developing thrombosis.1 In addition to inherited disorders, factors that contribute to VTE include prolonged immobilization, trauma, surgery, cancer, and critically ill patients.2 Routine assessment and prophylaxis are recommended in these groups to avoid DVT-related complications.2 Anticoagulants are the mainstay of drugs used in DVT/PE prevention and treatment. Despite the availability of evidence-based guidelines for anticoagulant therapy, there is suboptimal implementation of DVT prophylaxis in hospitalized patients.3 All anticoagulants are “high-alert” drugs, and judicious use is mandatory to prevent bleeding complications.4 This review discusses treatment guidelines, monitoring, side effects, and reversal agents available for some anticoagulant drugs approved for VTE. Dissemination of the knowledge via pharmacy education programs significantly improves the adherence to VTE prophylaxis.5 Understanding the clinical aspects of anticoagulant dispensing as presented in this review is hoped to facilitate implementation of the theoretical knowledge as well as evidence-based guidelines in order to maximize patient benefit.
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Konkle, Barbara A. "Monitoring target-specific oral anticoagulants." Hematology 2014, no. 1 (December 5, 2014): 329–33. http://dx.doi.org/10.1182/asheducation-2014.1.329.
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Abstract Target-specific oral anticoagulants are approved for use for the prevention of stroke in atrial fibrillation and for the prevention and treatment of venous thrombosis without the need for laboratory monitoring. However, there are clinical settings in which laboratory measurement of anticoagulant effect is needed. These may include patients with life-threatening bleeding or those requiring emergency surgery, in the setting of renal or hepatic failure, or patients with thrombosis on therapy. This chapter reviews the use of laboratory testing to assess the anticoagulant effect of these drugs. In addition, because these drugs can interfere with other laboratory testing, available data on these interactions are presented.
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Liesdek, Omayra C. D., Rolf T. Urbanus, Linda M. de Heer, Kathelijn Fischer, Willem J. L. Suyker, and Roger E. G. Schutgens. "Alternatives for Vitamin K Antagonists as Thromboprophylaxis for Mechanical Heart Valves and Mechanical Circulatory Support Devices: A Systematic Review." Seminars in Thrombosis and Hemostasis 47, no. 06 (May 31, 2021): 724–34. http://dx.doi.org/10.1055/s-0041-1722846.
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AbstractThe holy grail of anticoagulation in patients with intracardiac devices, such as mechanical heart valves (MHVs) and left ventricular assist devices (LVADs), comprises safe prevention of thrombosis without interrupting normal hemostasis. Device-induced thrombosis and anticoagulant-related bleeding problems are dreaded complications that may cause a significantly reduced quality of life and increased morbidity and mortality. Vitamin K antagonists are the current standard for oral anticoagulation therapy in patients with MHVs and LVADs. Even within the therapeutic range, hemorrhage is the primary complication of these drugs, which emphasizes the need for safer anticoagulants for the prevention of device-induced thrombosis. Device-induced thrombosis is a complex multifactorial phenomenon that likely requires anticoagulant therapy targeting multiple pathways. Here, we review the preclinical and clinical data describing the efficacy of a variety of anticoagulants as thromboprophylaxis after implantation of intracardiac devices.
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Ansell, Jack E., Jeffrey I. Weitz, and Anthony J. Comerota. "Advances in Therapy and the Management of Antithrombotic Drugs for Venous Thromboembolism." Hematology 2000, no. 1 (January 1, 2000): 266–84. http://dx.doi.org/10.1182/asheducation.v2000.1.266.20000266.
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This review focuses on antithrombotic therapy for venous thromboembolism and covers a diverse range of topics including a discussion of emerging anticoagulant drugs, a renewed focus on thrombolytic agents for selected patients, and an analysis of the factors leading to adverse events in patients on warfarin, and how to optimize therapy. In Section I Dr. Weitz discusses new anticoagulant drugs focusing on those that are in the advanced stages of development. These will include drugs that (a) target factor VIIa/tissue factor, including tissue factor pathway inhibitor and NAPc2; (b) block factor Xa, including the synthetic pentasaccharide and DX9065a; (c) inhibit factors Va and VIIIa, i.e., activated protein C; and (d) block thrombin, including hirudin, argatroban, bivalirudin and H376/95. Oral formulations of heparin will also be reviewed.In Section II, Dr. Comerota will discuss the use of thrombolysis for selected patients with venous thromboembolism. Fibrinolytic therapy, which has suffered from a high risk/benefit ratio for routine deep venous thrombosis, may have an important role to play in patients with iliofemoral venous thrombosis. Dr. Comerota presents his own results with catheter-directed thrombolytic therapy and the results from a large national registry showing long-term outcomes and the impact on quality of life.In Section III, Dr. Ansell presents a critical analysis of the factors responsible for adverse events with oral anticoagulants and the optimum means of improving outcomes. The poor status of present day anticoagulant management is reviewed and the importance of achieving a high rate of “time in therapeutic range,” is emphasized. Models of care to optimize outcomes are described, with an emphasis on models that utilize patient self-testing and patient self-management of oral anticoagulation which are considered to be the ultimate in anticoagulation care. The treatment of venous and arterial thromboembolism is undergoing rapid change with respect to the development of new antithrombotic agents, an expanding list of new indications, and new methods of drug delivery and management. In spite of these changes, many of the traditional therapeutics are still with us and continue to play a vital role in the treatment of thromboembolic disease. The following discussion touches on a wide range of therapeutic interventions, from old to new, exploring the status of anticoagulant drug development, describing a new intervention for iliofemoral venous thrombosis, and analyzing the critical factors for safe and effective therapy with oral anticoagulants.
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Ansell, Jack E., Jeffrey I. Weitz, and Anthony J. Comerota. "Advances in Therapy and the Management of Antithrombotic Drugs for Venous Thromboembolism." Hematology 2000, no. 1 (January 1, 2000): 266–84. http://dx.doi.org/10.1182/asheducation.v2000.1.266.266.
