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PubMed1985

Hemostatic effectiveness of fibrin glue derived from single-donor fresh frozen plasma.

Fibrin glue derived from pooled human blood is an effective sealant for high-porosity vascular grafts and a valuable topical hemostatic agent in heparinized patients. Use of this agent in the United States is prohibited because of potential transmission of hepatitis B, acquired immunodeficiency syndrome, and other serologically transmitted illnesses. We have developed a cryoprecipitation technique that allows preparation of fibrin glue from single-donor fresh frozen plasma. Use of this agent presumably entails no greater risk of disease transmission than intravenous administration of single-unit fresh frozen plasma. This report describes our early clinical experience with this material. Fibrin glue was used as a sealant for porous woven Dacron tubular prostheses and cardiovascular patches in 19 patients. The fibrin glue sealant has also been employed to control bleeding from needle holes and small anastomotic tears in 22 patients. No patient in this series had a bleeding complication from a suture line or graft treated with fibrin glue. This experience indicates that like fibrin glue from pooled blood, fibrin glue from single-donor plasma is effective as a graft sealant and topical hemostatic agent. Preparation of fibrin glue from single-donor plasma is simple and economical, and may provide cardiothoracic surgeons in the United States with a widely available, valuable hemostatic adjunct.

Blood Donors↗
PubMed2002

An open label, comparative study of the effects of a dose-reduced oral contraceptive containing 20 microg ethinyl estradiol and 100 microg levonorgestrel on hemostatic, lipids, and carbohydrate metabolism variables.

In this open label, randomized study we compared the influence of a dose-reduced oral contraceptive containing 20 microg ethinyl estradiol (EE) and 100 microg levonorgestrel (20 EE) with a reference preparation containing 30 microg EE and 150 microg levonorgestrel (30 EE) on hemostatic, lipids, and carbohydrate metabolism variables. Data from 48 volunteers were obtained. The direction of the change (increase or decrease) in most of the hemostatic variables were similar in both treatment groups. In particular, prothrombin fragment 1 + 2 increased during treatment, reaching a median percent change of 40% in the 20 EE group and of 17% in the 30 EE group after one year. D-Dimer fibrin split products remained virtually unchanged, with no change at Cycle 13. The median HDL2 cholesterol levels decreased by 26% in the 20 EE group and by 39.8% in 30 EE group (p = 0.0045 for group difference) after one year. The median one year change for LDL cholesterol was 3.23% in the 20 EE group, compared to 25% in the 30 EE group, for VLDL 11.1% compared to 38.8%, respectively, and for total triglycerides 10.0% compared to 37.5%, respectively. The median absolute change for the area under the curve (AUC)(0-3h) for glucose at treatment Cycle 13 was 41.25 mmol/L x min in the 20 EE group and 73.50 mmol/L x min in the 30 EE group. The AUC(0-3h) insulin at treatment Cycle 13 decreased in the 20 EE group by 1635.0 pmolL x min and increased in the 30 EE group by 11797.5 pmolL x min (p = 0.0491 for group difference). Both study treatments were safe and well tolerated by the volunteers. In conclusion, the balanced one-third dose reduction in this new oral contraceptive evoked similar effects on the hemostatic variables, but favorable results for the lipid and carbohydrate profiles.

Adolescent↗
PubMed1995

Characteristics of blood hemostatic markers in a patient with ovarian hyperstimulation syndrome who actually developed thromboembolism.

OBJECTIVE: To investigate whether a patient with ovarian hyperstimulation syndrome (OHSS) demonstrated characteristic changes in the blood hemostatic markers before she developed thromboembolism. DESIGN: Patients with OHSS had blood drawn to determine hemostatic markers and related factors. PATIENTS: Twenty-three OHSS patients, including a case complicated with thromboembolism. SETTING: The IVF-ET program of the Department of Obstetrics and Gynecology, The University of Akita, School of Medicine. MAIN OUTCOME MEASURES: Blood hemostatic markers and related factors. RESULTS: The patient with thromboembolism demonstrated marked leukocytosis and higher levels of activation in the blood markers related to fibrinolytic system, such as alpha 2 plasmin inhibitor, plasmin-alpha 2 antiplasmin complexes, and D-dimers, before the onset of this episode. CONCLUSION: Marked leukocytosis and higher levels of activation of the fibrinolytic system may be the signs of imminent thromboembolism in OHSS patients.

