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PubMed1998

Thrombelastographic changes and early rebleeding in cirrhotic patients with variceal bleeding.

BACKGROUND: Routine coagulation tests do not necessarily reflect haemostasis in vivo in cirrhotic patients, particularly those who have bleeding varices. Thrombelastography (TEG) can provide a global assessment of haemostatic function from initial clot formation to clot dissolution. AIM: To evaluate TEG changes in cirrhotic patients with variceal bleeding and their association with early rebleeding. PATIENTS/METHODS: Twenty cirrhotic patients with active variceal bleeding had serial TEG and routine coagulation tests daily for seven days. The TEG variables before the day of rebleeding (n = 6) were compared with those of patients without rebleeding (n = 14). RESULTS: Baseline characteristics of the rebleeding and non-rebleeding groups were comparable apart from a higher incidence of uncontrolled infection on the day of rebleeding in the rebleeding group (p = 0.007). The patients in the rebleeding group were more hypocoagulable before the day of rebleeding as shown by longer r (42 v 24 mm, p < 0.001) and k (48 v 13 mm, p < 0.001) and smaller a (12 v 38 degrees, p < 0.001) compared with the mean of daily results of the non-rebleeding group. Routine coagulation tests, however, showed no significant differences between the two groups. CONCLUSION: The results of serial TEG measurements suggest that hypocoagulability may be associated with early rebleeding in cirrhotic patients.

Adult↗
PubMed2005

Comparison of textilinin-1 with aprotinin as serine protease inhibitors and as antifibrinolytic agents.

Textilinin-1 (Q8008) was isolated from the venom of the Pseudonaja textilis and has a 47% sequence identity to the antihaemorrhagic therapeutic agent aprotinin. When equimolar concentrations of enzyme and aprotinin were pre-incubated, plasmin was inhibited 100%, plasma kallikrein 58%, and tissue kallikrein 99%. Under the same conditions, textilinin-1 inhibited plasmin 98%, plasma kallikrein 16% and tissue kallikrein 17%. Whole blood clot lysis was inhibited strongly by both aprotinin and textilinin-1, as shown by thrombelastography. At 2 microM inhibitor lysis initiated by t-PA was greater than 99% inhibited by aprotinin (LY60 = 0.4 +/- 0.1) whereas textilinin-1, inhibited lysis by 91% (LY60 = 8.9 +/- 0.7). The same trend was found with the lysis of euglobulin fractions. From these data textilinin-1 appears to be a more specific plasmin inhibitor than aprotinin but aprotinin inhibits clot lysis to a greater extent.

Animals↗
PubMed1994

Effects of hypertonic saline hydroxyethyl starch solution on collagen-induced platelet aggregation and ATP secretion.

OBJECTIVE: The purpose of this study was to investigate the effect of hypertonic (NaCl 7.5%) hydroxyethyl starch (HES 6%, molecular weight 200,000) (HHES) as used for small-volume resuscitation on global coagulation parameters and platelet function. DESIGN: Randomized, controlled clinical trial. SETTING: Intraoperative volume loading after induction of general anesthesia. PATIENTS: 27 consecutive patients [mean age 59 (22-76) years, mean body weight 69.8 (46-98) kg] undergoing abdominal surgery were studied. INTERVENTIONS: Global coagulation tests (aPTT: activated partial thromboplastin time; PT: prothrombin time; platelet count; thrombelastography: TEG), platelet aggregation and ATP release were measured before and 10 min after the application of 4 ml.kg-1 of HHES (study group H, n = 14) or HES (control group C, n = 13). RESULTS: The aPTT was prolonged and platelet count was significantly reduced in both study groups. In contrast to the HES group, clot formation time in the TEG was significantly prolonged and the maximum amplitude was reduced in the HHES group. Furthermore, platelet aggregation was significantly slowed down, whereas ATP release significantly increased in the HHES group. CONCLUSION: The changes in global coagulation parameters can be explained by dilutional effects of the infused solution. The hyperosmolar saline compound of the HHES solution obviously contributes to the slowing down of platelet aggregation. Osmotic stress and membrane pleating may aggravate HES-induced changes in membrane fluidity and microviscosity and thus explain this impaired interaction. The increase in ATP release suggests a change in receptor-second messenger interaction for delta granule release.

