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We have developed an AI-aided multiple time stepping (AI-MTS) algorithm and multiscale modeling framework (AI-MSM) and implemented them on the AiMOS supercomputer. AI-MSM is the first of its kind to integrate multi-physics, including intra-platelet, inter-platelet, and fluid-platelet interactions, into one system. It has simulated a record-setting multiscale blood clotting model of 102 million particles, of which 70 flowing and 180 aggregating platelets, under dissipative particle dynamics to coarse-grained molecular dynamics. By adaptively adjusting timestep sizes to match the characteristic time scales of the underlying dynamics, AI-MTS optimally balances speeds and accuracies of the simulations. [ABSTRACT FROM AUTHOR]

Introduction: Acute hypoxia has been suspected to cause blood coagulation and platelet activation. Our aim was to study blood coagulation and platelet function during a short hypoxic exposure. Methods: Healthy nonsmoking men (N = 10) inhaled a normobaric hypoxic gas mixture containing 8% of oxygen (92% nitrogen) for 7 min via a face mask. Venous blood was collected 5 min before and during the 5 to 7 min of hypoxia exposure (i.e., pretest and hypoxia samples, respectively) while monitoring arterial oxygen saturation (Sao2) with pulse oximetry. Blood sampling was completed in 2 min and the face mask was removed. Venous epinephrine and norepinephrine, complete blood counts, and a panel of coagulation markers were analyzed. Platelet aggregation induced by ristocetin, adenosine diphosphate (ADP), arachidonic acid, and thrombin receptor activating peptide was studied with MultiplateR and shear force-dependent functions with PFA-100R (collagen/epinephrine and collagen/ADP cartridges), both assays in whole blood. Results: During hypoxia, Sao2 declined from 98 to 58% (ranges 97-99% vs. 42-85%), while heart rate increased from 69/min to 94/min (SD 11 vs. SD 13). Venous epinephrine and norepinephrine levels also increased. This short hypoxia induced minor but uniform increases in red cells, reticulocytes, and leukocytes and decreases in platelet counts. Platelet functions and prothrombin time, APTT, thrombin time, D-dimer, fibrinogen levels or von Willebrand factor (VWF), antithrombin, factor V (FV) or FVIII activities did not change. Discussion: Profound acute hypoxia failed to affect blood coagulation or platelet functions in healthy individuals. [ABSTRACT FROM AUTHOR]

Abstract: In this paper, the concurrent numerical simulation of clotting and unsteady flow within a stenosed artery is described. The simplified blood clotting process is based on a residence time model, using a lattice Boltzmann flow solver with passive scalar advective–diffusive transport. Simulation results of a stenosed model artery are presented together with experimental blood analogue results. Aspects of an efficient unstructured implementation are briefly reviewed. [Copyright &y& Elsevier]

Some patients with systemic lupus erythematosus (SLE) develop anticoagulant (anticlotting) activity, which may be indicative of a deficiency of one or more clotting factors. Lupus anticoagulant (LAC) has been associated with the occurrence of thromboembolic events, or the development of clots that lodge in other blood vessels. The association of LAC with other SLE complications, such as miscarriage, is controversial. The reported prevalence of LAC varies widely. The prevalence and medical relevance of LAC was studied in 55 SLE patients (54 female and 1 male) in northern India. Thirteen percent of the patients had LAC, as identified by a prolonged clotting time. The patients with LAC had a significantly higher incidence of clot formation. Compared with the other SLE patients, those with LAC were significantly younger and had SLE for a shorter time, which may reflect more severe illness. No other SLE complications were significantly different in this small group of patients. The results suggest that SLE patients with LAC are at higher risk for thromboembolic events, and further study is needed on how best to treat them. (Consumer Summary produced by Reliance Medical Information, Inc.)