Adult↗
PubMed2000

Hemostatic disturbances in patients with systemic inflammatory response syndrome (SIRS) and associated acute renal failure (ARF).

Endothelial damage plays a central role in the development of an SIRS-related Multiple Organ Dysfunction Syndrome (MODS) as a consequence of the establishment of a hemostatic imbalance between coagulation and fibrinolysis systems. Until now, sepsis is the SIRS model that has been most studied. The aim of this study was to assess the endothelial damage and the hemostatic imbalance in early stages of an SIRS of different origins, and to study if there are any differences in these disturbances between infectious and noninfectious SIRS. The endothelial damage and hemostatic changes were studied in 40 patients with SIRS (with less than 12 h of evolution) and an acute renal failure. Infectious SIRS was diagnosed in 19 cases and noninfectious SIRS in the remaining 21 patients. Patients with SIRS presented significantly higher values (p<0.001) for factors related to endothelial damage [von Willebrand factor (vWF), thrombomodulin, tissue plasminogen activator (t-PA), and plasminogen activator inhibitor type 1 (PAI-1) antigen], hypercoagulability [prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complexes (TAT)], and fibrinolysis (D-dimer and PAI activity) with respect to the control group. However, although the group with infectious SIRS presented higher values for all the factors except for the t-PA and D-dimer with respect to SIRS of other origins, none of these differences reached statistical significance (p>0.05). Our data show that patients with SIRS and associated acute renal failure, irrespective of the origin (infectious or noninfectious), show signs of intense endothelial damage and hypercoagulability throughout the process.

Acute Disease↗
PubMed2002

Markers of hemostatic system activation during treatment of deep vein thrombosis with subcutaneous unfractionated or low-molecular weight heparin.

Prothrombin fragments (F1+2), thrombin-antithrombin complexes (TAT) and D-dimers, markers of hemostatic system activation, were measured in 59 consecutive patients with deep vein thrombosis (DVT). Patients were randomly treated either with subcutaneous unfractionated heparin (UH) administered in two to three subcutaneous doses adjusted to activated partial thromboplastin time (APTT) or with low-molecular weight heparin (LMWH) (dalteparin) administered in a fixed dose of 200 IU/kg body weight in one subcutaneous injection daily. Before treatment, F1+2, TAT and D-dimer were above the cut-off level in 27/59 (46%), 34/59 (58%) and all (100%) patients, respectively. Significant associations were observed between F1+2 and TAT (r=.66, P<.001), TAT and D-dimer (r=.36, P<.005) and F1+2 and D-dimer (r=.30, P<.050). On the third day of treatment, F1+2 and TAT significantly decreased to reference values in almost all patients (in 64/66 determinations of both F1+2 and TAT) and remained low on the seventh day of treatment. Compared to pretreatment values, a nonsignificant decrease of D-dimer was noted in both groups, but all values remained above the cut-off value. When markers of hemostatic system activation in the UH and LMWH groups were compared, no significant differences were observed. It was concluded that subcutaneous UH in an APTT-adjusted dose and subcutaneous LMWH in a once-daily weight-adjusted dose controlled these markers of hemostatic system activation in a similar manner.

Adult↗
PubMed1999

Endothelial cell and hemostatic activation in relation to cytokines in patients with sepsis.

Sepsis is commonly associated with disturbances of the hemostatic balance. Most of the pathophysiological changes in sepsis are caused by endotoxin acting directly through endothelial injury or indirectly through release of cytokines with procoagulant effects. The relation between cytokines and hemostatic parameters was assessed in 32 patients with sepsis. Prothrombin fragment 1+2 (F1+2), thrombin-antithrombin III complexes (TAT), tissue type plasminogen activator (t-PA) functional and antigen, plasminogen activator inhibitor-1 (PAI-1), plasminalpha2-antiplasmin complexes (PAP), D-Dimer, thrombomodulin (TM) and von Willebrand factor (vWF) were measured in patients and in 30 healthy subjects. The levels of cytokines TNF-alpha and interleukin-6 (IL-6) also were determined. A significant increase of F1+2, TAT, PAI-1, PAP, and D-Dimer was observed in septic patients as compared with controls (p<0.0001), whereas t-PA activity was significantly reduced (p<0.01). The markers of endothelial cell activation TM, vWF, and t-PA antigen also were elevated significantly as compared with the control group (p<0.01). Finally, we found a marked increase of TNF-alpha and IL-6 (p<0.0001). Whereas the increase of cytokine levels could be partially responsible for the hemostatic activation, it did not correlate with markers of endothelial activation in patients with sepsis.