Abdomen↗
PubMed2003

Role of blood coagulation factor XIII in patients with acute pulmonary embolism. Correlation of factor XIII antigen levels with pulmonary occlusion rate, fibrinogen, D-dimer, and clot firmness.

In patients with acute pulmonary embolism (PE), pulmonary occlusion rate is directly related to D-dimer and inversely related to fibrinogen levels. The role of coagulation factor XIII (FXIII) levels in acute venous thromboembolism is not known. A total of 120 consecutive patients with suspected PE and VIDAS D-dimer levels >500 micro g/L were investigated by helical computed tomography (CT). Pulmonary occlusion rate was assessed by CT using the modified Miller index. D-dimer, fibrinogen, and FXIII A- and B-subunit antigen levels were taken on admission. Thrombelastography (TEG) was performed in a subset of patients (n = 12). The 71 patients with PE had lower FXIII A-subunit levels than the 49 patients with excluded PE (78.6 +/- 24.5% vs. 91.3+/-28.8%, p=0.01). In both groups, FXIII A-subunit was inversely related to D-dimer levels. FXIII A-subunit correlated with fibrinogen levels in patients with PE but not in patients without PE. FXIII A-subunit decreased with increasing pulmonary occlusion rate. The risk of PE was increased in the presence of A-subunit levels < 60% (OR 7.0 [95% CI 1.4-35.3], p = 0.019). Clot firmness determined by TEG was lower in patients with PE than in patients without PE. In patients with PE, circulating FXIII A-subunit is decreased compared to patients with suspected but excluded PE. The higher the clot burden within the pulmonary arteries the lower the FXIII antigen. In these patients, direct relation of FXIII A-subunit to fibrinogen levels argues for significant consumption of these coagulation factors in PE. This consumption of FXIII can also be detected by a global coagulation test like TEG.

Acute Disease↗
PubMed2001

Haemodilution-induced enhancement of coagulation is attenuated in vitro by restoring antithrombin III to pre-dilution concentrations.

Moderate haemodilution enhances coagulability in vitro and in vivo as measured by thrombelastography (TEG). The mechanism has never been established. We have conducted an in vitro study to determine whether the effect can be moderated or prevented when the reduction in antithrombin III caused by dilution is prevented by supplementation. Blood from 20 volunteers was divided into four samples. One sample was not diluted and served as control (C). Another was diluted (by 20%) with saline (S). The third was diluted by 20% with saline plus two units of antithrombin (AT III) (SA). The fourth remained undiluted, with two units of added AT III (CA). Coagulation was measured in all four samples using the TEG. In a separate laboratory study, the levels of AT III were measured in control samples and compared with levels after 20% dilution, and 20% dilution with two units of AT III added to the diluent. Enhanced coagulation was demonstrated in saline-diluted samples (S) by shortening of r- and k-times, and increased alpha angle. In the SA samples, r-time shortening was prevented; k-time shortening and alpha-angle increase persisted, but to a reduced degree (difference from saline-only dilution P<0.051). There were no differences between samples C and CA. A predictable drop of AT III (24.2%) occurred with saline dilution, while AT III levels in the AT III/Saline group were similar to the undiluted control. Haemodilution-induced coagulation enhancement is attenuated, but not prevented, if AT III levels are maintained in the normal range. This is in keeping with the established concept of an antithrombin threshold preventing positive coagulation feedback into the intrinsic pathway.

Antithrombin III↗
PubMed1994

Thrombelastographic patterns following abdominal aortic surgery.

Postoperative changes in thrombelastographic patterns were studied in thirty patients undergoing elective abdominal aortic bypass surgery. Native whole blood thrombelastography was performed preoperatively and on days 1, 2, and 3 postoperatively. The thrombelastographic changes included a decrease in r on day one (P < 0.0001), with concurrent increases in alpha (P < 0.0001) and MA (P < 0.001). On days 2 and 3 there were further increases in MA (P < 0.0001). These changes indicate enhanced procoagulant activity and progressive increases in maximum clot strength. The results confirm that hypercoagulability occurs in whole blood following abdominal aortic bypass surgery. Further studies are warranted to determine whether modification of postoperative hypercoagulability reduces the incidence of thrombotic complications in this group of patients.