Activation of the blood coagulation system is thought to occur at the time of delivery. This is evidenced by the development of deep vein thrombosis, the formation of a blood clot in the deep veins of the legs, in the postpartum period. Coagulation occurs through the interaction of a number of factors, namely platelets, fibrinogen, factor VIII and plasminogen. It is not clear whether the balance of the clotting system is altered through a change in the production or the consumption of coagulation factors. New advances in blood analysis permit the measurement of markers in the blood that indicate clotting activity. The blood markers reveal the degree of fibrinolysis (mechanism of clot dissolving) and activation of platelets (cells that aggregate during clotting). These markers were used to study the changes in hemostatic activity experienced during delivery and immediately afterwards. Tests to measure 11 blood clotting functions were performed on 70 healthy pregnant women. There was an increase in activation of platelets and formation of fibrin, a stringy protein found in clots, at the time of delivery. The clotting system is activated immediately after the delivery of the placenta and this activation continues for the first three postpartum hours. Fibrinolysis is increased in the first three hours postpartum, followed by gradual decrease in activity during the next 48 hours. Women who do not experience a dramatic increase in fibrinolytic activity during the postpartum period may be at risk for deep vein thrombosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

The country said it has identified 26 suspected cases of bleeding and clotting among recipients of the vaccine. [ABSTRACT FROM AUTHOR]

Byline: Angelo Salvucci, Jr., MD, FACEP Literature Review: Is TXA Safe for Lesser Injuries? Roberts I, Perel P, Prieto, et al. Effect of tranexamic acid on mortality in patients with [...]

* Although coagulopathy is a well-known complication of severe niacin-induced hepatotoxic reaction, it is not found in patients with minimal aminotransferase level elevations. Three patients with significant clotting factor synthesis deficiency and coagulopathy (prothrombin times, > 1.5 times control) from sustained-release niacin had only mild aminotransferase level elevations (1.5 to 2.0 times normal). In each case, protein deficiency, coagulopathy, and aminotransferase level elevation resolved promptly after withdrawal of niacin therapy. In one case, this syndrome recurred after rechallenge with sustained-release niacin, whereas the coagulopathy did not recur in a second patient rechallenged with crystalline niacin. Deficiency in protein synthesis, including coagulation factors, and coagulopathy are unrecognized complications of sustained-release niacin therapy. These cases indicate the need to measure prothrombin times routinely in patients who develop even mild aminotransferase level elevation while receiving sustained-release niacin therapy. These data are important in light of the increasing use of sustained-release niacin in the treatment of patients with lipid disorders. (Arch Intern Med. 1992;152:861-863)

While ionic contrast media (CM) are stronger anticoagulants and antiplatelet agents, both nonionic and ionic CM retard clotting, fibrinopeptide A generation and platelet aggregation (at least by Born-O'Brien aggregometry). Thus, nonionic CM do not cause clots and thrombi. Rather, the driving force for clot or thrombus formation, when it occurs, is blood contact with and activation by the foreign surface of a syringe or catheter itself. A marked enhancement of clotting by glass syringes in comparison to plastic ones supports this view. Blood in any suringe or catheter, therefore, will clot more slowly in the presence of nonionic or ionic CM, the inhibitory effects of the latter being more profound. With respect to models of thrombosis at sites of vascular injury or stenosis, the antithrombotic effecgs of CM may either be transient owing to the dynamic nature of blood flow (local endothelial cell denudation model), or as in the case of ionic CM, actually to enhance local platelet aggregation (stenosis model). In these situations, preservation of the antithrombotic functions of endothelium with nonionic CM may be quite critical., Nonionic contrast agents, used for visualizing blood vessels on X-ray, have been shown to produce fewer side effects than high-osmolarity ionic contrast agents. Since these side effects may include loss of consciousness or cardiac arrest, there is significant reason to use nonionic agents, and by 1989, 70 percent of the procedures visualizing arteries of the heart relied upon nonionic agents. The percentage would likely be 100 percent were it not for the far greater cost of the nonionic agents. There has been some suggestion, however, that nonionic contrast agents may contribute to the formation of blood clots in the syringes and catheters used in the procedures; if this were the case, it would provoke serious concern for the safety of the patient. Laboratory investigation of blood clotting, however, has revealed that nonionic contrast media do not contribute to clotting. Both ionic and nonionic contrast media reduce the likelihood of clotting. The observed clotting is a result of the effect of the synthetic materials of the syringe and catheter. Two ionic contrast media (ioxaglate 320 and diatrizoate) and two nonionic contrast media (iohexol 370 and iopamidol 350) were studied; both reduced the rate of clot formation in catheters and plastic and glass syringes when compared with saline solution. However, the antithrombic activity of the ionic contrast media was found to be greater than that of the nonionic contrast media. (Consumer Summary produced by Reliance Medical Information, Inc.)

