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PubMed2004

Periprocedural thromboprophylaxis in patients receiving chronic anticoagulation therapy.

Patients receiving chronic anticoagulation therapy pose a clinical challenge when therapy needs to be interrupted for surgical or invasive procedures. Maintaining anticoagulation places them at risk for serious bleeding complications, whereas discontinuing anticoagulation puts them at risk of thromboembolic complications. Most patients can undergo dental procedures, cataract surgery, and diagnostic endoscopy without discontinuing anticoagulation. The main patient groups that may require a periprocedural alternative to oral anticoagulation (periprocedural thromboprophylaxis or bridging) include patients with prosthetic heart valves, atrial fibrillation, and hypercoagulable states and patients with chronic venous thrombosis who are undergoing surgery. Currently, there is little consensus on the appropriate perioperative treatment of patients on long-term warfarin therapy. There are an increasing number of studies that evaluate the benefits of periprocedural bridging with low-molecular-weight heparin (LMWH) in place of unfractionated heparin (UFH). An advantage of LMWH over UFH is that perioperative conversion from warfarin therapy with LMWH can be carried out in the outpatient setting, which is more convenient for patients and is cost effective. As with the use of UFH, there are reports of maternal thromboembolic complications with LMWHs in pregnant women with mechanical heart valves. This review brings together the available data on periprocedural bridging to assess the available options for patients on long-term warfarin therapy who are undergoing surgical procedures. It provides a rationale for using LMWHs while individualizing the risks versus benefits in a given patient population.

Anticoagulants↗
PubMed2005

Smoking cessation in patients with coronary artery disease.

BACKGROUND: Smoking cessation is an important factor in the primary and secondary prevention of cardiac events. Although multiple clinical trials have examined the efficacy of various smoking cessation aids, a systematic review of the efficacy and safety of smoking cessation aids has not been done. METHODS: This paper reviews the effects of smoking on coronary artery disease. In addition, we identify randomized controlled trials examining the efficacy and safety of smoking cessation aids from the years 1970 to 2004. We then pooled the trial results for 6- and 12-month rates of continuous smoking abstinence. RESULTS: The 4 principal mechanisms of cardiovascular damage caused by cigarette smoking are induction of a hypercoagulable state, reduction of oxygen delivery because of carbon monoxide, coronary vasoconstriction, and nicotine-induced hemodynamic effects. Our review of clinical trials suggests that each smoking cessation aid improved continuous smoking abstinence rates at both 6 and 12 months compared with placebo. The 12-month abstinence rates for the active versus placebo treatments were the following: nicotine patch 11.1% versus 5.5%, nicotine gum 27.3% versus 16.5%, nicotine inhaler 16.9% versus 9.1%, bupropion 18.5% versus 6.6%, and behavioral therapy 20.0% versus 13.9%. CONCLUSIONS: Several smoking-related mechanisms are responsible for the development of atherosclerosis and the induction of cardiac events. Smoking cessation aids effect a modest increase in smoking abstinence at 12 months compared with placebo. In spite the apparent success of cessation aids, smoking relapse rates are quite high.

Administration, Cutaneous↗
PubMed2006

Acute thrombotic disorders.

The acquired hypercoagulable states are responsible for a broad range of thrombotic and thromboembolic disorders. Symptoms and signs of acute ischemia or organ dysfunction will lead many of these patients to seek care in EDs. Proper diagnosis and therapy must be based on an understanding of epidemiology and pathophysiology. Immediate anticoagulation with heparin may not always be the treatment of choice; careful analysis of clinical and laboratory parameters is necessary to arrive at the safest and most effective course of action. Newer anticoagulants, including low-molecular-weight heparins and nonheparin compounds, are changing the therapeutic approach to many of these disorders.

Acute Disease↗
PubMed2006

Deep venous thrombosis and pulmonary embolism in hospitalized patients with sickle cell disease.