Aged↗
PubMed2002

Thrombelastographic changes in OPCAB surgical patients.

The purpose of this study was to determine whether thrombelastography could detect hypercoagulability in the off-pump coronary artery bypass (OPCAB) patient. Seventeen OPCAB and six cardiopulmonary bypass (CPB) patients were studied pre- and postprocedure, as well as on each of the first three postoperative days (POD). In the OPCAB patients, there was a small reduction in the postprocedure coagulation index (CI). This was followed by an increase in the CI on each of the next three POD, reaching a level exceeding the mean preprocedure CI by 2.32 units, indicative of a state of relative hypercoagulability. The mean CI for the CPB patients decreased significantly in the postprocedure sample. Over the next 72 h, the CI increased to a level that nearly equaled the preprocedure 'baseline'. We concluded that our study identified a state of relative hypercoagulability in the OPCAB patient 72 h after surgery. The mechanism of this hypercoagulation, as well as the clinical significance of this finding, is yet to be determined.

Aged↗
PubMed2004

Peroxynitrite decreases rabbit tissue factor activity in vitro.

UNLABELLED: Tissue factor (TF) is a primary initiator of physiological coagulation in vivo. Peroxynitrite (OONO(-)), a molecule formed from nitric oxide (NO) and superoxide (O(2). (-)), decreases human TF activity in vitro. Coagulopathy has been associated with hepatoenteric ischemia-reperfusion known to involve formation of OONO(-). Further, circulating TF activity decreases in rabbits after hepatoenteric ischemia-reperfusion. We hypothesized that exposure of rabbit TF to OONO(-) would result in a decrease in activity. OONO(-) generation was performed with 3-morpholinosydnonimine (SIN-1), a molecule that produces both nitric oxide and superoxide. Rabbit brain TF was incubated at 37 degrees C for 90 min with 1) 0 mM SIN-1, 2) 5 mM SIN-1, 3) 5 mM SIN-1 and 2000 U/mL recombinant human superoxide dismutase (hSOD1), or 4) 2000 U/mL hSOD1 (n = 8 per condition). TF activity was assessed by addition of TF samples to human plasma and measuring clot formation kinetics with a thrombelastograph(R). TF exposure to SIN-1 resulted in a 48% decrease in activity that was significantly different from the other three conditions (P < 0.001). There were no significant differences between the other conditions. We conclude that rabbit TF is inhibited by OONO(-), and further investigation to determine the role of OONO(-) in coagulopathies associated with hepatoenteric ischemia-reperfusion is warranted. IMPLICATIONS: Tissue factor (TF) initiates physiological coagulation in vivo. Hepatoenteric ischemia-reperfusion injury is associated with peroxynitrite (OONO(-)) formation, coagulopathy and decreased TF activity in rabbits. We determined that OONO(-) decreased rabbit TF activity in vitro via thrombelastography(R).

Animals↗
PubMed2004

Peroxynitrite inactivates tissue plasminogen activator.

UNLABELLED: Tissue plasminogen activator (tPA) has a prominent role in physiological fibrinolysis in vivo. Thrombosis has been associated with clinical scenarios (e.g., atherosclerotic disease) known to involve local decreases in tPA activity with concomitant formation of reactive nitrogen species such as peroxynitrite (OONO(-)), a molecule formed from nitric oxide and superoxide. We hypothesized that exposure of tPA to OONO(-) would result in a decrease in tPA activity. OONO(-) was generated with 3-morpholinosydnonimine (SIN-1), a molecule that produces both nitric oxide and superoxide. Recombinant tPA was incubated at 37 degrees C for 60 min with 0 microM SIN-1; 100 microM SIN-1; 100 microM SIN-1 and 4000 U/mL recombinant human superoxide dismutase; or 4000 U/mL recombinant human superoxide dismutase (n = 8 separate reactions per condition). Changes in tPA activity were assessed by addition of tPA samples to tissue factor-exposed human plasma and measuring clot fibrinolysis with a thrombelastograph. Exposure to SIN-1 resulted in a decrease in tPA-mediated fibrinolysis (<1% activity of tPA not exposed to SIN-1) that was significantly (P < 0.001) different from the other three conditions. There were no significant differences between the other conditions. We conclude that tPA is inhibited by OONO(-), and that OONO(-) may have a role in clinical thrombotic scenarios. IMPLICATIONS: Tissue plasminogen activator (tPA) has a prominent role in fibrinolysis in vivo. Thrombosis has been associated with clinical scenarios involving decreases in tPA activity with concomitant formation of the oxidant peroxynitrite. We determined that peroxynitrite decreased tPA activity via thrombelastography. Peroxynitrite-mediated tPA inactivation may have a role in thrombotic states.