Antithrombin III↗
PubMed1999

The relationship between the onset of labor mechanisms and the hemostatic system.

The relationship between onset of labor and the hemostatic system was evaluated in 38 pregnant women. The hemostatic system consists of blood coagulation, kinin-kallikrein system, the fibrinolytic system, and platelet function. The most prominent changes take place in the kinin-kallikrein system. After the onset of labor, prekallikrein decreases rapidly which may trigger changes in blood coagulation and the fibrinolytic system. Platelet hemostatic capacity (PHC) was also measured using the PFA-100 (platelet function analyzer) system. Closure times (CT) were shorter during pregnancy, compared to non-pregnant controls, suggesting an increase in PHC. Platelet aggregation by ADP at the end of pregnancy was decreased at the onset of labor. At the same time a slight increase in FDP (fibrin degeneration product) was also seen. While FDP increased, platelet aggregation decreased, which seems to suggest FDP inhibits platelet aggregation. In this manner, these three systems(kinin-kallikrein system, blood coagulation, and fibrinolytic system) and platelet aggregation are closely interrelated, possibly affecting uterine contractility during pregnancy and the onset of labor.

Factor XII↗
PubMed1999

Pravastatin therapy in hyperlipidemia: effects on thrombus formation and the systemic hemostatic profile.

OBJECTIVES: The study sought to determine the effects of lipid-lowering with pravastatin on the systemic fibrinolytic profile and on thrombus formation under dynamic flow conditions. BACKGROUND: Lowering cholesterol (C) decreases clinical events in coronary artery disease (CAD) patients, but an analysis of the effects of lipid-lowering on the entire hemostatic and thrombotic profile has not been conducted. METHODS: We prospectively studied 93 stable patients with untreated low-density lipoprotein cholesterol (LDL-C) >145 mg/dl. The CAD patients received pravastatin, and non-CAD patients were randomized to pravastatin versus placebo (double-blind). Thrombus formation upon an injured vascular surface was assessed in a substudy of 40 patients with a previously validated ex vivo perfusion chamber system. Systemic hemostatic markers and thrombus formation were evaluated at baseline, three and six months. RESULTS: Placebo produced no changes in either the lipid profile, any of the hemostatic markers, or the ex vivo thrombus formation. Both pravastatin groups (CAD and non-CAD) showed decreased LDL-C by 30% within 6 weeks (188 to 126 mg/dl, p < 0.001 vs. baseline), and decreased plasminogen activator inhibitor-1 at 3- and 6-month follow-up compared to baseline (15% to 18% decrease at 3 months and 21% to 23% at 6 months). For the tissue plasminogen activator antigen, CAD and non-CAD groups showed significant decreases at 6 months compared to baseline (10% and 13%, respectively). No significant changes were observed with treatment in d-dimer, fibrinopeptide A, prothrombin fragment F1.2, factor VIIa, von Willebrand factor, or C-reactive protein. Fibrinogen levels were significantly increased at 6 months compared to baseline, though still below the upper normal limit. In the perfusion chamber substudy, there was a decrease in thrombus area in non-CAD patients treated with pravastatin at both 3 and 6 months compared to baseline (by 21% and 34%, respectively). The CAD patients showed decreases in thrombus formation by 13% at 3 months, and by 16% at 6 months. The change in LDL-C- correlated modestly with the change in thrombus formation (r = 0.49; p < 0.01). CONCLUSIONS: Pravastatin therapy significantly decreased thrombus formation and improved the fibrinolytic profile in patients with and without CAD. These early effects may, in part, explain the benefit rendered in primary and secondary prevention of CAD.