BACKGROUND: As would be expected with a hypercoagulable state, pulmonary embolism (PE) occurs in sickle cell disease (SCD). Its frequency, however, is undetermined, largely because of difficulties in distinguishing it from thrombosis in situ. The prevalence of deep venous thrombosis (DVT) is also undetermined in patients with SCD. Knowing the prevalence of DVT would be an important step in the overall assessment of the risk of PE in these patients. METHODS: Data from the National Hospital Discharge Survey were assessed. RESULTS: In patients <age 40 years, 7000 of 1,581,000 (0.44%) with SCD had a discharge diagnosis of PE compared with 59,000 of 48,611,000 (0.12%) of African Americans without SCD. The prevalence of DVT was similar in patients < age 40 with SCD, 7000 of 1,581,000 (0.44%) and in African Americans who did not have SCD, 193,000 of 48,611,000 (0.40%). CONCLUSION: The high prevalence of apparent PE in patients with SCD, compared with non-SCD African-American patients of the same age and the comparable prevalence of DVT in both groups are compatible with the concept that thrombosis in situ might be present in many. On the other hand, the data suggest that PE is not rare in patients with SCD. This suggests that PE might be an etiologic factor in patients with SCD who develop respiratory symptoms. In such patients, an imaging procedure might be appropriate.

Adolescent↗
PubMed2004

[Peri-operative anticoagulation with danaparoid for a patient with Budd-Chiari syndrome and heparin-induced thrombocytopenia].

We report a case of Budd-Chiari syndrome revealing a polycythemia vera and complicated by heparin-induced thrombocytopenia. A surgical porto-caval shunt was inserted with danaparoid as anticoagulant during the peri-operative period. The doses of danaparoid were as follows: a continuous intravenous infusion of 200 U/h with a target between 0.5 et 0.8 U/ml antifactor Xa activity during the preoperative period, followed by 100 U/h with a target of 0.3 U/ml during the peroperative period; an increase in doses of danaparoid to 150 and 200 U/h with a target above 0.5 U/ml was used during the postoperative period. This case report is a rare situation of hypercoagulable state, in a surgical context, treated with danaparoid.

Adult↗
PubMed2005

[Manageability and potential for haemostasis monitoring by near-patient modified thromboelastometer (Rotem) in intensive care unit].

OBJECTIVE: Preliminary assessment of a rotary thromboelastometer (Rotem) in the haemostasis monitoring in ICU. STUDY DESIGN: Prospective, open. PATIENTS AND METHODS: The device: the Rotem is a rotary thromboelastometer, which measures continuously and retranscribes numerically viscoelastic properties of a clot after an in vitro haemostasis activation. 83 patients with various haemostasis disorders that 122 blood samples have been subjected to a double analysis: extemporaneous by Rotem and at the laboratory for conventional haemostasis tests (aPTT, PT, fibrinogen, platelets). We assessed Rotem's manipulation duration, time for the first results. We compared Rotem variables with conventional haemostasis parameters and haemostasis diagnosis with each method. RESULTS: Mean Rotem manipulation duration was measured at 2 minutes 51 seconds+/-1 minute 48 seconds and time for results at 13+/-6 minutes. Plasma fibrinogen level was strongly correlated with the kinetic of clot formation (CFT) and the maximun clot firmness (MCF) measured by Rotem (R>0.7, coefficient of Pearson). Platelets were strongly correlated with MCF. The PT and aPTT had a weak correlation with Rotem parameters (R< or =0.53). The diagnosis concordance between the two techniques was good with a pondered kappa coefficient measured at 0.68. Hypocoagulability thromboelastographic profile with Rotem was in agreement with conventional parameters diagnosis in 92 percent of cases. Hypercoagulability thromboelastographic profile was associated with a significant increase of conventional parameters (supranormal value in 78%). Normal thromboelastography profile was associated with normal conventional parameters in 49%. Different reagents used on several simultaneous tests specified the thromboelastographic diagnosis. A diagnostic algorithm showed the interest of the Rotem for the prediction of conventional test results. CONCLUSION: Rotem is an easy manipulation device whose concordant and rapid results allow its emergency use in the framework of haemorrhagic situations. It also allows an approach of hypercoagulability states so that the therapeutic implication remains to evaluate. The Rotem offers a dynamic multifactorial approach on total blood of haemostasis that is what makes it a prime aid of haemostasis monitoring, in complement of usual analytic haemostasis evaluation.