Antioxidants↗
PubMed2004

Peroxynitrite decreases hemostasis in human plasma in vitro.

Coagulopathy has been associated with clinical scenarios that involve reactive nitrogen species such as peroxynitrite (OONO-). Further, OONO- decreases tissue factor and fibrinogen function in vitro. Thus, we hypothesized that exposure of plasma to the OONO- generated with 3-morpholinosydnonimine (SIN-1), a molecule that produces both nitric oxide and superoxide, would result in a decrease in hemostatic function via diminished coagulation protein activity. Hemostatic function of plasma exposed to SIN-1 (0, 1, 5, and 10 mM for 60 min at 37 degrees C) was assessed with thrombelastography, activated partial thromboplastin time, and prothrombin time in the presence or absence of superoxide dismutase (SOD) or an OONO- scavenger. SIN-1 exposure resulted in a significant (P < 0.05), dose-dependent decrease in plasma hemostatic function and concurrent significant (P < 0.05) decreases in activities of factor VII, factor VIII complex, and factor X. Fibrinogen concentration was not affected by SIN-1. Antithrombin and protein C activity also decreased significantly (P < 0.05). Coincubation with SOD or an OONO- scavenger significantly (P < 0.05) attenuated SIN-1 mediated changes in hemostasis and procoagulant/ anticoagulant activity. We conclude that OONO- may decrease hemostatic function in human plasma by nitration of key procoagulants and that OONO- may play a significant role in hemorrhagic states.

Blood Coagulation Factors↗
PubMed2004

Changes in thrombelastograph variables associated with aging.

Aging is associated with hypercoagulability. To assess thrombelastography (TEG) variables associated with aging, 132 adult patients of various ages undergoing orthopedic surgery for fracture repair had venous blood samples withdrawn for testing of recalcified TEG before the induction of anesthesia. Age was weakly correlated with all TEG variables: r time (R) (r = -0.45, P < 0.001; R = 19.5 - 0.09 x age), k time (K) (r = -0.49, P < 0.001; K = 6.5 - 0.04 x age), maximum amplitude (MA) (r = 0.25, P < 0.01; MA = 53.3 + 0.07 x age), and alpha (r = 0.52, P < 0.001; alpha = 52.8 + 0.2 x age). The correlation was stronger for men than for women. Only R was significantly correlated with age when the women were separately analyzed. Part of the correlation may be attributable to a concurrent decrease in hemoglobin with aging, but age remained an independent predictor of R, K, and alpha on forward stepwise linear multiple regression analysis. Aging was weakly associated with changes in TEG variables, which should be allowed for when interpreting TEG measurements in the elderly.

Adolescent↗
PubMed2004

Decreased factor XIII availability for thrombin and early loss of clot firmness in patients with unexplained intraoperative bleeding.