Cut yourself while cooking? Stop the bleeding with dehydrated potato flakes. Mayo Clinic researchers found that a powder made from dried potatoes can cause blood to clot better than applying [...]

Use of heparin or heparinoid for acute ischemic stroke has been controversial for a long time. Theoretically there are benefits in prevention of thrombus propagation. and fibrin formation. Nevertheless data from 16 randomized controlled trials of heparin or heparinoid involving 22,000+ patients show that they are not of significant net benefit in the long term. Use of heparin in acute stroke is not justified unless it is as a part of an approved controlled clinical trial It is possible that false-negative error may have affected data from 22,000+ patients, but unlikely. Types of heparin, administration routes, bolus, or loading, doses, and other factors should be investigated.

Platelets, cells involved in the clotting process, can be transfused in patients with certain bleeding disorders. Platelet therapy is indicated in patients diagnosed with thrombocytopenia, a decreased production of platelets by the bone marrow. Bleeding occurs in blood vessels and capillaries (the smallest of blood vessels) mostly in the skin and mucous membranes, but can occur in the blood vessels of the brain. Platelet therapy can also be given to prevent anticipated bleeding produced by chemotherapy, surgery, lumbar puncture (the removal of spinal fluid) and liver biopsies. Patients with thrombotic thrombocytopenic purpura (TTP) however, are not good candidates for platelet therapy, which can accentuate this disease. Platelet therapy should only be used when bleeding in the brain appears life-threatening. Additional drugs, such as vitamin K, can be given to help the blood clotting during platelet therapy. Platelets are short-lived and expensive, and therapy causes some associated complications, such as transfusion and immune reactions. The infusion of platelets can transmit infectious diseases such as hepatitis, HIV (the human immunodeficiency virus) and the cytomegalovirus. It is suggested that since platelet therapy is not without risk, it should be used only when necessary. Close patient monitoring is essential. (Consumer Summary produced by Reliance Medical Information, Inc.)

The time it takes blood to coagulate or clot, known as thrombin time, was prolonged in four surgical patients, although other coagulation factors were normal and they had no history of blood clotting abnormalities. Further laboratory studies suggested that there were factors in the patients' blood that interfered with the action of the blood clotting factor thrombin. Bovine thrombin (thrombin derived from cows) had been used in all patients in a previous surgery as a clotting agent. When human thrombin was used instead of bovine thrombin, the clotting ability of the blood was normal. This suggested that the factors in the patients' blood were specifically directed against bovine thrombin. Immunological tests showed that the blood of these patients contained immunoglobulin antibodies, specialized proteins that inactivate foreign substances, and these antibodies were specifically directed against bovine thrombin. Thus, antibodies to bovine thrombin were produced during previous exposure to bovine thrombin, and accounted for the prolonged clotting time after the later surgery. (Consumer Summary produced by Reliance Medical Information, Inc.)