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Abstract This review focuses on antithrombotic therapy for venous thromboembolism and covers a diverse range of topics including a discussion of emerging anticoagulant drugs, a renewed focus on thrombolytic agents for selected patients, and an analysis of the factors leading to adverse events in patients on warfarin, and how to optimize therapy. In Section I Dr. Weitz discusses new anticoagulant drugs focusing on those that are in the advanced stages of development. These will include drugs that (a) target factor VIIa/tissue factor, including tissue factor pathway inhibitor and NAPc2; (b) block factor Xa, including the synthetic pentasaccharide and DX9065a; (c) inhibit factors Va and VIIIa, i.e., activated protein C; and (d) block thrombin, including hirudin, argatroban, bivalirudin and H376/95. Oral formulations of heparin will also be reviewed. In Section II, Dr. Comerota will discuss the use of thrombolysis for selected patients with venous thromboembolism. Fibrinolytic therapy, which has suffered from a high risk/benefit ratio for routine deep venous thrombosis, may have an important role to play in patients with iliofemoral venous thrombosis. Dr. Comerota presents his own results with catheter-directed thrombolytic therapy and the results from a large national registry showing long-term outcomes and the impact on quality of life. In Section III, Dr. Ansell presents a critical analysis of the factors responsible for adverse events with oral anticoagulants and the optimum means of improving outcomes. The poor status of present day anticoagulant management is reviewed and the importance of achieving a high rate of “time in therapeutic range,” is emphasized. Models of care to optimize outcomes are described, with an emphasis on models that utilize patient self-testing and patient self-management of oral anticoagulation which are considered to be the ultimate in anticoagulation care. The treatment of venous and arterial thromboembolism is undergoing rapid change with respect to the development of new antithrombotic agents, an expanding list of new indications, and new methods of drug delivery and management. In spite of these changes, many of the traditional therapeutics are still with us and continue to play a vital role in the treatment of thromboembolic disease. The following discussion touches on a wide range of therapeutic interventions, from old to new, exploring the status of anticoagulant drug development, describing a new intervention for iliofemoral venous thrombosis, and analyzing the critical factors for safe and effective therapy with oral anticoagulants.
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Jain, Nishank, and Robert F. Reilly. "Clinical Pharmacology of Oral Anticoagulants in Patients with Kidney Disease." Clinical Journal of the American Society of Nephrology 14, no. 2 (May 25, 2018): 278–87. http://dx.doi.org/10.2215/cjn.02170218.
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Oral anticoagulants are commonly used drugs in patients with CKD and patients with ESKD to treat atrial fibrillation to reduce stroke and systemic embolism. Some of these drugs are used to treat or prevent deep venous thrombosis and pulmonary embolism in patients with CKD who undergo knee and hip replacement surgeries. Warfarin is the only anticoagulant that is approved for use by the Food and Drug Administration in individuals with mechanical heart valves. Each oral anticoagulant affects the coagulation profile in the laboratory uniquely. Warfarin and apixaban are the only anticoagulants that are Food and Drug Administration approved for use in patients with CKD and patients with ESKD. However, other oral anticoagulants are commonly used off label in this patient population. Given the acquired risk of bleeding from uremia, these drugs are known to cause increased bleeding events, hospitalization, and overall morbidity. Each anticoagulant has unique pharmacologic properties of which nephrologists need to be aware to optimally manage patients. In addition, nephrologists are increasingly asked to aid in the management of adverse bleeding events related to oral anticoagulant use in patients with CKD and patients with ESKD. This article summarizes the clinical pharmacology of these drugs and identifies knowledge gaps in the literature related to their use.
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Nieto, Elena, Marcelo Suarez, Ángela Roco, Juan Carlos Rubilar, Francisca Tamayo, Mario Rojo, Gabriel Verón, et al. "Anticoagulation Management With Coumarinic Drugs in Chilean Patients." Clinical and Applied Thrombosis/Hemostasis 25 (January 1, 2019): 107602961983434. http://dx.doi.org/10.1177/1076029619834342.
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Warfarin and acenocoumarol are used in various cardiovascular disorders to improve the prognosis of patients with thromboembolic disease. However, there is a lack of substantial efficacy and safety data on antithrombotic prophylaxis in several countries, particularly in Latin America. The aim of this study was to provide information about the efficacy of anticoagulants in Chilean patients. Data were collected from databases of the Western Metropolitan Health Service, Santiago, Chile. We identified 6280 records of patients receiving anticoagulant treatment. The three most common diagnoses were rhythm disorder (43.7%), venous thrombosis (22%), and valvular prosthesis (10.7%). The majority of patients (98.5%) received acenocoumarol while 1.5% of patients received warfarin, at weekly therapeutic doses of 13.6 mg and 30.4 mg, respectively. For total diagnoses, the median time in the therapeutic range was 50%. However, better results, 66.7%, were observed when a telemedicine strategy was used only in Santiago Province. Our findings emphasize that in Chile, where the number of patients receiving anticoagulant treatment increases every year, telemedicine, by committed teams, improves the use of oral anticoagulants and is able to increase quality indicators of anticoagulant treatment care.
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Fredenburgh, James C., and Jeffrey I. Weitz. "Factor XI as a Target for New Anticoagulants." Hämostaseologie 41, no. 02 (April 2021): 104–10. http://dx.doi.org/10.1055/a-1384-3715.
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AbstractDespite advances in anticoagulant therapy, thrombosis remains the leading cause of morbidity and mortality worldwide. Heparin and vitamin K antagonists (VKAs), the first anticoagulants to be used successfully for the prevention and treatment of thrombosis, are associated with a risk of bleeding. These agents target multiple coagulation factors. Thus, by activating antithrombin, heparin mainly inhibits factor Xa and thrombin, whereas VKAs lower the levels of the vitamin K–dependent clotting factors. Direct oral anticoagulants, which have replaced VKAs for many indications, inhibit only factor Xa or thrombin. Although the direct oral anticoagulants are associated with less bleeding than VKAs, bleeding remains their major side effect. Epidemiological and animal studies have identified factor XI as a target for potentially safer anticoagulant drugs because factor XI deficiency or inhibition protects against thrombosis and is associated with little or no bleeding. Several factor XI–directed strategies are currently under investigation. This article (1) reviews the rationale for the development of factor XI inhibitors, (2) identifies the agents in most advanced stages of development, (3) describes the results of completed clinical trials and provides a summary of those underway, and (4) highlights the opportunities and challenges for this next generation of anticoagulants.
Dissertations / Theses on the topic "Thrombosis; Anticoagulant drugs"
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Glossop, Paul. "Thrombin inhibition." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244533.
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Bouchnita, Anass. "Mathematical modelling of blood coagulation and thrombus formation under flow in normal and pathological conditions." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSE1300/document.