Aged↗
PubMed1999

Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction.

OBJECTIVES: The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND: Increased plasma hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical data concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS: Blood samples were obtained from 64 patients (mean age 67 +/- 11 years; 49 male) with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasma concentrations of fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS: The follow-up time was 27 +/- 17 months, and 19 patients died of cardiac causes during the follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86; 95% confidence interval [CI] 1.55-15.19), left ventricular ejection fraction (hazard ratio 0.94; 95% CI 0.90-0.99), FPA (hazard ratio 1.54; 95% CI 1.13-2.10), F1+2 (hazard ratio 2.03; 95% CI 1.17-3.53) and TAT (hazard ratio 1.88; 95% CI 1.27-2.79) as significant factors associated with cardiac mortality. In multivariate analyses, only FPA level (hazard ratio 1.84; 95% CI 1.03-3.30) and left ventricular ejection fraction (hazard ratio 0.93; 95% CI 0.88-0.98) were independent predictors of cardiac mortality. CONCLUSIONS: Elevated FPA in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction.

Adult↗
PubMed2002

Hyperhomocyst(e)inemia and hemostatic factors: the atherosclerosis risk in communities study.

PURPOSE: To determine whether homocyst(e)ine (H(e)) is related to hemostatic factors in a population-based sample without evidence of cardiovascular disease. METHODS: A subsample of 660 participants--67 African-American women, 53 African-American men, 201 white women, and 339 white men--was selected from the Atherosclerosis Risk in Communities Study baseline cohort. This was based on carotid intimal-medial wall thickness above the 90th percentile or below the 75th percentile of the population distribution, assessed by B-mode ultrasonography. Unadjusted and multivariable-adjusted associations between fasting plasma H(e) and the hemostatic factors fibrinogen, factor VII:c, factor VIII:c, protein C antigen, hematocrit, platelet count, beta-thromboglobulin (beta-TG), tissue plasminogen activator (tPA), PAI-1, D-dimer, and lipoprotein[a] were examined. RESULTS: Mean age-adjusted H(e) was positively, albeit weakly, correlated with beta-TG, tPA, hematocrit, D-dimer and PAI-1; inversely correlated with protein C; and was higher in smokers, men and African-Americans. In multivariable regression, beta-TG, tPA, and factor VII:c were positively associated with H(e), as well as age, black race, male sex, and current cigarette smoking. CONCLUSIONS: These cross-sectional data for a biracial group of middle-aged individuals suggest that H(e) levels falling below values consistent with homocyst(e)inemia are associated with several prothrombotic factors after adjustment for sociodemographic factors. If H(e) change is antecedent to altered hemostasis, FDA-mandated fortification of grain products with folic acid for prevention of fetal neural tube defects may lead to both reduced plasma H(e) levels and improved hemostatic profiles.

Age Factors↗
PubMed2002

Genetic variants of the hemostatic system and development of transplant coronary artery disease.

BACKGROUND: The occurrence of coronary artery disease (CAD) after heart transplantation may represent an accelerated inflammatory and thrombotic response to coronary vascular endothelial cell injury. Several common mutations involving hemostasis and cellular adhesion proteins have been associated with genetic susceptibility to native coronary heart disease. The clinical setting of heart transplantation provides a unique opportunity to examine the relative contribution of circulating (i.e., recipient) vs local vascular (i.e., donor) hemostatic components to the occurrence of CAD. METHODS: We performed genotyping for several common hemostatic polymorphisms among 53 cardiac transplant patients and their heart donors. Patients were observed for an average of 43 months, and the presence of transplant CAD was determined by coronary angiography. RESULTS: The development of transplant CAD did not relate to recipient hemostatic genotype, but 2 donor polymorphisms (PAI-1 4G/5G and alpha(2) integrin C807T) were important predictors of transplant CAD. The risk ratio (RR) of transplant CAD associated with donor PAI-1 4G/4G genotype was 2.6 (95% confidence interval [CI] 1.1-6.2) and was modified by recipient cytomegalovirus status, hyperlipidemia, diabetes, and recipient factor XIII Val34Leu genotype. The RR of transplant CAD associated with donor alpha(2) integrin 807 T/T genotype was 7.4 (95% CI, 2.5-22.0). CONCLUSIONS: Genetic and metabolic factors contributed by both donor and recipient may interact at the level of the coronary vessel wall in the development of transplant-associated CAD, and this finding may provide additional support for the importance of local thrombotic response to endothelial injury in the pathogenesis of this disorder.

