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PubMed2002

Utility of whole blood hemostatometry using the clot signature analyzer for assessment of hemostasis in cardiac surgery.

BACKGROUND: A hemostatic monitor capable of rapid, accurate detection of clinical coagulopathy within the operating room could improve management of bleeding after cardiopulmonary bypass (CPB). The Clot Signature Analyzer is a hemostatometer that measures global hemostasis in whole blood. The authors hypothesized that point-of-care hemostatometry could detect a clinical coagulopathic state in cardiac surgical patients. METHODS: Fifty-seven adult patients scheduled for a variety of elective cardiac surgical procedures were studied. Anesthesia, CPB, heparin anticoagulation, protamine reversal, and transfusion for post-CPB bleeding were all managed by standardized protocol. Clinical coagulopathy was defined by the need for platelet or fresh frozen plasma transfusion. The Clot Signature Analyzer collagen-induced thrombus formation (CITF) assay measured platelet-mediated hemostasis in vitro. The activated clotting time, platelet count, prothrombin time, activated partial thromboplastin time, and fibrinogen concentration were also measured. RESULTS: The postprotamine CITF was greater in patients who required hemostatic transfusion than in those who did not (17.6 +/- 8.0 min vs. 10.5 +/- 5.7 min, respectively; P < 0.01). Postprotamine CITF values were highly correlated with platelet and fresh frozen plasma transfusion (Spearman r = 0.50, P < 0.001 and r = 0.40, P < 0.005, respectively). Receiver operator characteristic curves showed a highly significant relation between the postprotamine CITF and intraoperative platelet and fresh frozen plasma transfusion (area under the curve, 0.78-0.81, P < 0.005) with 60-80% sensitivity, specificity, positive and negative predictive values at cutoffs of 12-14 min. Logistic regression demonstrated that the CITF was independently predictive of post-CPB hemostatic transfusion, but standard hemostatic assays were not. CONCLUSIONS: The Clot Signature Analyzer CITF detects a clinical coagulopathic state after CPB and is independently predictive of the need for hemostatic transfusion. Hemostatometry has potential utility for monitoring hemostasis in cardiac surgery.

Algorithms↗

PubMed2001

Vascular bed-specific hemostasis: role of endothelium in sepsis pathogenesis.

OBJECTIVES: To examine the role of vascular bed-specific pathways in determining the hemostatic phenotype in sepsis. DATA SOURCES/STUDY SELECTION: Published research and review articles related to hemostasis and endothelial cell biology. DATA EXTRACTION AND SYNTHESIS: The results of published studies have been used to generate a hypothesis of vascular bed-specific hemostasis in sepsis. CONCLUSIONS: In sepsis, coagulation is initiated by the extrinsic pathway and is amplified through the intrinsic pathway. In addition, the body's natural anticoagulant mechanisms are significantly dampened. Together, these changes result in a net imbalance of hemostasis. The nature of this imbalance varies from one vascular bed to the next according to the local set point of the endothelium. These concepts lay an important foundation for understanding the pathophysiology of sepsis.

Animals↗

PubMed1996

Monitoring hemostasis.

As our understanding of the normal mechanisms of coagulation grows, so does our ability to monitor hemostasis. Evaluation of hemostasis will become more specific and accurate and instrumentation techniques will become simpler and more efficient as technology progress, facilitating the monitoring of hemostasis in the perioperative setting.

Blood Coagulation↗

PubMed1990

Enhanced in vitro hemostasis and reduced thrombolysis in cyclosporine-treated renal transplant recipients.