Adult↗
PubMed2006

Blood coagulation unaffected by ozonated autohemotherapy in patients on maintenance hemodialysis.

BACKGROUND: Ozonated autohemotherapy (O(3)-AHT) is a clinically useful therapeutic procedure in hemodialyzed patients with peripheral arterial occlusive disease (PAOD). The majority of patients on dialysis are in a hypercoagulable state. Thrombotic complications are the major cause of morbidity and mortality in hemodialyzed patients. Effects of O(3)-AHT on blood coagulation were evaluated in 11 hemodialyzed patients affected by PAOD. METHODS: We performed an oxygen-controlled, crossover study in which nine sessions of autohemotherapy with oxygen administration (AHT) as a control were followed by nine sessions of O(3)-AHT. Blood coagulation was assessed by antithrombin III, activated partial thromboplastin time, prothrombin time, D-dimer and fibrinogen plasma concentrations. RESULTS: The extents of all the measured parameters after nine sessions of O(3)-AHT did not differ statistically from the values after nine sessions of AHT. Similarly, there were no differences in the measured variables after the first session of O(3)-AHT as compared to the values before therapy. We did not observe any thrombotic accidents during the study. CONCLUSIONS: O(3)-AHT with ozone concentration of 50 microg/mL and citrate as an anticoagulant does not influence blood coagualation parameters in hemodialyzed patients with PAOD.

Aged↗
PubMed2006

Pregnancy and puerperium are high susceptibility periods for the development of catastrophic antiphospholipid syndrome.

It is well known that antiphospholipid syndrome (APS) is associated with recurrent pregnancies losses, but is also associated with other obstetric features such as preeclampsia, uteroplacental insufficiency and preterm birth. Pregnancy is a hypercoagulable state than can be complicated by thrombosis, especially in those patients with an underlying thrombophilic disorder. Catastrophic APS is a rare form of presentation of the APS. Several trigger factors have been related with the catastrophic APS, including infections, anticoagulation withdrawal, surgery, neoplasms and lupus "flares". In around 6% of the cases, the catastrophic APS can appear during pregnancy or puerperium. We review this specific subset of the catastrophic APS and propose a therapeutical approach for this particular situation.

Antiphospholipid Syndrome↗
PubMed2006

Pathophysiology of venous thrombosis, thrombophilia, and the diagnosis of deep vein thrombosis-pulmonary embolism in the elderly.

This article reviews Virchow's triad to provide clinicians with the pathophysiologic basis for the development of venous thromboembolism (VTE). Armed with these data physicians should be vigilant of the development of VTE when these factors are present. The second clinical point is the appropriate need to evaluate elderly patients for primary or secondary thrombophilia. By using statistical probability and clinical history selected geriatric patients with VTE should be assessed for the etiology of their hypercoagulable state. Finally, evaluating symptomatic patients for VTE should be structured to use the appropriate testing to confirm the diagnosis.

Age Factors↗
PubMed2004

Transient global amnesia heralding basilar artery thrombosis.

The cause of transient global amnesia (TGA) remains controversial. Focal cerebral ischemia, seizure, venous congestion, and migraine have all been proposed as underlying mechanisms. We describe a patient presenting with typical TGA who two days later developed a posterior circulation stroke due to basilar artery occlusion. He was treated successfully with intra-arterial thrombolytic therapy. Shortly thereafter, he had recurrent basilar artery thrombosis and jugular vein thrombosis, and was found to have a mucinous adenocarcinoma believed to be causing a hypercoagulable state. We believe this case supports the hypothesis that TGA can on occasion be caused by cerebral ischemia.