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Cette thèse est consacrée à la modélisation mathématique de la coagulation sanguine et de la formation de thrombus dans des conditions normales et pathologiques. La coagulation sanguine est un mécanisme défensif qui empêche la perte de sang suite à la rupture des tissus endothéliaux. C'est un processus complexe qui est règlementé par différents mécanismes mécaniques et biochimiques. La formation du caillot sanguin a lieu dans l'écoulement sanguin. Dans ce contexte, l'écoulement à faible taux de cisaillement stimule la croissance du caillot tandis que la circulation sanguine à fort taux de cisaillement la limite. Les désordres qui affectent le système de coagulation du sang peuvent provoquer différentes anomalies telles que la thrombose (coagulation exagérée) ou les saignements (insuffisance de coagulation). Dans la première partie de la thèse, nous présentons un modèle mathématique de coagulation sanguine. Le modèle capture la dynamique essentielle de la croissance du caillot dans le plasma et le flux sanguin quiescent. Ce modèle peut être réduit à un modèle qui consiste en une équation de génération de thrombine et qui donne approximativement les mêmes résultats. Nous avons utilisé des simulations numériques en plus de l'analyse mathématique pour montrer l'existence de différents régimes de coagulation sanguine. Nous spécifions les conditions pour ces régimes sur différents paramètres pathophysiologiques du modèle. Ensuite, nous quantifions les effets de divers mécanismes sur la croissance du caillot comme le flux sanguin et l'agrégation plaquettaire. La partie suivante de la thèse étudie certaines des anomalies du système de coagulation sanguine. Nous commençons par étudier le développement de la thrombose chez les patients présentant une carence en antihrombine ou l'une des maladies inflammatoires. Nous déterminons le seuil de l'antithrombine qui provoque la thrombose et nous quantifions l'effet des cytokines inflammatoires sur le processus de coagulation. Puis, nous étudions la compensation de la perte du sang après un saignement en utilisant un modèle multi-échelles qui décrit en particulier l'érythropoïèse et la production de l'hémoglobine. Ensuite, nous évaluons le risque de thrombose chez les patients atteints de cancer (le myélome multiple en particulier) et le VIH en combinant les résultats du modèle de coagulation sanguine avec les produits des modèles hybrides (discret-continues) multi-échelles des systèmes physiologiques correspondants. Finalement, quelques applications cliniques possibles de la modélisation de la coagulation sanguine sont présentées. En combinant le modèle de formation du caillot avec les modèles pharmacocinétiques pharmacodynamiques (PK-PD) des médicaments anticoagulants, nous quantifions l'action de ces traitements et nous prédisons leur effet sur des patients individuelsThis thesis is devoted to the mathematical modelling of blood coagulation and clot formation under flow in normal and pathological conditions. Blood coagulation is a defensive mechanism that prevents the loss of blood upon the rupture of endothelial tissues. It is a complex process that is regulated by different mechanical and biochemical mechanisms. The formation of the blood clot takes place in blood flow. In this context, low-shear flow stimulates clot growth while high-shear blood circulation limits it. The disorders that affect the blood clotting system can provoke different abnormalities such thrombosis (exaggerated clotting) or bleeding (insufficient clotting). In the first part of the thesis, we introduce a mathematical model of blood coagulation. The model captures the essential dynamics of clot growth in quiescent plasma and blood flow. The model can be reduced to a one equation model of thrombin generation that gives approximately the same results. We used both numerical simulations and mathematical investigation to show the existence of different regimes of blood coagulation. We specify the conditions of these regimes on various pathophysiological parameters of the model. Then, we quantify the effects of various mechanisms on clot growth such as blood flow and platelet aggregation. The next part of the thesis studies some of the abnormalities of the blood clotting system. We begin by investigating the development of thrombosis in patients with antihrombin deficiency and inflammatory diseases. We determine the thrombosis threshold on antithrombin and quantify the effect of inflammatory cytokines on the coagulation process. Next, we study the recovery from blood loss following bleeding using a multiscale model which focuses on erythropoiesis and hemoglobin production. Then, we evaluate the risk of thrombosis in patients with cancer (multiple myeloma in particular) and HIV by combining the blood coagulation model results with the output of hybrid multiscale models of the corresponding physiological system. Finally, possible clinical applications of the blood coagulation modelling are provided. By combining clot formation model with pharmacokinetics-pharmacodynamics (PK-PD) models of anticoagulant drugs, we quantify the action of these treatments and predict their effect on individual patients
Books on the topic "Thrombosis; Anticoagulant drugs"
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Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York: Oxford University Press, 2006.
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Becker, Richard C. Fibrinolytic and antithrombotic therapy: Theory, practice, and management. 2nd ed. New York, NY: Oxford University Press, 2005.
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, and Johannes de Vos. Haemostasis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199683307.003.0010.
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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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Provan, Drew, Trevor Baglin, Inderjeet Dokal, Johannes de Vos, and Angela Theodoulou. Haemostasis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199683307.003.0010_update_001.
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Assessing haemostasis - The coagulation system - Laboratory tests - Platelets - Bleeding - Bleeding: laboratory investigations - Bleeding: therapeutic products - von Willebrand disease - Haemophilia A and B - Rare congenital coagulation disorders - Congenital thrombocytopenias - Congenital platelet function defects - Congenital vascular disorders - Haemorrhagic disease of the newborn - Thrombocytopenia (acquired) - Specific thrombocytopenic syndromes - Disseminated intravascular coagulation - Liver disease - Renal disease - Acquired anticoagulants and inhibitors - Treatment of spontaneous FVIII inhibitor - Acquired disorders of platelet function - Henoch–Schönlein purpura - Perioperative bleeding and massive blood loss - Massive blood loss - Heparin - Heparin induced thrombocytopenia/with thrombosis (HIT/T) - Oral anticoagulant therapy (warfarin, VKAs) - New oral anticoagulant drugs - Thrombosis - Risk assessment and thromboprophylaxis - Example of VTE risk assessment - Heritable thrombophilia - Acquired thrombophilia - Thrombotic thrombocytopenic purpura (TTP) - Haemolytic uraemic syndrome (HUS) - Heparin-induced thrombocytopenia (HIT)
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Valentin, Fuster, and Verstraete M, eds. Thrombosis in cardiovascular disorders. Philadelphia: Saunders, 1992.
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Thrombosis in cardiovascular diseases. Philadelphia: Saunders, 1992.