In vitro hemostatometry and assessment of thrombolysis was carried out in three groups of 72 renal transplant recipients. In one (triple, n = 21) immunosuppression was with cyclosporine, azathioprine, and prednisolone, while a second group (CsA, n = 29) received cyclosporine and prednisolone alone, and the third group (Aza, n = 22) azathioprine and prednisolone. Results were compared with those in 30 normal controls. A statistically significant increase in hemostasis compared with controls was seen in the triple group and in patients in the CsA group studied within 2 years of transplantation. Hemostasis in the Aza group did not differ from normal. All patients in this group had been transplanted more than 2 years before study. Thrombolysis times were significantly prolonged compared with controls in all three groups. Cyclosporine treatment is associated with enhanced hemostasis and reduced thrombolysis, especially during the first 2 years after renal transplantation. If these in vitro findings reflect events in vivo, this may throw light upon the pathogenesis of the obliterative arteriolopathy that is a feature of cyclosporine nephrotoxicity.

Azathioprine↗

PubMed2003

Increased hemostasis potential persists in women with previous thromboembolism with or without APC resistance.

BACKGROUND: Activated thrombin generation and depressed fibrinolysis due to the presence of activated protein C (APC) resistance with or without factor (F)V Leiden mutation are associated with development of deep venous thrombosis (DVT). OBJECTIVE: A better understanding of the mechanism behind the risk of recurrence of DVT, using our new, recently developed assay of overall hemostasis potential (OHP). PATIENTS AND METHODS: Levels of OHP, as well as APC resistance and FV Leiden mutation, were determined in 88 women (cases) who had previously experienced DVT in connection with pregnancy, and in 25 young healthy individuals (controls). Clotting time and clot lysis time were also investigated. RESULTS: OHP levels in the patients were increased compared with the controls. In the cases with APC resistance and the Leiden mutation this imbalance in hemostasis potential was more severe than in those without. The group with the more severe imbalance had shorter clotting times and longer clot lysis times. CONCLUSIONS: A procoagulant state perseveres in patients with a history of pregnancy-related DVT, even after the symptomatic phase is over. The mechanisms behind such an imbalance in overall hemostasis are enhanced thrombin generation and depressed fibrinolysis. These findings may underscore the need for thromboprophylaxis to prevent recurrence of thromboembolism in risk situations.

Activated Protein C Resistance↗

PubMed2004

Synthetic selective inhibitors of coagulation factor Xa strongly inhibit thrombin generation without affecting initial thrombin forming time necessary for platelet activation in hemostasis.

DX-9065a and JTV-803, synthetic selective inhibitors of activated factor X (FXa), have recently been demonstrated as strongly effective antithrombotic agents in animal thrombosis models, yet with a low risk of bleeding. The aim of the present study was to elucidate these characteristics. Using a chromogenic assay with purified coagulation factors, 73.9% of thrombin generation was suppressed by the addition of DX-9065a (0.20 microm) and 75.7% by JTV-803 (0.18 microm). Inhibition by argatroban (0.19 microm) was less (36.0%) and initial thrombin forming time (T50), the time required to generate 50% thrombin activity in vitro, which is considered important for platelet aggregation in hemostasis, was significantly prolonged by argatroban. In contrast, DX-9065a and JTV-803 had no apparent influence on T50, suggesting that initial thrombin was formed immediately, as in the control. We also investigated platelet aggregation in defibrinated plasma induced by tissue factor, to clarify whether initial thrombin contributes to hemostasis. Aggregation was not affected by the addition of either FXa inhibitor, whereas it was significantly reduced by argatroban. Our results suggest that initial thrombin, which is formed despite the presence of a FXa inhibitor, can activate platelets. We concluded that DX-9065a and JTV-803 are able to inhibit thrombin generation significantly without affecting the formation of initial thrombin for platelet activation, which may contribute to hemostasis through the preservation of normal bleeding time.

Anticoagulants↗

PubMed1992

Femoral arterial hemostasis using a collagen plug after coronary artery stent implantation.

We have investigated the safety and efficacy of sealing the femoral arterial puncture site using purified bovine collagen in the catheter laboratory immediately after coronary stent implantation. Ten consecutive patients, mean age 64.6 years, pretreated with heparin, aspirin, and dextran underwent the insertion of a collagen plug immediately after coronary stent implantation. The mean activated clotting time was 512 seconds (range 320-999). Femoral arterial hemostasis was achieved before leaving the catheterization laboratory in nine of ten patients. Seven of these patients received additional mild groin compression with an air cushion compression device after hemostasis was successful. One of ten patients had persistent bleeding after delivery of the collagen plug and later required blood transfusion. The collagen plug may be a useful adjunct to obtaining hemostasis following coronary stent implantation, but further trials are required to test its reliability in fully anticoagulated patients.