Adolescent↗
PubMed1998

Lack of Correlation Between Activation of Hemostatic Mechanism and Inflammation in Unstable Angina Pectoris.

In the acute phase of unstable angina, activation of the hemostatic mechanism is demonstrated by an increase in the plasma levels of markers of thrombin generation (prothrombin fragment 1+2) and thrombin activity (fibrinopeptide A). Increased concentrations of plasma C-reactive protein, an acute-phase reactant, have also been reported in patients with unstable angina. However, whether there is a correlation between the activation of the hemostatic mechanism and the acute-phase reaction of inflammation remains unclear. We measured the plasma levels of prothrombin fragment 1+2, fibrinopeptide A, and C-reactive protein in 91 patients consecutively hospitalized with recent-onset rest angina (Class IIIB Braunwald's classification), finding that they were above the normal limits in 48 (53%), 45 (49%), and 30 (33%) patients, respectively. There was no correlation between prothrombin fragment 1+2 and fibrinopeptide A (P = 0.34), prothrombin fragment 1+2 and C-reactive protein (P = 0.10), or fibrinopeptide A and C-reactive protein (P = 0.75). Plasma levels of prothrombin fragment 1+2 and fibrinopeptide A were both above normal levels in 32% of patients; 19% had both prothrombin fragment 1+2 and C-reactive protein, and 18% both fibrinopeptide A and C-reactive protein levels above the upper normal limits. All three markers were abnormally high in 11% of patients. According to the kappa cofficient test, the agreement between the elevation of the plasma concentrations of the markers was "random." In approximately half of the patients with acute unstable angina, there was an increase in the markers of the activation of the hemostatic mechanism and, in a smaller proportion, an increase in plasma C-reactive protein levels. The activation of the coagulation cascade and the acute-phase reaction of inflammation were infrequently associated in individual patients.

Journal Article↗
PubMed2003

The hemostatic defect of cardiopulmonary bypass.

Cardiac surgery involving cardiopulmonary bypass is a common yet complex procedure that results in considerable disruption of hemostasis during and following surgery. Despite the relatively common and widespread use of this procedure, there remains a significant peri-operative risk of both thrombosis and hemorrhage in some patients. This is known as the hemostatic defect of cardiopulmonary bypass. Strategies including the use of pharmacological agents, hemodilution, autologous blood transfusion, rapid in-theatre monitoring of hemostatic potential with fine-tuning of the degree of heparinization, minimally invasive surgery and the use of biologically coated cardiopulmonary bypass equipment have been employed to ameliorate the effects of cardiopulmonary bypass on hemostasis. However there exists a fine line between preventing hemorrhage and promoting thrombosis. Likewise attempts to prevent thrombosis may result in increased hemorrhage. Research into many strategies for minimizing the hemostatic defect of cardiopulmonary bypass is incomplete, with safety and efficacy the subjects of intensive investigation.

Blood Platelet Disorders↗
PubMed2002

Low plasma levels of hemostatic proteins during the induction phase in children with acute lymphoblastic leukemia: A retrospective study by the JACLS. Japan Association of Childhood Leukemia Study.