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Frost & Sullivan., ed. U.S. thrombosis markets: Anticoagulants, antithrombotics, and thrombolytics : new drugs, new indications expand market. Silicon Valley, Mountain View, CA (2525 Charleston Rd., Mountain View, 94043): Frost & Sullivan, 1994.
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Wijdicks, Eelco F. M., and Sarah L. Clark. Anticoagulation and Reversal Drugs. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190684747.003.0007.
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Management of anticoagulation, is a common practice. This chapter discusses best approaches, heparin choices, and safety issues. Anticoagulation is required in immobilized patients in the neurosciences intensive care unit to prevent deep venous thrombosis and the more consequential pulmonary embolus. There are very few strong indications for anticoagulation in ischemic stroke and exceptions are discussed. Reversal of anticoagulation is also needed in some patients and certainly in patients with recent significant trauma or spontaneous hemorrhages. Current reversal protocols require intravenous vitamin K, fresh-frozen plasma, and more often, prothrombin complex concentrate. Reversal of the effect of the direct oral anticoagulants is more difficult but options are discussed.
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Stanworth, Simon, and Stuart McKechnie. Pathophysiology of disordered coagulation. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0269.
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Imbalances in the regulation of haemostasis may manifest as bleeding (depletion of pro-coagulant factors) or thrombosis (deficiency of anti-coagulants). Disordered haemostasis is common in critically-ill patients and may result from infection, trauma, haemorrhage, inflammation, organ dysfunction (notably renal and liver dysfunction), or drug therapy. Complex patterns of coagulopathy where both bleeding and prothrombotic tendencies co-exist are well recognized in critical illness. The limitations of standard laboratory coagulation tests to predict bleeding risk, including activated partial thromboplastin time and prothrombin time, are well recognized. These assays were developed for diagnosis of inherited bleeding disorders or for monitoring of anticoagulant therapy. This has led to increased interest in global haemostatic tests, such as viscoelastic and thrombin generation tests. Thromboembolism is an important cause of morbidity and mortality in critically-ill patients. While inherited causes of bleeding appear to be often related to single gene abnormalities, thrombotic tendencies appear to reflect more complex interactions between inherited and acquired factors. Many interactions exist between coagulation pathways and inflammation. Systemic inflammation triggers widespread activation of coagulation, with pro-inflammatory cytokines activating pro-coagulant pathways and downregulating anticoagulant pathways. A net result of this interaction between inflammatory and coagulation pathways in sepsis is thrombin generation, intravascular fibrin deposition and a consumptive coagulopathy.
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Frost & Sullivan., ed. European thrombotic drug markets: Cost containment pressures intensify the competitive environment. Mountain View, Calif: Frost & Sullivan, 1995.
Find full textBook chapters on the topic "Thrombosis; Anticoagulant drugs"
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"Overview of New Anticoagulant Drugs." In New Therapeutic Agents in Thrombosis and Thrombolysis, 155–76. CRC Press, 2016. http://dx.doi.org/10.3109/9781420069242-14.
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Weitz, Jeffrey, and Jack Hirsh. "Overview of New Anticoagulant Drugs." In New Therapeutic Agents In Thrombosis And Thrombolysis, Revised And Expanded. Informa Healthcare, 2002. http://dx.doi.org/10.1201/9780203909317.pt2.
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"Overview of New Anticoagulant Drugs." In New Therapeutic Agents In Thrombosis And Thrombolysis, Revised And Expanded, 78–91. CRC Press, 2002. http://dx.doi.org/10.3109/9780203909317-7.
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"Commonly used anticoagulant and antiplatelet drugs." In Thrombosis in Clinical Practice, 33–59. CRC Press, 2005. http://dx.doi.org/10.3109/9780203640357-4.
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Mazzeffi, Michael, and Ashleigh Lowery. "Anticoagulation Options." In Coronary and Cardiothoracic Critical Care, 474–98. IGI Global, 2019. http://dx.doi.org/10.4018/978-1-5225-8185-7.ch022.
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There are multiple indications for anticoagulation in the cardiac surgery intensive care unit including cardiac valve replacement, mechanical circulatory pumps (ECMO and ventricular assist devices), deep vein thrombosis prophylaxis, treatment of heparin-induced thrombocytopenia, and treatment of other thrombotic conditions including pulmonary embolism. Anticoagulant medications broadly fall into two categories: antiplatelet drugs and inhibitors of protein clotting factors. In this chapter we will review anticoagulant medications, therapeutic drug monitoring, common indications for anticoagulation, and the risks associated with anticoagulation after cardiac surgery.
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Verheugt, Freek. "Thrombosis." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Heinz Drexel and Massimo Francesco Piepoli, 59–68. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0004.
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Blood coagulation plays a role in the pathogenesis of acute and chronic vascular disease. Acute myocardial infarction is generally associated with partial or complete thrombotic occlusion of one of the coronary arteries, whereas embolic stroke usually is associated with clot formation in the left atrium, left ventricle, or carotid arteries. Arteries in the lower extremities may get occluded by thrombosis, leading to ischaemia or amputation. Finally, venous thromboembolism is mainly caused by thrombus formation in the veins of the pelvis and/or the legs. This chapter deals with the effectiveness and safety of antiplatelet and anticoagulant drugs in primary and secondary prevention of cardiovascular disease.
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Verheugt, Freek. "Thrombosis." In The ESC Handbook on Cardiovascular Pharmacotherapy, edited by Heinz Drexel and Massimo Francesco Piepoli, 59–68. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198759935.003.0004_update_001.
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Blood coagulation plays a role in the pathogenesis of acute and chronic vascular disease. Acute myocardial infarction is generally associated with partial or complete thrombotic occlusion of one of the coronary arteries, whereas embolic stroke usually is associated with clot formation in the left atrium, left ventricle, or carotid arteries. Arteries in the lower extremities may get occluded by thrombosis, leading to ischaemia or amputation. Finally, venous thromboembolism is mainly caused by thrombus formation in the veins of the pelvis and/or the legs. This chapter deals with the effectiveness and safety of antiplatelet and anticoagulant drugs in primary and secondary prevention of cardiovascular disease.
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Mannucci, Pier Mannuccio. "An overview of haemostasis, in relation to atherothrombotic, thromboembolic, and venous cardiovascular disease." In ESC CardioMed, edited by Raffaele DeCaterina, 239–43. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0046.