Aged↗

PubMed1994

The role of progestationally regulated stromal cell tissue factor and type-1 plasminogen activator inhibitor (PAI-1) in endometrial hemostasis and menstruation.

The physiologic mechanisms whereby the human endometrium maintains hemostasis during endovascular trophoblast invasion, yet permits menstrual hemorrhage, are unknown. This paradoxical relationship was investigated by evaluating endometrial expression of tissue factor (TF), the primary initiator of hemostasis, and plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of fibrinolysis. We observed increased immunostaining for TF and PAI-1 in sections of decidualized stromal cells from luteal phase and gestational endometrium. To determine whether TF and PAI-1 expression are directly linked to decidualization, both endpoints were monitored in a well described in vitro model of decidualization. Thus, confluent stromal cell cultures were exposed to vehicle control, 10(-8) M estradiol (E2), 10(-8) to 10(-6) M medroxyprogesterone acetate (MPA) or both E2 + MPA for 2-24 days in serum-containing or defined media. The progestin enhanced the content of stromal cell-associated immunoreactive and functionally active TF and PAI-1 released into the medium and elevated levels of stromal cell TF and PAI-1 mRNA. While E2 alone was ineffective, it greatly augmented MPA-enhanced TF and PAI-1 protein and mRNA content. Dose-dependent effects on TF and PAI-1 content were observed between 10(-8) to 10(-6) M MPA +/- E2. Similar results were observed for decidual cells derived from first trimester endometrium and cultured in type 1 collagen gels. Following optimal induction of TF and PAI-1 expression by E2 + MPA in stromal cell cultures, removal of these steroids greatly reduced levels of both TF and PAI-1 protein and mRNA within 4 days. These studies suggest a mechanism whereby endometrial hemostasis is maintained during trophoblast invasion yet reduced at the end of nonfertile cycles to permit menses.

Cells, Cultured↗

PubMed2005

Maintenance of hemostasis in transoral robotic surgery.

BACKGROUND: The last decade has seen a tremendous growth in the field of robotic surgery with an increasing number of cardiac and urologic procedures performed each year. Several attributes of this technology may offer advantages to laryngeal and pharyngeal surgery in that it allows for exceptional visualization of the operative field, precise handling of soft tissues, and multiplanar transection of tissues. One potential limitation is the management of bleeding in transoral pharyngeal and laryngeal surgery, which is critical to prevent both intravascular volume loss and aspiration. OBJECTIVES: To demonstrate methods for management of bleeding in the surgical field during transoral robotic surgery (TORS). METHODS: We developed a canine robotic surgery model for the evaluation of the ability to control bleeding in laryngeal and pharyngeal procedures using the daVinci surgical robot (Intuitive Surgical, Inc., Sunnyvale, Calif., USA). Both large- and small-vessel hemostasis was obtained with both robotically controlled monopolar and bipolar cautery and with robotically controlled small hemoclips. Additionally, manually controlled large hemoclips were applied by an assistant surgeon viewing on a video monitor for management of large arterial vessels. Suction was performed with both flexible suction catheters controlled by the robotic arms and with manually controlled conventional suction catheters. Data were collected with still and video photography. RESULTS: The lingual artery as well as small arteries and veins were easily controlled and there were no difficulties with maintenance of hemostasis. CONCLUSIONS: Effective hemostasis with control of both large and small vessels can be obtained using both surgical hemoclips and electrocautery during TORS in a canine model.

Animals↗

PubMed1999

Hormone replacement therapy, inflammation, and hemostasis in elderly women.