Fibrinogen is a protein found in the plasma (the fluid portion of the blood), which, when acted on by the blood enzyme thrombin, is changed into fibrin, the material which forms the framework of a blood clot. The blood clot is essential in hemostasis (stopping bleeding). Lack of circulating fibrinogen may cause severe hemorrhage or bleeding, and abnormalities in fibrinogen itself may produce either hemorrhage or thrombosis, formation of clots or deposits in the blood vessels. Disorders of fibrinogen (fibrinogenopathies) include a total lack of fibrinogen (afibrinogenemia), an insufficient amount of fibrinogen (hypofibrinogenemia), or an overabundance of fibrinogen (hyperfibrinogenemia). Afibrinogenemia is a genetic disorder. Hypofibrinogenemia may be either congenital or acquired. Acquired hypofibrinogenemia may be the result of medication intended to reduce fibrinogen, intravascular coagulation, liver failure, snake venom, or treatment with L-asparaginase. Congenital hypofibrinogenemia is frequently a factor in liver diseases, tumors and kidney cancers. Hyperfibrinogenemia is an acquired disorder and is a risk factor for heart attacks and strokes. Smoking is thought to be a factor contributing to hyperfibrinogenemia. Fibrinogen is an acute-phase reactant and is present when there is an inflammatory state, such as rheumatic disease. This process is reflected in elevated erythrocyte sedimentation rates. Neoplasms (tumors) are also associated with elevated fibrinogen levels. Fibrinogen disorders that may cause hemorrhage can be detected by delayed clotting time. Genetic causes of fibrinogen disorders and the biochemical and molecular biologic aspects of fibrinogen are discussed.

Pulmonary embolism is the movement of blot clots formed elsewhere in veins into the capillary beds of the lung. Once lodged in the lung tissue, the embolism can severely affect the normal physiologic gas exchange mechanism, and death frequently results. However, not all clots in peripheral veins are associated with a high risk of pulmonary embolism. Research has demonstrated a close association between clots forming in deep peripheral veins and the development of pulmonary embolism. A new strategy has been developed to avoid unnecessary treatment of peripheral vein thrombosis, clot formation, while protecting patients from the dangers of pulmonary embolism associated with clots in the deep proximal veins. A group of 874 patients with suspected pulmonary embolism was studied for the presence of proximal vein disease. The data suggest that two types of populations are involved: those with deep vein disease who require treatment with anticoagulant drugs, and those without deep vein disease, who have an excellent prognosis without anticoagulation therapy. This classification has resulted in patient management strategies that can significantly reduce the number of patients who undergo anticoagulation therapy when pulmonary embolism is detected.

Kawasaki syndrome (KS) is an illness that usually occurs in infants and children under five years of age, and is characterized by fever and inflammation of the lymphatic system. Children suffering from KS have active blood coagulation with elevated levels of beta-thromboglobulin (BTH), indicating platelet activity and development of aneurysms, weak spots in the wall of a coronary artery. Researchers evaluated the effects of immune globulin on platelet count, platelet activation, and coagulation in 28 children with KS. This study confirms previous observations regarding activation of coagulation in children with KS. BTG levels could not be used to distinguish patients at high risk for coronary artery disease resulting from KS. Furthermore, the means by which intravenous immune globulin reduces the prevalence of coronary artery abnormalities and decreases other measures of acute inflammation remains unknown. While immune globulin does reduce the prevalence of coronary artery aneurysms, it does not have an early effect on reducing platelet activation or other measures of coagulopathy (defects in blood clotting).

The relationship between taurine (amino acid in bile) and platelet (component of blood responsible for clot formation) function was explored in cats and humans. Under laboratory conditions, platelets from taurine-depleted cats were twice as sensitive to clotting as those from healthy cats. Platelets from healthy humans became 30 percent more resistant to clotting when subjects were given 400 milligrams of taurine per day, and 70 percent more resistant when subjects were given 1600 milligrams per day. Decreased clotting was associated with increased levels of taurine and glutathione (aids various chemical reactions in body) and decreased release of thromboxane (induces clotting) during blood clotting. This indicates that taurine stabilizes platelets against aggregation, so that a lack of taurine makes them clot too easily and an excess makes them clot less.

An 86-year-old man sails through gallbladder surgery like a champ, only to die a week later of a blood clot in the lung. After completing long airplane flights in cramped [...]