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Haemostasis, a physiological mechanism employed by the human body to stop bleeding when a vessel wall is severed, results from complex interactions between the vessel wall, blood platelets, coagulation, and fibrinolysis proteins. Haemostasis is regulated by such naturally occurring biological systems as anticoagulant proteins and fibrinolysis that limit the formation of blood clots at the level of the injured blood vessel and help to avoid the formation of intravascular thrombi. Arterial thrombosis and venous thrombosis, the causes of the most frequent cardiovascular diseases (acute coronary syndromes, non-valvular atrial fibrillation, ischaemic stroke, and venous thromboembolism) are the consequences of dysregulated haemostasis in the wrong place. Heightened platelet reactions are the main mechanism of arterial thrombosis, in association with a damaged arterial wall, but hypercoagulability also plays an important role, particularly in acute coronary syndromes. These cooperative mechanisms explain why in the latter mechanism, antiplatelet and anticoagulant drugs are often used in association. Venous thromboembolism is mechanistically explained not only by the onset of blood flow stasis, but also by a hypercoagulable state (thrombophilia) due to gain of function of some coagulation factors and, less often, by genetic deficiencies or dysfunctions of naturally occurring anticoagulant proteins. Blood stasis and thrombus formation in the asystolic left atrium is also the main mechanism of systemic thromboembolism in atrial fibrillation. Accordingly, drugs that inhibit coagulation are the mainstay of primary and secondary prophylaxis of venous thromboembolism and the primary prevention of systemic embolization in patients with non-valvular atrial fibrillation.
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Waldmann, Carl, Andrew Rhodes, Neil Soni, and Jonathan Handy. "Haematological drugs." In Oxford Desk Reference: Critical Care, 235–43. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198723561.003.0015.
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This chapter discusses haematological drugs and includes discussion on anticoagulants and heparin-induced thrombocytopenia (including unfractionated heparin, low-molecular weight heparins, danaparoid, coumarins, synthetic pentasaccharides, the direct oral anticoagulants, and thromboprophylaxis in critical care patients), thrombolysis (definition of thrombolysis, physiology of fibrinolysis, contraindications to thrombolysis, factors influencing a successful outcome, myocardial infarction, acute limb ischaemia, and pulmonary embolism), and antifibrinolytics (describing the efficacy of tranexamic acid in reducing traumatic bleeding, the efficacy of tranexamic acid in reducing surgical bleeding, and the efficacy of tranexamic acid in postpartum haemorrhage).
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Becker, Richard C., and Frederick A. Spencer. "Anticoagulants." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0040.
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Anticoagulant therapy, particularly when used in combination with fibrinolytics and less often platelet antagonists, can cause life-threatening hemorrhage. This supports the importance of coagulation proteases in several phases of thrombus development; paradoxically, several anticoagulants can also cause microvascular and macrovascular thrombotic disorders. Hemorrhage is the most common adverse effect associated with warfarin administration. To predict the risk of bleeding, Beyth and colleagues (1998) developed a 5-point scoring system, with 1 point given for each of the following: . . . • Age greater than 65 . . . . . . • History of stroke . . . . . . • History of gastrointestinal bleeding . . . . . . • Specific comorbid conditions (recent myocardial infarction [MI], elevated serum creatinine, hematocrit <30%, or diabetes) . . . Low-risk patients have a score of 0; intermediate-risk patients, 1 or 2; and high-risk, 3 or 4. The risk of bleeding in these three groupings at 12 months was 3%, 8%, and 30%, respectively. Many commonly used medications have significant interactions with warfarin. In 1994, Wells and colleagues (1994) reviewed all reports of warfarin–drug interactions and found original reports totaling 186. Potentiation of warfarin effect was observed with six antibiotics, five cardiac drugs, two antiinflammatory agents, two histamine2-blockers, and alcohol in persons with concomitant liver disease. Inhibition of warfarin effect was noted with three antibiotics, three central nervous system (CNS) drugs, cholestyramine, and sucralfate. An important interaction between acetaminophen and warfarin has also been recognized (Hylek et al., 1998), and certain herbal remedies, such as ginkgo biloba, ginseng, and garlic, may enhance the effects of warfarin. The first step in the management of bleeding is to stop the drug; however, recovery of clotting factor levels may take several days, depending upon the vitamin K content of the patient’s diet and rate of intrinsic metabolism. To rapidly raise coagulant factor concentrations in patients with life-threatening hemorrhage, clotting factor concentrates are given (Makris et al., 1997). The older concentrates were plasma-derived and consisted mainly of activated prothrombin complex factors. They had the disadvantages of thrombogenicity and potential for transmission of infectious agents.
Conference papers on the topic "Thrombosis; Anticoagulant drugs"
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Day, H. J., R. Cherrey, D. O'Hara, and J. Carabello. "INCIDENCE OF PROCAINAMIDE-INDUCED LUPUS ANTICOAGULANT." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644241.
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Isolated cases of lupus anticoagulants (LA) in association with procainamide have been reported. This study was done to estimate the frequency of LA in patients taking procainamide. Two groups of patients were evaluated: Group A: 110 hospitalized patients (84 males, 26 females, ages 51-78, mean age 74.3) and Group B: 80 ambulatory patients (54 males, 26 females, ages 36-89, mean 67.5 years). The latter group of patients was on this drug for a period of two-five years, while the former group hadbeen on drug at least two full days. All patients were screened with baseline laboratory data including activated partial thromboplastin time (APTT) and prothrombin time (PT) which were performed using Auto APTT® and Simplastin® on a Coagulamate X2® (General Diagnostics/Organon Teknika). Patients taking drugs known to alter the APTT and PT were excluded. All patients were followed with daily (hospital patients) or weekly (ambulatory patients) APTT and PT. Prolongation of the APTT of 5 sec or PT of 3 sec over baseline was considered as a positive LA screening test. Patients with a positive screening test were further evaluated with tissue thromboplastin inhibitor assay (TTI), platelet neutralization procedure (PNP, anti-nuclear antibodies (ANA) and blood serology (RPR). In Group A. 11 out of 110 (1096) developed prolonged APTT while on procainamide . Of these, 9 developed abnormal TTI and 2 had positive PNP. The ANA was positive (titers of 1:320-1:2560) in 10 patients with the only positive RPR test, being in the patient with the highest ANA titer. In Group B, 12 out of 80 (1596) developed prolonged APTT, 11 had positive TTI. The ANA titer was elevated in all positive cases, although one patient's titer was 1:30. The PNP was positive in 1/12. All blood serologies were negative in this group. The difference in incidence between Groups A and B may reflect longer exposure to drug in the latter group. This difference is not statistically significant. This study indicates that the incidence of procainamide-induced lupus antocoagulant is between 10-1596 when the APTT (or PT) is used as a screening test. The TTI and ANA seem to have equal sensitivity in this syndrome when taking this drug. The failure of the PNP to be sensitive to LA may be due to the minimal prolongation of the APTT arbitrarily chosen as representing a positive screening test.