BACKGROUND: Thromboembolic and bleeding events are serious complications associated with the administration of L-asparaginase (ASP) during the induction phase in children with acute lymphoblastic leukemia (ALL). Prophylactic supplementation of plasma-derived coagulation products remains controversial. The purposes of this study were to examine the plasma levels of hemostatic proteins during the induction phase and the efficacy of prophylactic replacement of plasma-derived products. METHODS: A multicenter retrospective survey on the incidence of hemostatic complications and the frequency of prophylactic replacement of plasma-derived products among children with ALL who under went ASP therapy was conducted. All patients were treated according to the Japan Association of Childhood Leukemia Study (JACLS) ALL-97 protocol. RESULTS: Thirty-six (67%) of the 54 JACLS-treatment centers responded and provided information on 127 patients. Clinically relevant hemostatic complications occurred in two patients (1.6%;2/127); one patient suffered intracranial bleeding 5 days after beginning the protocol, and the second patient suffered an ischemic attack during an ASP treatment. The administration of ASP(10 000 u/m2 x six doses) led to significant reductions in the plasma fibrinogen (180 +/- 74 to 105 +/- 57 mg/dL),antithrombin III (AT III) (126 +/- 21 to 73 +/- 18%),and plasminogen levels (97 +/- 17 to 52 +/- 18%). These laboratory parameters returned to normal levels 2 weeks after completion of the ASP treatment. Forty-eight patients (38%)received AT III concentrate (AT III-supplement group). The AT III level of the AT III-supplement group was significantly lower than that of the AT III non-supplement group, not only during the ASP therapy, but also prior to the ASP therapy. A greater percentage of patients in the AT III-supplement group received fresh-frozen plasma and in greater amounts than those in the AT III non-supplement group. CONCLUSIONS: Severe hemorrhage and thrombosis were uncommon in the ALL patients who underwent ASP therapy in comparison with the degree of coagulation changes. Prophylactic administration of AT III concentrate or fresh-frozen plasma did not demonstrate clear beneficial effects in the treatment of ALL in preventing thromboembolic events.

Antineoplastic Agents↗
PubMed1994

Platelet concentrates stored for 5 days in a reduced volume of plasma maintain hemostatic function and viability.

BACKGROUND: Platelet concentrates prepared from whole blood are generally suspended in a standard volume of 50 to 60 mL of plasma and can be stored thus at 20 to 24 degrees C for up to 5 days. In vitro studies suggested that this plasma volume could be reduced to 30 to 35 mL without impairing platelet function. STUDY DESIGN AND METHODS: This study evaluated whether platelets stored for 5 days in a reduced volume (30-35 mL) of plasma maintained their in vivo viability, hemostatic function, and recovery in recipients. Paired autologous platelet survival studies were done in 20 adult volunteers to assess platelet viability. A rabbit ear bleeding-time model was used to compare the hemostatic effectiveness of human platelet concentrates stored for 5 days in the standard or reduced volume of plasma. Platelet recovery was compared in thrombocytopenic hospital patients. RESULTS: Paired platelet survival studies indicated no significant difference between the values in platelet concentrates stored for 5 days in the reduced volume of plasma and the values in those stored in the standard volume. In the animal model, there was no significant difference in the bleeding times achieved by either set of platelet concentrates. The platelet count increments in thrombocytopenic patients were measured. The platelet count increments in patients who received reduced-volume platelet concentrates were as good as the increments achieved in patients given standard-volume concentrates. CONCLUSION: The in vivo viability, recovery, and hemostatic function of platelets collected in polyvinylchloride plastic containers and stored in 30 to 35 mL of plasma for 5 days are maintained as well as those of platelets stored in 50 to 60 mL of plasma.

Adult↗
PubMed2002

A randomized, blinded trial comparing the hemostatic effects of pentastarch versus hetastarch.

BACKGROUND: HES solutions provide a sterile, alternative colloidal fluid to albumin solutions and/or plasma in the management of patients who need plasma volume expansion. Solutions of HES are widely accepted internationally but are used only modestly in the United States, largely because of concerns over hemostasis. STUDY DESIGN AND METHODS: A randomized, blinded, two-arm trial comparing the hemostatic effects of pentastarch versus hetastarch when infused in the clinically relevant dose of 90 g of HES dissolved in 1.5 L of saline was conducted. Multiple studies of fibrin clot formation, fibrinogen/fibrinolysis, and platelet (PLT) functions were performed before and on multiple occasions for 70 days following HES infusion. RESULTS: Several significant abnormalities of hemostasis assay results occurred following HES infusions, with hetastarch causing significantly greater abnormalities than pentastarch. Individual clotting proteins and blood PLTs fell modestly because of plasma volume expansion and hemodilution. A fall in excess of that caused by hemodilution was demonstrated for von Willebrand factor antigen plus its associated FVIII and ristocetin cofactor activities. The partial thromboplastin time was prolonged, whereas the thrombin time was shortened. Plt function abnormalities were seen in most subjects to a modest degree. Studies of fibrinolysis were normal. CONCLUSIONS: Solutions of hetastarch produce significant abnormalities of some hemostasis laboratory results when infused at clinically relevant doses, but it is unlikely that the modest hemostatic abnormalities produced at these doses per se would lead to clinical bleeding. Hetastarch causes greater hemostatic abnormalities than pentastarch, and because both HES solutions have comparable plasma volume-expanding effects, it is reasonable to prefer pentastarch as a plasma volume expander.