Lipid-lowering by postmenopausal hormone therapy (HRT) explains only partly the assumed coronary risk reduction associated with therapy. To explore other possible mechanisms, we studied associations of HRT use with inflammation and hemostasis risk markers in women >/=65 years of age. Subjects were selected from 3393 participants in the fourth year examination of the Cardiovascular Health Study, an observational study of vascular disease risk factors. After excluding women with vascular disease, we compared levels of inflammation and hemostasis variables in the 230 women using unopposed estrogen and 60 using estrogen/progestin, with those of 196 nonusers selected as controls. Compared with nonusers, unopposed estrogen use was associated with 59% higher mean C-reactive protein (P<0.001), but with modestly lower levels of other inflammation indicators, fibrinogen, and alpha-1 acid glycoprotein (P<0.001). Factor VIIc was 16% higher among estrogen users (P<0.001), but this was not associated with higher thrombin production (prothrombin fragment 1-2), or increased fibrin breakdown (D-dimer). Concentration of plasminogen activator inhibitor-1 was 50% lower in both using groups (P<0.001) compared with nonusers, and this was associated with higher plasmin-antiplasmin complex: 8% higher in estrogen and 18% higher in estrogen/progestin users (P<0. 05). Relationships between the markers and hormone use were less pronounced in estrogen/progestin users, with no association for C-reactive protein except in women in upper 2 tertiles of body mass index (P for interaction, 0.02). The direction and strength of the associations of HRT use with inflammation markers differed depending on the protein, so it is not clear whether HRT confers coronary risk reduction through an inflammation-sensitive mechanism. Associations with hemostasis markers indicated no association with evidence of procoagulation and a possible association with increased fibrinolytic activity.

Aged↗

PubMed2004

Anti-glycoprotein VI treatment severely compromises hemostasis in mice with reduced alpha2beta1 levels or concomitant aspirin therapy.

BACKGROUND: Platelet inhibition is a major strategy to prevent arterial thrombosis, but it is frequently associated with increased bleeding because of impaired primary hemostasis. The activating platelet collagen receptor, glycoprotein VI (GP VI), may serve as a powerful antithrombotic target because its inhibition or absence results in profound protection against arterial thrombosis but no major bleeding in mice. METHODS AND RESULTS: Mice lacking (-/-) or expressing half-levels (+/-) of the other major platelet collagen receptor, integrin alpha2beta1, were injected with the anti-GP VI antibody JAQ1 and analyzed on day 5. Anti-GP VI treatment resulted in a marked hemostatic defect in alpha2-/- or alpha2+/- mice, as shown by dramatically prolonged tail bleeding times. Platelet adhesion to collagen was studied in an ex vivo whole-blood perfusion system under high shear conditions. Weak integrin activation by thromboxane A2 (TxA2) receptor stimulation restored defective adhesion of anti-GP VI-treated wild-type but not alpha2-/- or alpha2+/- platelets to collagen. This process required the simultaneous activation of the G(q) and G13 signaling pathways, as demonstrated by use of the respective knockout strains. Conversely, inhibition of TxA2 production by aspirin severely compromised hemostasis in anti-GP VI-treated or GP VI/Fc receptor gamma-chain-deficient but not control mice. CONCLUSIONS: Anti-GP VI therapy may result in defective hemostasis in patients with reduced alpha2beta1 levels or concomitant aspirin therapy. These observations may have important implications for a potential use of anti-GP VI-based therapeutics in the prevention of cardiovascular disease.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1988

Abnormal blood pathways in left ventricular cavity in acute myocardial infarction. Experimental observations with special reference to regional wall motion abnormality and hemostasis.