Budd-Chiari syndrome, a disorder of the blood circulation in the liver, is caused by blockage of the veins leading from the liver. The condition has rarely been seen to occur in pregnant women after delivery. A 29-year-old woman, who delivered her third child three weeks earlier, developed swelling in her abdomen and legs, epigastric pain, and weakness. On examination, her liver appeared enlarged, and she had ascites, an abnormal accumulation of fluid in the abdomen. Deep vein thrombosis, blood clot formation in the deep veins in the legs, was also noted. Magnetic resonance imaging revealed the collapse of the veins leading from the liver and detected a clot in the inferior vena cava vein. Heparin anticoagulation therapy cleared the deep vein thrombosis but did little to correct the ascites. The clot-dissolving drug streptokinase improved the blood flow through the vena cava but liver veins remained blocked. An artificial bypass shunt was inserted to help the flow of blood. The patient's coagulation system entered a heightened state. Despite efforts to improve widespread coagulation, kidney and liver functioning deteriorated and the patient died nine months after delivery. The unusually long state of hypercoagulability and continued cascading of events after delivery contributed to the development of deep vein and liver vein thrombosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

FDA has approved a third intravenous blood-clot-dissolving (thrombolytic) drug for preventing permanent damage to the heart muscle following a heart attack. Known generically as anistreplase, the product is being marketed [...]

When one of my geriatric residents had a tooth removed, the dentist ordered that a tea bag be placed over the extraction site in the event of bleeding. How does [...]

Oral anticoagulant therapy requires constant management of the level of the anticoagulant, because the risk of serious hemorrhage is high, affecting approximately five percent of all patients. The ability of patients to monitor and adjust their own anticoagulant therapy is discussed. An instrument to measure the time required for blood to clot, known as the prothrombin time (PT), and the effective level of anticoagulant can be used by patients to adjust their levels of anticoagulant. The device is hand-held and battery- driven and uses a small portable laser to perform the measurement. The device allows accurate and virtually instantaneous assessments of PT. The system was evaluated by a group of 16 patients who were under anticoagulant therapy with the drug warfarin during an average period of 43 weeks. During that time, 458 measurements of PT were obtained with the device, and in 393 measurements the level of warfarin was found to be appropriate. In the 65 readings that were outside of the acceptable range, the patients made the correct adjustment 75 percent of the time. When adjustment mistakes were made by the patients, they were minor and, because warfarin levels only adjust slowly, not dangerous. Analysis of the reasons for the mistakes reveals that they stemmed from a lack of understanding of proper levels. This pilot study demonstrates that more responsibility for the maintenance of effective anticoagulant drug titer can be borne by the patient.

NEW YORK - Streptokinase, the oldest of three drugs studied for their use in dissolving blood clots, has been found to be not only the safest but also the least [...]

Corvas raises $6.6 million for its blood-clot research Corvas Inc., a biopharmaceutical company involved in blood clot research, has raised $6.6 million in a second round of venture capital financing. [...]

Since the 1940s researchers have tried to develop a surgical procedure to place a baffle in the inferior vena cava (the main vein which returns blood to the heart) to prevent clots or venous thrombi from entering the right side of the heart and, through it, the lungs. Difficulties with this task caused researchers to intensify their search for an ideal filter. The ideal filter should be based on several concepts: (1) it should not increase instances of clot formation; (2) it should break the large cross-sectional face of the vena cava into smaller channels so as to prevent the movement of large clots; and (3) it should be able to be placed without extensive surgery. Several filters have been developed and tried, and although good results have been recorded with most, there are considerable risks and unanswered questions regarding their use and time of removal. Several can now be installed and removed through a simple needle-like inserter system through the skin. Several devices under study have either been modified or withdrawn from further study. It has not yet been determined which of the commercially available devices and methods are best. A collaborative, multicenter study to evaluate these important devices is proposed.

Early Stroke Data Implicate Antiphospholipid Antibodies San Antonio, Texas--Stroke researchers are cautiously enthusiastic about early work with a class of autoantibodies that have been linked to thrombosis, cerebral ischemia, and […]