Amnesia, Transient Global↗
PubMed2004

NTPDase and 5'-nucleotidase activities in rats with alloxan-induced diabetes.

Diabetes is associated with a hypercoagulable state. In this study, we investigated the potential effects of alloxan-induced diabetes on the activities of the enzymes NTPDase (E.C. 3.6.1.5, apyrase, ATP diphosphohydrolase, ecto/CD39) and 5'-nucleotidase (E.C. 3.1.3.5, CD73) that can control the levels of ADP and adenosine, two substances that regulates platelet aggregation. In the alloxan-treated rats, NTPDase activity was significantly increased by 88 and 35% with ATP as substrate and by 156 and 58% with ADP as substrate in platelets and synaptosomes, respectively (P< 0.05). AMP hydrolysis was increased by 142% (platelets) and 70% (synaptosomes) in diabetic rats compared to control. These results demonstrate that alloxan-induced diabetes interferes with ATP, ADP, and AMP hydrolysis in platelets and synaptosomes. Taken together, these results may indicate that in diabetic rats both NTPDase and 5'-nuleotidase from the central nervous system (CNS) and platelets respond similarly with increased activity. Thus, we speculate that platelets could be used as a potential peripheral marker of central alterations in NTPDase and 5'-nucleotidase activities in diabetes.

5'-Nucleotidase↗
PubMed2006

Analysis of risk factors for early hepatic artery thrombosis after liver transplantation. Possible contribution of reperfusion in the early morning.

BACKGROUND: Since the incidence of myocardial infarction and other cardiovascular ischaemic events is highest in early morning, on account of a relative hypercoagulable state occurring in this time period, an attempt was made to test whether reperfusion of the hepatic artery at this time of the day, at liver transplantation, produces an increased risk of early thrombosis. METHODS: The records of 255 consecutive patients receiving a first transplant for chronic liver disease were retrospectively analysed. As possible risk factors, for early post-operative thrombosis (<30 days from transplantation), several medical and surgical parameters were taken into consideration. Arterial reperfusion was considered to have taken place at a time of high coagulability when occurred between 6.00 a.m. and 10.00 a.m. on the basis of previous reports. RESULTS: Logistic regression identified donor age (OR for age >60: P=0.017), bench reconstruction of the artery (OR: 5.06, P=0.013) and time of high coagulability at reperfusion (OR 2.93, P=0.087), as independently associated with early hepatic artery thrombosis. CONCLUSIONS: The present findings identified three independent predictors of early hepatic thrombosis, warranting stricter post-surgical follow-up of patients presenting such conditions. Interestingly, these factors are consistent with arterial reperfusion in the early morning being associated with an increased risk of early hepatic artery thrombosis, suggesting relative coagulative imbalances to provide a contribution in the pathogenesis of this severe complication of liver transplantation.

Blood Coagulation↗
PubMed2006

Heparin resistance and increased platelet activation in coronary surgery patients treated with enoxaparin preoperatively.