To elucidate the mechanism of regional hemostasis in the left ventricular (LV) cavity during myocardial infarction, the blood pathway in LV cavity was examined with contrast echocardiography injected from the left atrium before and after coronary ligation in nine canines. Before coronary ligation, contrast echoes spread over LV cavity with one rush. After ligation, smokelike echoes indicating hemostasis were observed at the apical middle of the LV cavity in five dogs with apical akinesis and at the apical area in four dogs with apical dyskinesis. The contrast echoes did not reach the apex within one diastolic period but turned upward to the outflow tract in the middle of the cavity in all dogs. In the cardiac beats that followed, some contrast echoes spread slowly toward the apex, forming a thin layer along the posterior wall in cases with akinesis but not in cases with dyskinesis. The area separated from the blood pathway developed where the smokelike echoes had been developed. Tachycardia exaggerated the abnormality of blood pathway and widened the contrast echo-free area. The abnormal pathway of the blood in apical myocardial infarction develops hemostasis in the apex. This should be one of the mechanisms of thrombus formation in myocardial infarction.

Animals↗

PubMed1988

Altered in vitro hemostasis, clotting, and thrombolysis after oral nifedipine in normal volunteers.

In this study the authors used the Haemostatometer, a new instrument to monitor the pattern of hemostatic plug formation that occurs in holes in polyethylene tubing through which nonanticoagulated blood is flowing under standard conditions. The pattern and speed of blood coagulation, subsequent to hemostasis, was also monitored. Simultaneously, the time until expulsion of hemostatic plugs formed was measured and considered as spontaneous thrombolysis time (STT). In 10 healthy volunteers, blood samples were drawn and tested before and ninety minutes after administration of 10 mg oral nifedipine. After nifedipine, the initial phase of primary hemostasis was delayed (p less than 0.05), the clotting time lengthened (p less than 0.01), and the STT shortened (p less than 0.01). The authors conclude that the effect of nifedipine on hemostasis and thrombolysis could contribute to its therapeutic efficacy.

Administration, Oral↗

PubMed1993

An overview of hemostasis.

Hemostasis is a remarkable and a remarkably complex mechanism. It can maintain blood in a fluid state intravascularly but very quickly changes blood to a jellylike mass upon disruption of the vasculature. This review will give a synopsis of the 3 phases of hemostasis: platelet, vascular, and coagulation. Fibrinolysis and control mechanisms of hemostasis will also be covered. In addition, brief descriptions of the clinical and laboratory evaluation of patients and the diagnosis of bleeding disorders will be presented.

Animals↗

PubMed1996

Effects of serotonin reuptake inhibitors on hemostasis.

OBJECTIVE: To examine the hematologic safety profile of the selective serotonin reuptake inhibitors (SSRIs), with particular emphasis on the effects of these drugs on platelet aggregation. METHODS: Platelet aggregation studies were undertaken at baseline, and repeated 2 and 4 weeks after the initiation of treatment with an SSRI. Other investigations undertaken included analysis of serum electrolyte and liver enzyme concentrations, complete blood count, and coagulation studies. Patients were also assessed for clinical signs of bleeding. Eight patients (7 treated with fluoxetine, 1 with paroxetine) completed the study protocol. RESULTS: Repeated ANOVA revealed no abnormalities in platelet aggregation, hematopoiesis, or coagulation profile. No patient developed clinical signs of abnormal hemostasis during the study period. A statistically significant elevation in the mean serum bilirubin concentration was detected, but this was not of clinical significance. CONCLUSIONS: Although the SSRIs may cause abnormal hemostasis, this effect is probably rare. Another possibility is that abnormal hemostasis is more likely to occur when high doses of SSRIs are administered.

Analysis of Variance↗

PubMed2001

The peculiar features of changing the hemostasis in children with chronic constipation.