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Rouvier, J., H. Vidal, J. Gallino, M. Boccia, A. Scazziota, and R. Altman. "ACUTE INTERRUPTION OF ORAL ANTICOAGULANT THERAPY: A THROMBOTIC RISK?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643265.
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It is still on discussion how oral anticoagulant therapy must be interrupted. A progressive diminution of drug intake have been proposed in order to avoid a MreboundM of vitamin K-dependent procoagulant factors. At the present, it is well known that coumarin drugs affect not only the biologic activity of factors II, VII, IX and X but also Protein C (PC), an inhibitor of coagulation kinetics, and their cofactor Protein S. With the aim to determine the recovery level of PC in relation with the others vitamin K-dependent factors, the effect of suppression of anticoagulant therapy in patients under chronic treatment with acenocoumarin was studied.Quick time, functional factors II, VII, X (one stage methods), functional PC (Francis method) and immunological Factor II and Protein C (Laurell) were determined before and 36 hours after suspension of acenocoumarin administration.Results showed that: 1) Recovery levels of functional Protein C (increased from 28.55% ±2.57 to 72.64% ±5.9) were significantly higer than functional Factor II (22.09% ±2.34 to 30.73% ±8.64), Factor VII (22.55% ±2.01 to 40.73% ±4.85) and Factor X (23.27% ±2.66 to 39.18% ±3.19). Statistical analysis (Newmann-Keuls test) showed at least a p<0.01 between PC increase and factors II, VII or X increment.2) No significant differences were seen between immunological levels of Factor II before and after suspension of acenocoumarin.3) Levels of immunological PC in patients under anticoagulant therapy were higer than functional PC. After acenocoumarin suppression, not correlation was seen between immunological and functional Protein C recovery.It is concluded that acute suppression of acenocoumarin does not induce a thrombotic tendency because the recuperation of functional Protein C is more important than factors II, VII and X recovery.
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Heptner, W., J. R. Suárez, and V. Lütgendorf. "STUDIES ON PLATELET AGGREGATION BY IMPEDANCE AGGREGOMETRY AND ATP SECRETION IN NON-ANTICOAGULANT BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644810.
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Investigations in vitro on the time-dependent increase in thrombin activityand platelet function have been used tocharacterize the kinetics of the clotting process in nonanticoagulated blood. The test procedures described involve great effort and expense and therefore are not suitable for routine tests in pharmacology and clinical pharmacology. The present contribution describes the determination of clotting times in ATP secretion in the Chrono-Log Whole Blood Aggregometer.Blood was taken from healthy donors who had not used any drug in the two weeks before the trial. 0.5 ml blood wereimmediately transfered into siliconizedglass cuvettes containing 0.4 ml salineand 0.1 ml luciferin-luciferase cocktail prewarmed to 37°C. Impedance and luminescence were recorded continuously. Clotting at the electrodes is indicated by an immediate steep rise in both impedance and luminescence. Clotting time is defined as the time from diluting the blood in the cuvettes until the point at which marked elevation of these variables begins.In the blood of twelve subjects the mean clotting time was 3.8 min and intersubject variation (SD) was 0.45 min. Drastic interindividual differences in response to collagen and ADP in citratedwhole blood were observed in the study group.In vitro addition of 20 μl Fibraccel(Behringwerke AG, Marburg, FRG),a platelet factor 3 containing plateletextract decreased clotting time by 35 %(n=10). In the presence of 0.2 U heparin a slow and lona-lasting increase in impedance was seen. 1 g oral AspirinR didnot influence clotting time measured ex vivo.The results indicate that whole blood aggregometry is a simple, fast, and precise method of determining blood clotting and the effects of drugs in a medium reflecting almost physiological conditions.
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Roncaglioni, M. C., I. Reyers, A. P. Bolognese Dolessandro, C. Cerletti, M. B. Donati, and G. de Gaetano. "SALICYLATE-WARFARIN INTERACTION: EFFECTS ON SYSTEMIC ANTICOAGULATION, BLEEDING TIME, AND EXPERIMENTAL VENOUS THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643270.
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The potential benefit of the aspirin/warfarin association as an antithrombotic treatment has been matter of debate in view of the major haemorrhagic effect reported with this drug combination. We have tested the effect of such association in a model of venous thrombosis already shown to be prevented by a fully anticoagulant schedule of warfarin. CD-COBS male rats were treated for three days with either warfarin (0.1 mg/kg i.v. once a day) or salicylate (175 mg/kg i.p. twice a day) or their combination (W+S). Systemic anticoagulation (thrombotest), template bleeaing time and occurrence of experimental venous thrombosis (ligature of inferior vena cava) were followed. Treatment with W or S alone did not affect template bleeding time, whereas the association (W+S) did (320+35 sec versus 120± 10 sec in the control group, p<0.01). Thrombotest was only slightly prolonged by single drug treatment (W= 43%, S=48% versus 90% of controls) but strongly prolonged in the association group (S+W=5%; p<0.001). The mechanism of this combined effect may be multifaceted; competition of both drugs for protein binding and the anticoagulant effect of salicylate itself could contribute. In any case, neither the incidence nor the weight of the thrombus were reduced by any drug treatment. Thus, W+S, in contrast to W alone (<5% thrombotest), was unable to prevent or reduce venous thrombosis, while prolonging bleeding time. Bleeding complications reported in clinical trials by the association of W and aspirin might not be solely due to the antiplatelet effect of aspirin.
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Merton, R. E., T. W. Barrowcliffe, and D. P. Thomas. "A COMPARISON OF DERMATAN SULPHATE AND HEPARIN AS ANTITHROMBOTIC DRUGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642933.