OBJECTIVE: Patients with unstable coronary disease have changes in the hemostatic system. These patients are often treated with low molecular weight heparin. In patients who are accepted for coronary artery bypass grafting, treatment with low molecular weight heparin is frequently continued until surgery. We hypothesized that in coronary artery bypass grafting, the hypercoagulable state seen in unstable patients persists into the intra- and postoperative phase despite preoperative treatment with low molecular weight heparin. The aim of this study was to explore and describe the perioperative hemostatic process in patients with unstable coronary artery disease undergoing coronary artery bypass grafting. METHODS: Thirty-two patients with unstable coronary disease treated preoperatively with enoxaparin, and 32 stable control patients not treated with enoxaparin, were included. All patients were taking low dose aspirin until the day before surgery. Before cardiopulmonary bypass, all patients were given tranexamic acid as a bolus injection. Blood samples for analysis of platelet counts, international normalized ratio, activated partial thromboplastin time, fibrinogen, protein S, protein C, prothrombin fragment 1 + 2, thrombin-antithrombin complex, antithrombin, plasmin-antiplasmin complex, D-dimer, neutrophil-activating peptide 2, platelet-monocyte complexes, and heparin concentrations were drawn preoperatively, after 30 min on cardiopulmonary bypass, and 30 min, 3 h, and 20 h postoperatively. Heparin was given during cardiopulmonary bypass to maintain an activated clotting time above 480 s. RESULTS: Patients in the enoxaparin group needed more heparin to maintain an activated clotting time above 480 s, and had higher heparin concentrations and lower antithrombin values compared with control patients. Neutrophil-activating peptide 2 concentrations were higher in the enoxaparin group. CONCLUSIONS: Patients treated with enoxaparin before coronary artery bypass grafting showed signs of heparin resistance intraoperatively. Enoxaparin-treated patients also had increased perioperative platelet activation. Reasons for the observed difference in platelet activation remain unclear.

Aged↗
PubMed2006

Fulminant Budd-Chiari syndrome associated with polycythemia rubra vera and factor V Leiden mutation.

Budd-Chiari syndrome (BCS) is a severe disorder characterized by hepatic venous outflow obstruction. Hypercoagulable states are the major etiological factors for the development of BCS and can be identified in about 75% of patients. Multiple etiological factors can be found in the same patient. Hematologic abnormalities, especially myeloproliferative disorders, are the most common causes of BCS. Furthermore, the prevalence of factor V Leiden mutation is three times greater in patients with BCS. Although the clinical course tends to be chronic, BCS may, on rare occasions, cause acute liver failure. Herein, we report a patient who had factor V Leiden mutation and polycythemia rubra vera, presented as fulminant BCS.

Journal Article↗
PubMed2005

Antiphospholipid syndrome with anti-prothrombin autoantibodies in a patient with an axial-flow left ventricular assist device.

Autoantibodies to prothrombin, first described almost 50 years ago, are paradoxically associated with thrombosis. Described is an unusual case of fatal hypercoagulability in a patient with multiple arterial and venous thromboembolic complications despite intense anticoagulation while being bridged to transplantation with a left ventricular assist device. Serum analysis revealed the presence of prothrombin autoantibodies and high titers of anti-nuclear antibodies, and autopsy revealed pulmonary arteriolar vasculitis. These findings suggest an autoimmune basis for the presence of anti-prothrombin antibodies and the hypercoagulable state observed in the present case.

Antibodies, Antiphospholipid↗
PubMed2004

Activation of coagulation occurs after electrical cardioversion in patients with chronic atrial fibrillation despite optimal anticoagulation with warfarin.

BACKGROUND: There is evidence for the activation of the coagulation system and a hypercoagulable state following cardioversion. The aim of the study was to determine whether electrical cardioversion in patients with chronic atrial fibrillation induced a prothrombotic state despite optimal anticoagulation. We studied the effects of electrical cardioversion on plasma levels of fibrinogen, antithrombin III, protein C and D-dimers. METHODS: We studied 24 patients with chronic atrial fibrillation who were on optimal anticoagulation and were referred for electrical cardioversion. Samples of venous blood were taken 2 h pre and post cardioversion and 1 month later. RESULTS: Plasma median concentrations of fibrinogen decreased significantly from 3.8 g/l (interquartile range 3.1-4.2 g/l) before cardioversion to 3.5 g/l (interquartile range 2.9-3.9 g/l) 2 h after cardioversion levels (P=0.004). The fibrinogen levels at 1 month post cardioversion (3.45 g/l, interquartile range 3.1-3.9 g/l) were also significantly lower than baseline (P=0.02). Plasma median levels of antithrombin III fell from 93.5 U/dl (interquartile range 89.3-97.0 U/dl) pre cardioversion to 89.5 U/dl (interquartile range 83.0-93.0 U/dl) 2 h after cardioversion (P=0.001) and returned to normal by 1 month (94.0 U/dl; interquartile range 89.3-98.5 U/dl; P=0.0001). There were no significant changes in plasma median D-dimer or protein C levels at any time. CONCLUSIONS: We have demonstrated a significant fall in the plasma fibrinogen and antithrombin III levels in patients with chronic atrial fibrillation early after electrical cardioversion, indicating thrombin generation. This study suggests that there are haemostatic changes of thrombogenesis induced by cardioversion despite optimal anticoagulation with warfarin.