Adult↗
PubMed2004

Understanding the hemostatic effects of recombinant factor VIIa by clot wave form analysis.

The monitoring of coagulation-inhibitor bypassing agents, including recombinant factor VIIa (rFVIIa), remains a major issue in the management of clinical hemophilia. Clotting assays using prothrombin time (PT) and measurements of factor VII (FVII) activity do not always reflect the hemostatic effects of treatment. Thrombelastography can be used to observe the global effects of treatment on the overall coagulation process and is especially useful for observing the effects of hemostatic treatment in hemophilia patients with inhibitors. Waveform analysis is another technique for evaluating global hemostatic condition where changes in light transmission during routine clotting assays, such as the activated partial thromboplastin time (aPTT), are measured. We found that waveforms differed between individual patients with severe hemophilia A (FVIII:C < 1.0 IU/dL) with levels of sensitivity at below FVIII:C 1.0 IU/dL. Clot waveforms indicated dose-dependent improvements in clot formation after the addition of rFVIIa to both FVIII-deficient and factor IX (FIX)-deficient plasma. The improvements were further enhanced in the presence of both platelets and synthetic phospholipids, and were more pronounced with FVIII-deficient plasma than with FIX-deficient plasma. It appears that clot waveform analysis provides a very useful means for monitoring hemostasis in hemophilia A patients with inhibitors.

Blood Coagulation↗
PubMedDate not supplied

Hemostatic profiles in 39 dogs with congenital portosystemic shunts.

OBJECTIVES: To determine if there were significant changes in prothrombin time (PT), partial thromboplastin time (PTT), and fibrinogen levels in dogs with naturally occurring congenital portosystemic shunts (CPSS) and to determine if there was any association between these values, serum albumin concentration, and the ability to attenuate the shunt vessel. STUDY DESIGN: Retrospective clinical study. ANIMALS: Thirty-nine client-owned dogs. METHODS: Medical records of 60 dogs with confirmed CPSS were retrospectively evaluated. Hemostatic profiles had been performed before surgery in 39 cases. RESULTS: Dogs with CPSS had significantly higher values for PTT (P < .001) when compared with normal dogs. Of the total number of dogs, 64.1% had a PTT greater than 16 seconds (25/39). PTT was prolonged by 25% or more in 51.3% of dogs (20/39). PT tended to be higher in dogs with CPSS (P = .036), although only 7.7% (3/39) of dogs had a PT greater than 12 seconds (the maximum reference value). Dogs with CPSS had significantly lower values for albumin and fibrinogen (P < .001). Platelet numbers were within the normal range in 87.2% of cases (34/39). Of the 5 dogs with platelet numbers outside the normal range, 3 were mildly thrombocytopenic. Fibrin degradation product concentrations were not elevated in any dogs tested (N = 22). There was no significant difference in any of the measured variables between dogs with extrahepatic shunts and those with intrahepatic shunts (P > .1). For PT, PTT, albumin, and fibrinogen, there was no significant difference between dogs that underwent total, partial, or no attenuation (P > .3). CONCLUSIONS: Dogs with CPSS have a tendency to have a prolonged PTT. There was no significant difference in hemostatic profile results between dogs with intrahepatic shunts versus extrahepatic shunts. Preoperative hemostatic profile abnormalities were not useful as predictors of ability to attenuate CPSS. CLINICAL RELEVANCE: Prolonged PTT was not associated with bleeding tendencies in any of the dogs. Assays of individual clotting factors may help to further characterize the abnormalities present in animals with CPSS and may identify specific factor deficiencies. This might enable identification of a noninvasive diagnostic or prognostic indicator.

Animals↗