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Dermatan sulphate (DS) has been shown to accelerate thrcmbin inhibition by its action on heparin cofactor II (HCII) but has no effect on anti thrombin III (Tollefson et al., 1983). In this study, we have examined the in vitro anticoagulant effect of a purified preparation of DS (free from heparin and heparan sulphate), m comparison with that of unfractionated heparin (UEH). We have also studied the effect of DS and UEH in preventing experimental venous thrombosis in rabbits and in inhibiting thrombin generation, both in vitro and in ex vivo plasma samples.Dermatan had low activity in vitro by APTT and anti-Xa assays (< 5 iu/ mg). When thrombin generation was measured in vitro, 1 μg/ml UEH was sufficient to inhibit thrombin formation. Although 1 μg/ml DS reduced thrombin generation to 40% of control values, there was no further reduction when the concentration of DS was increased to 8 μg/ml.When DS was injected into rabbits (n = 10), a dose of 150 μg/kg inpaired thrombogenesis m a Wessler stasis model. The mean thrombus score was reduced to 25% of the control values, although thrombosis could not be completely prevented, even after an eight-fold increase m dose (1250 μg/kg). When the duration of stasis was extended from 10 to 20 minutes, there was no impairment of thrombosis (mean thrombus score 100%) following 1250 μg/kg of DS. Thrombin generation measured in ex vivo plasma after 150 μg/kg of DS was 72% (s.e.m. 63-81) of that measured in pre-injection plasma. In contrast, 150 μg/kg of heparin prevented thrombosis after both 10 and 20 minutes stasis (mean score 0%) and thrombin generation was reduced to 17% (s.e.m. 12-23) of control values m ex vivo plasma samples.Unlike heparin, DS does not completely abolish thrcmbin generation in vitro and is not as potent as UEH in inhibiting thrombin generation m ex vivo plasma. While DS has demonstrable antithrombotic activity under defined conditions, it is less effective than heparin and increasing doses of DS do not improve antithrombotic effectiveness in this model.
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Poort, S. R., C. Krommenhoek-van Es, I. K. van der Linden, N. H. van Tilburg, and R. M. Bertina. "DEFECTS OF VITAMIN K-DEPENDENT FACTORS IN CA(11)-STABILI ZED STRUCTURE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644320.
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Vitamin K-dependent (anti)coagulation factors (factor II, VII, IX, X protein C and S) undergo a conformational transition upon binding of Ca(II), which is a prerequisite for their normal function. Abnormalities in these properties occur during vitamin K deficiency or treatment with anti vitamin K drugs and in some genetic variants of coagulation factors. Immunological assays utilizing antibodies against the Ca(II)-stabilized structure are useful to detect such abnormalities.Starting from specific rabbit antisera antibody populations specific for the Ca(II)-dependent conformation of factor II, VII, IX, X and protein C and S were isolated using immuno-affinity procedures. Subsequently immunoradiometric assays specific for the Ca(II)-dependent (Ca(II)Ag) and Ca(II)-independent (NonCa(II)Ag) conformations of the different proteins were developed. These assays were used for the analysis of plasmas of patients stably treated with oral anticoagulants; Ca(II)Ag, NonCa(II)Ag and their ratio were measured as function of the intensity of the treatment (INR 2.4 to 4.8). The same parameters were measured in plasmas of patients with hereditary coagulation disorders. After treatment with oral anticoagulation with an antivitamin K drug reduced ratios of Ca(II)Ag/-NonCa(II)Ag were observed for factor II, VII, IX, protein C and protein S. However, the actual degree of reduction and its dependence on the intensity of treatment varied for the different vitamin K-dependent proteins. In general Ca(II)Ag levels correspond nicely with the procoagulant activity of the concerning proteins. These data provide indirect evidence for the existence of abnormal (non and/or subcarboxylated) forms of the vitamin K-dependent proteins during oral anticoagulant treatment.Genetic variants with a mutation in one of the sites involved in the formation of the Ca(II)-s tab i1ized structure could be detected for factor IX, factor VII and factor II. However, the extent of reduction of the ratio Ca(II)Ag/-NonCa(II)Ag differed considerably in those variants.
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Borowska, A., D. Lauri, A. Maggi, E. Dejana, G. de Gaetano, and J. Pangrazzi. "IMPAIREMENT OF PRIMARY HAEMOSTASIS BY LMW-HEPARINS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643172.
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Low molecular weight (LMW) heparlns have been developed with the aim of reducing anticoagulant activity thereby minimizing the bleeding complications of conventional heparin. Unexpectedly, bleeding events were reported during treatment with some LMW-heparins, in clinical and experimental studies. We studied the effect of four different LMW-heparlns on primary haemostasis In male rats (CD COBS, Charles River) after l.v. administration of 0.75 mg/kg b.w. of the drugs. LMW heparin A was devoid of any activity on an experimental model of “template” bleeding time in rats (110.6±5.9 sec versus 108.7±4.1 control values) whereas LMW-heparins B, C and D prolonged the bleeding time to a different extent (228.7±19.9, 161.5±6.4 and 161.7±8.6 respectively). Pretreatment of animals with aspirin (100 mg/kg b.w. per o.s). resulted In a significant potentiation of the “template” bleeding time. In vitro platelet aggregation Induced by collagen (20 μg/ml) or by collagen in combination with ADP (5-10 μM) was strongly inhibited by LMW-heparln B, while LMW-heparln A showed no effect. LMW-heparins C and D exerted an Intermediate level of Inhibition of platelet aggregation. The same pattern of aggregating response was found when LMW-heparins A and B were given i.v. to rats (0.75 mg/kg b.w.) and platelet aggregation was studied “ex vivo” 15 min after drug administration.These data may help explain the impairment of primary haemostasis associated with some LMW-heparin preparations.
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Roth, A., G. I. Barbash, H. I. Miller, G. Keren, S. Laniado, and U. Seligsohn. "BLEEDING COMPLICATIONS DURING RT-PA THROMBOLYSIS RELATED TO USE OF ANTI-INFLAMMATORY DRUGS PRIOR TO ACUTE MYOCARDIAL INFARCTION ADMISSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642977.