Adult↗
PubMed2006

Atorvastatin reduces tissue factor expression in adipose tissue of atherosclerotic rabbits.

BACKGROUND: We have recently demonstrated that tissue factor (TF) expression increases in adipose tissues/adipocytes of cholesterol-fed rabbit, which is associated with a hypercoagulable state that contributes to thrombosis. In this study, we evaluated the ability of atorvastatin to modulate TF expression in cholesterol-fed rabbit and the regulatory mechanism. METHODS: Male rabbits were randomly fed with normal diet and high-cholesterol diet for 8 weeks, following 4 weeks, those fed high-cholesterol diet were randomly assigned to atorvastatin or starch. At the end of 12 weeks, subcutaneous adipose was collected, and culture adipocyte. TF mRNA was detected by reverse transcription-polymerase chain reaction (RT-PCR). TF concentrations were determined with ELISA. The in vitro effect of atorvastatin and mevalonate (MVA) on TF production in adipocytes was observed. RESULTS: Atorvastatin reduced serum TC and LDL-C levels (P<0.05), and decreased plasma TF concentration and expression in adipose tissues/adipocytes from cholesterol-fed rabbits. In vitro, atorvastatin dose-dependently suppressed TF expression and protein secretion in adipocytes. MVA reversed the inhibitory effect of atorvastatin on TF expression in concentration-dependent manner. CONCLUSIONS: Results provide further support for the antithrombotic effect of atorvastatin. It also indicated that mevalonate pathway may play an important role in TF expression in adipocyte.

Animals↗
PubMed2004

A flow cytometric method for determining the binding of coagulation factor X to monocytes in whole human blood.

It is known that inflammation affects the coagulation pathway, but the mechanisms are not clear. Because a persistent inflammatory condition is associated with several chronic diseases, including cardiovascular disorders, there is intense interest in determining if and how chronic inflammation contributes to a hypercoagulable state. One pathway by which inflammation interacts with coagulation is via monocyte binding and activation of coagulation Factor X (FX). Upon activation, monocytes express the alphaMbeta2 integrin CD11b/CD18, which has a binding site for the plasma protein FX. Binding is followed by the cleavage of FX into its activated form Xa(FXa) which, in turn, is responsible for the conversion of prothrombin to thrombin. To assess the contribution of this pathway, a straightforward assay in whole blood is needed for studies of inflammation-induced coagulation and thrombosis. The current assay for FXa binding requires isolation of the monocytes and measurement of bound FXa activity with a chromogenic substrate. Harvesting a sufficient number of monocytes for analysis requires a relatively large blood sample. In addition, it is known that the process of isolating neutrophils and monocytes from whole blood induces an upregulation of CD11b. Thus, the measurement process itself causes an artifact in receptor expression resulting in an overestimate of true state of monocyte activation and FX binding. To address these limitations, we developed a flow cytometric assay to directly measure the binding of FX to monocytes in whole blood. In this report we describe the methods of the procedure in detail and apply the procedure to demonstrate a significant increase of both monocyte CD11b expression and FXa binding when human blood samples were activated with the endotoxin, lipopolysaccharide in-vitro.

CD11b Antigen↗