To explore relevant changes in unexplained intraoperative bleeding, we evaluated elements of the final steps of the coagulation cascade in 226 consecutive patients undergoing elective surgery. Patients were stratified for the occurrence of unexplained intraoperative bleeding according to predefined criteria. Twenty patients (8.8%) developed unexplained bleeding. The median intraoperative blood loss was 1350 mL (bleeders) and 400 mL (nonbleeders) (P < 0.001). Fibrinogen and Factor XIII (F. XIII) were more rapidly consumed in bleeders (P < 0.001). Soluble fibrin formation (fibrin monomer) was increased in bleeders throughout surgery (P < or = 0.014). However, F. XIII availability per unit thrombin generated was significantly decreased in bleeders before, during, and after surgery (P < or = 0.051). Computerized thrombelastography showed a parallel, significant reduction in clot firmness. We suggest that mild preexisting coagulopathy is not rare in surgical patients and probably can result in clinically relevant intraoperative bleeding. This hemostatic disorder shows impaired clot firmness, probably secondary to decreased cross-linking (due to a loss of F. XIII, both in absolute measures and per unit thrombin generated). We suggest that the application of F. XIII might be worthwhile to test in a prospective clinical trial to increase clot firmness in patients at risk for this intraoperative coagulopathy.

Adolescent↗
PubMed2004

A novel method to assess platelet inhibition by eptifibatide with thrombelastograph.

We examined a novel method to detect platelet inhibition with thrombelastography (TEG). We hypothesized that this method would be suitable for monitoring the antiplatelet effects of eptifibatide (Integrilin). Whole blood from healthy volunteers was anticoagulated with 3.2% citrate or unfractionated heparin (7 IU/mL). For the platelet aggregation test, both citrate and heparinized samples were spiked with increasing concentrations of eptifibatide (0, 0.2, 0.4, 0.8, 1.6, and 4 microg/mL). Conventional kaolin TEG was performed with citrated samples, and batroxobin-modified TEG was performed with heparinized samples, which were spiked with eptifibatide at concentrations of 0, 0.4, 0.8, 1.6, 4, 8, and 24 microg/mL. Adenosine 5'-diphosphate-induced platelet aggregation was reduced to 6.4% +/- 2.9% (citrate) and 10.3% +/- 4.8% (heparin) with eptifibatide at the concentration of 4 mug/mL. The kaolin TEG showed a decrease in maximum amplitude (MA) only at the eptifibatide concentration of 24 mug/mL and no change in alpha angle, whereas with the batroxobin-based TEG, the difference in MA and alpha angle was observed at concentrations >/=0.8 microg/mL. Additionally, the time to achieve maximum MA was much shorter for batroxobin TEG than for kaolin TEG. We conclude that the batroxobin-modified TEG is a sensitive method that detects platelet inhibition induced by eptifibatide.

Adenosine Diphosphate↗
PubMed2006

The effect of fibrinogen substitution on reversal of dilutional coagulopathy: an in vitro model.

Colloids and crystalloids are usually administered as treatment for hypovolemia in severely injured patients. However, dilution of clotting factors and platelets together with impaired fibrinogen polymerization are associated with fluid therapy and may aggravate hemorrhage, thus worsening final outcome of these patients. We investigated, in an in vitro model, whether the addition of fibrinogen to diluted blood samples can reverse dilutional coagulopathy. Blood from 5 healthy male volunteers was diluted by 60% using lactated Ringer's solution, 4% modified gelatin solution, or 6% hydroxyethyl starch 130/0.4, as well as the combination of lactated Ringer's solution with either of the 2 colloid solutions. Thereafter, aliquots of diluted blood samples were incubated with 3 different concentrations of fibrinogen (0.75, 1.5, and 3.0 mg/mL). Measurements were performed by modified thrombelastography (ROTEM; Pentapharm, Munich, Germany). After 60% dilution, clotting times increased, whereas clot firmness and fibrin polymerization decreased significantly. After administration of fibrinogen, clotting times decreased and clot firmness, as well as fibrin polymerization, increased in all diluted blood samples. The effect of in vitro fibrinogen substitution on ROTEM variables was dependent on the fibrinogen dosage and the type of solution used to dilute the blood samples.

Adult↗
PubMed2006

A head-to-head comparison of the in vitro coagulation effects of saline-based and balanced electrolyte crystalloid and colloid intravenous fluids.