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Of 57 patients with acute myocardial infarction (AMI) treated with rt-PA, we observed 2 major bleeding complications, both in patients who had been treated with anti-inflammatory drugs prior to admission. The thrombolytic protocol included: lOmg rt-PA in bolus and continuous infusion of 110 mg over 6 hr 5,000 iu heparin in bolus and continuous infusion of 25,000 iu/ 24hr, and aspirin 250 mg/24hr. The first patient, a 64 year old woman had been taking indomethacin 25 mg × 3 daily, during 3 weeks prior to the AMI. Rt-PA protocol was initiated with relief of chest pain and disappearance of ST elevation, but at 2 hr rt, sciatic pain developed. Treatment was continued accor ding to protocol in spite of the pain, but on the 3rd day hemoglobin decreased to 7.8%. Abdominal CT scan disclosed retroperitoneal hemorrhage. All anticoagulant medications were stopped, and 4 units of blood were transfused. The retro-peritoneal mass dissolved gradually. The second patient, a 68 year old male was treated by diclofenac 100 mg for 5 days prior to admission for AMI, and consequently aspirin was removed from the rt-PA protocol. However, 2 hr after completion of the 6 hr rt-PA infusion, gross hematuria and a “coffee ground” vomiting developed. Heparin infusion was discontinued and antacid treatment initiated, resulting in cessation of bleeding within a few hrs. In both patients the anticipated prolongation of APTT (heparin) and about 30% decrease in fibrinogen level were observed as the sole abnormality, and thus we related the bleeding episodes to the anti-aggregating effect of indomethacin and diclofenac respectively. We suggest that the use of anti-inflammatory drugs prior to administration of rt-PA protocol can be hazardous, and that special prudence (possibly protocol modification) is warranted.
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Pérez-Requejo, J. L., J. Aznar, T. Santos, and J. Vallés. "ANTIPLATELET ACTIVITY OF DYPIRIDAMOLE IN HUMAN WHOLE BLOOD WITH PHYSIOLOGICAL LEVELS OF IONIZED CALCIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643421.
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In spite of the windespread use of dypiridanole (DP) as an anti thrombotic drug, its usefullnes has not been generally proved. The clinical trials have been somewhat inconclusive or challenge and most of the studies were not able to snow a clear inhibitory action of DP on platelet aggregation. Using the impedance aggre gometer it has been shewn that the antiplatelet action of DP can be demonstrated in whole blood (WB) ex vivo an it was suggested that this was due to the inhibition of adenosin reuptake by the red cells. We have recently described (Thrombos & Haerostas 54: 799, 1985) a method, that detects the early platelet-collagen interaction in whole blood, which has been called BASIC wave. Using slight modifications of the BASIC wave method, we were able to study the platelet-collagen interactions in native WB with physio logical levels of calcium and its inhibition by DP ex vivo. We performed the BASIC wave in 25 human healthy volunteers in WB without sodium citrate, WB with citrate and citrated platelet rich plasma (PRP) before and 2 hours after the oral administration of DP 3mg/kg. We observed that in WB with citrate, DP produced a 66% inhibition of the BASIC wave (p<0.005) in PRP the inhibition was 40.7% (p< 0.005) but it was a non-significant 21.7% in WB without citrate. Using hirudin 40U/ml as anticoagulant, the inhi bition was the same as in WB without citrate. There were no correlation between the oral dose and the DP plasma levels or with the observed inhibition of the BASIC wave. We postulate that the antiplatelet action of DP is only demonstrable in citrated samples, beer negligible in native blood with physiological levels of calcium. The present report could explain the lack of firm da ta supporting the antithrombotic action of DP in clinical trials. Furthermore, the method here presented allows the study of anti -thrombotic drugs ex vivo in whole blood in its normal calcium environement.
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Roberts, H. R. "PREVENTION OF DEEP VENOUS THROMBOSIS: CONCLUSIONS OF A CONSENSUS DEVELOPMENT CONFERENCE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642966.
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Deep venous thrombosis (DVT) and pulmonary embolism (PE) are major health problems that lead to significant morbidity and mortality. In the United States, it is estimated that these two problems result in over 300,000 hospitalizations annually and available data indicate that 50,000 to 100,000 patients per year die of pulmonary embolism.The advent of several diagnostic tests has permitted the identification of groups of patients at high risk for development of deep venous thrombosis and subsequent pulmonary embolism. Identification of these patient groups has led to therapeutic measures designed to prevent both deep venous thrombosis and subsequent embolic episodes. However, the efficacy of these preventive measures have not been widely adopted and reservations have been expressed regarding use of low dose anticoagulant drugs for prevention of DVT and PE, especially in surgical patients. Because of the apparent reluctance to adopt putative preventive measures for DVT and PE, the National Heart, Lung and Blood Institute convened a Consensus Development Conference on the issue of prevention in 1986. Experts from North America, Europe, and South Africa presented data, both pro and con, on prevention of DVT and PE, using one or more therapeutic regimens. An impartial Panel was then asked to arrive at a consensus statement on the following questions: 1) the level of risk of DVT and PE in different patient groups; 2) the efficacy and safety of prophylactic measures in these groups; 3) the recommended prophylactic regimens for different patient groups, and 4) remaining questions related to prevention of DVT and PE. Recommendations for prevention were based on the assumption that reduction in DVT would also result in reduction of pulmonary embolism. Furthermore, the consensus was based, at least in part, upon data combined from multiple clinical trials. Thus, combined data on 12,000 individuals in randomized clinical trials indicated that in appropriate patient groups, treated with low dose heparin, there was a 68 percent reduction in DVT, as measured by the 125I-fibrinogen uptake test and venography, and that there was a reduction of 49% in pulmonary embolism and a significant decrease in overall mortality resulting from pulmonary embolism.Prophylactic measures for the following different patient groups were assessed: 1) general surgery; 2) orthopedic surgery; 3) urology; 4) gynecology-obstetrics; 4) neurosurgery and neurology; 5) trauma; and 6) medical conditions.Basically, the following prophylactic regimens were considered: 1) low dose heparin; 2) low dose dihydroergotamine heparin; 3) dextran; 4) low dose warfarin; and 5) external pneumatic compression. In general terms, low dose heparin appears to be one of the more effective prophylactic regimens in certain groups of high risk patients. This regimen is not useful in orthopedic or certain neurosurgical procedures where heparin has been shown to be of little value or hazardous. In these cases, dextran, warfarin, or external pnuematic compression may be more beneficial. In some groups of high risk patients, combination of mechanical measures with anticoagulant agents appear to be of value in prevention of DVT and PE.The recommendations of the Consensus Panel for Prevention of DVT and PE for each patient group will be assessed.