Our purpose was to study the peculiarities of changing the hemostasis in children with chronic constipation. In the course of our investigation of hemostasis in children with chronic constipation, we found chronometric hypocoagulation with impairment of internal (XII, XI, IX, VIII) and external (II, V, VII, X) mechanisms of blood clotting, at the base of which is a deficit of vitamin K-dependent factors (II, VII, IX, X) and a slight impairment of the final stage of coagulation. In thrombocytovascular hemostasis, thrombocytopathy demonstrated increased adenosine-5-diphosphate aggregation and suppression of the internal route of fibrinolysis and endotheliosis. We must point out that all these changes lead to impairment of microcirculation in the form of thromboses, particularly in the submucous and mucous membrane vessels, which is confirmed by the morphologic findings. In the compensated form, chronometric hypocoagulation with a deficit of II, IX, and X factors is noted. In the subcompensated form, hypocoagulation increases, and the deficit of V and VII factors is in part the cause. Endotheliosis and the increase of the thrombogenesis dynamics are noted in the thrombocytovascular section. In the decompensated form, there is marked hypocoagulation. Low activity of antithrombin III leads to high content of fibrinmonomeasured complexes in combination with reduction of the thrombocytes quantity and to hypercoagulation. The present changes are confirmed by the morphologic research methods of studying the vascular channel of the large intestine wall, where organized thrombi and a marked plethora of neutrophil tissue infiltration are often revealed.

Adolescent↗

PubMed2001

Hemostasis in children with dysbacteriosis in chronic constipation.

The purpose of the study was to investigate hemostasis in children with dysbacteriosis disturbance in chronic constipation. The disturbance of factors in the inner mechanism of blood coagulation (VII, IX, XI, XII) in compensated chronic constipation was defined based on the reduction in colon bacillus levels. We observed hypocoagulation caused by the reduced activity of the prothrombin complex factors, disaggregate thrombocytopathy, and endotheliosis with fibrinolysis inhibition in subcompensated chronic colostasis with continuous reduction of colon bacillus levels and pathogenic microflora appearance. In decompensated colostasis there was an increase in pathogenic microorganisms and a continuous reduction of colon bacillus levels. In hemostasis there was a factor deficiency in inner (XII, XI, IX, VIII) and outer (II, V, VII, X) blood coagulation mechanisms. Fibrinolysis inhibition, endotheliosis development with thrombocyte aggregation, and microthrombosis formation were determined. Thus, in children with chronic constipation, there was a marked reduction in the amount of colon bacillus, which led to the reproduction of pathogenic bacteria. We also observed chronometric hypocoagulation with the inner (XII, XI, IX, VIII) and outer (II, V, VII, X) mechanisms of blood coagulation, at the base of which there is the deficiency of vitamin K-dependent factors (II, VII, IX, X) and a slightly marked disturbance in the final stage of coagulation. In thrombocyte vascular hemostasis, thrombocytopathy was observed with increased adenosine-5-diphosphate aggregation and the inhibition of the inner mechanism with fibrinolysis and endotheliosis.

Adolescent↗

PubMed1999

Evaluation of the Clot Signature Analyzer as a hemostasis test in healthy volunteers exposed to low doses of aspirin.

Several variables affect bleeding time that make it difficult to obtain consistent measurements. The Clot Signature Analyzer (CSA) has been developed to assess in vitro hemostasis using well-controlled flow chambers. In this study, the equivalencies in the CSA parameters with the conventional bleeding time or platelet aggregation methods were evaluated in subjects exposed to aspirin. The CSA parameters, platelet hemostasis time (PHT) and collagen-induced thrombus formation (CITF), were compared to bleeding time (Surgicutt2) and collagen-induced platelet aggregation, respectively. Fifty-three healthy volunteers were given two doses of aspirin (81 and 243 mg) in one day. Following the baseline period, the volunteers took 81 mg of aspirin and then took 243 mg 2 hours later. The changes in each value from the baseline to that at either aspirin dose (2 hours after dosing) were evaluated. Platelet hemostasis time and CITF correlated well with bleeding time and aggregation, respectively, but PHT was not significantly increased after 81 mg of aspirin, whereas bleeding time was significantly increased. The variation in PHT was slightly higher than that of bleeding time. At 81 mg, CITF was significantly increased but aggregation was not, even though the variation was comparable. This suggests that PHT and CITF can simulate the changes in bleeding time and aggregation, respectively, but the sensitivity of PHT for detecting the changes in bleeding time was no better than the conventional method. Also, CITF was more sensitive than aggregation in detecting platelet response to collagen. In conclusion, the proposed CSA is not always suitable for detecting hemostatic abnormalities.

Adolescent↗