Both fluid composition (e.g., type of hydroxyethyl starch) and formulation (e.g., saline or balanced salt carrier solution) may alter whole blood coagulation. We therefore enrolled 10 healthy volunteers to test ex vivo, thrombelastograph-based blood coagulation differences of eight crystalloid and colloid solutions at 20%, 40%, and 60% dilutions. Saline and lactated Ringer's solution produced a hypercoagulable state at 20%-40% dilutions. Saline, hetastarch in saline, pentastarch in saline, tetrastarch in saline, and human albumin solutions all produced a hypocoagulable state at 60% dilution. Hetastarch in saline also produced a hypocoagulable state at 40% dilution. The larger molecular weight starches produced more intense coagulation abnormalities than the medium molecular weight compounds formulated similarly (i.e., suspended in saline or balanced salt solution). The balanced salt solutions caused fewer coagulation abnormalities, especially pentastarch in balanced salt solution. This balanced salt pentastarch preparation produced the least derangement of coagulation of the colloid solutions at all dilutions, causing hypercoagulability at the lower dilutions and minimal coagulation derangement at 60% dilution. These data support the theory that smaller molecular weight hydroxyethyl starches and colloids suspended in balanced salt solutions preserve coagulation better than large molecular weight starches and saline-based colloids, as judged by thrombelastography.

Analysis of Variance↗
PubMed2006

Fibrinogen concentrate reverses dilutional coagulopathy induced in vitro by saline but not by hydroxyethyl starch 6%.

Severe bleeding often induces coagulopathy via loss, consumption, and dilution of clotting factors and platelets. The aims of our in vitro study were to characterize the influence of progressive hemodilution with either NaCl 0.9% or hydroxyethyl starch (HES) 6% on blood clot formation and to analyze the effect of substitution of fibrinogen and platelets on dilutional coagulopathy. Whole blood samples drawn from 8 volunteers were diluted from 20% to 80% of the sample volume with both diluents separately. Clot formation was measured by thrombelastography. At a 60% dilution, either fibrinogen and/or platelets were added to the samples. Clot firmness became critical after 40% dilution with HES 6% but not until 60% dilution with NaCl 0.9%. When platelet function was blocked, fibrin polymerization was severely impaired after 20% dilution with HES 6%, whereas such an effect was only seen after 80% dilution with NaCl 0.9%. The addition of fibrinogen reconstituted the clot firmness in the presence of NaCl 0.9%, but this had only a minor effect after dilution with HES 6%. Platelets alone or in addition were not able to improve clot firmness to a clinically relevant extent. Dilutional coagulopathy induced by crystalloids can, in vitro, be effectively reversed by supplementation of fibrinogen. In contrast, HES molecules interfere with fibrin polymerization and, thus, administration of fibrinogen after dilution with HES 6% failed to significantly improve clot firmness.

Analysis of Variance↗
PubMed2007

Qualitative thrombelastographic detection of tissue factor in human plasma.

BACKGROUND: Tissue factor (TF) is the principal in vivo initiator of coagulation, with normal circulating TF concentrations reported to be approximately 23-158 pg/mL. However, patients with atherosclerosis or cancer have been reported to have TF concentrations ranging between 800 and 9000 pg/mL. Of interest, thrombelastographic (TEG)-based measures of clot initiation and propagation have demonstrated hypercoagulability in such patients at risk for thromboembolic events. Thus, our goal in the present investigation was to establish a concentration-response relationship of the effect of TF on TEG variables, and determine specificity of TF-mediated events with a monoclonal TF antibody. METHODS: Thrombelastography was performed on normal human plasma exposed to 0, 500, 1000, or 2000 pg/mL TF. Additional experiments with plasma exposed to 0 or 750 pg/mL TF in the presence or absence of a monoclonal TF antibody (1:360 dilution, 10 min incubation) were also performed. Clot initiation time (R) and the speed of clot propagation (MRTG, maximum rate of thrombus generation) were determined. RESULTS: The addition of TF to normal plasma resulted in a significant, concentration-dependent decrease in R and increase MRTG values. The addition of TF antibody to samples with TF significantly increased R and decreased MRTG values compared to samples with TF addition. CONCLUSIONS: In conclusion, changes in TEG variables in conjunction with use of a TF antibody can detect pathological concentrations of TF in human plasma in vitro. Further investigation is warranted to determine if TEG(R)-based monitoring could assist in the detection and prevention of TF-initiated thromboembolic events.

Blood Coagulation↗