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PubMed1997

Prospective, randomized evaluation of the efficacy of fibrin sealant as a topical hemostatic agent at the cannulation site in neonates undergoing extracorporeal membrane oxygenation.

BACKGROUND: The topical hemostatic effect of fibrin sealant that has been solvent/detergent treated and plasminogen depleted was evaluated in a multicenter prospective, randomized controlled study at the cannulation site wound of infants undergoing extracorporeal membrane oxygenation (ECMO). METHODS: The test group received standard cauterization and Fibrin sealant, while the control group was given cauterization alone to control hemostasis at this site. Efficacy data were available on 173 randomized study subjects of whom 149 met study entry criteria. All were managed according to standard ECMO practice. RESULTS: Fibrin sealant reduced the risk of bleeding, was associated with less shed blood, and was associated with shorter duration of hemorrhage. Further, control infants showed an increased bleeding risk with less depressed fibrinogen levels and prothrombin time elevations >18 seconds prior to ECMO. CONCLUSION: Fibrin sealant is useful as a topical hemostatic agent in patients with coagulopathy not responding to standard surgical techniques.

Blood Loss, Surgical↗
PubMed2000

Hemostatic effects of third- and second-generation oral contraceptives: absence of a causal mechanism for a difference in risk of venous thromboembolism.

Some observational studies have found a difference in the risk of nonfatal venous thromboembolism (VTE) with low-dose, oral contraceptives (OCs) containing desogestrel (DSG) or gestodene (GSD) and those containing levonorgestrel (LNG). However, this does not agree with current pathophysiological concepts. This review compares all 17 comparative studies on the hemostatic effects of DSG/GSD- and LNG- or norgestimate (NGM)-containing OCs, and comments on two recent cross-sectional studies on the effects of third- and second-generation OCs on activated protein C (APC) sensitivity. In the comparative studies, the only difference in hemostatic parameters between DSG/GSD- and LNG- or NGM-containing OC users was a tendency towards higher factor VII (FVII) levels with DSG/GSD OCs. Differential effects on APC sensitivity were observed with the endogenous thrombin generation potential (ETP) assay, but not with the classical APC resistance test. FVII is not a risk marker for VTE, but is affected by dietary fat, estrogens and androgens and may interfere with the ETP assay. As no differences in established VTE risk markers were observed, there is no plausible reason for a differential risk of VTE with DSG/GSD- and LNG-containing OCs. In fact, the lack of differences with regard to established risk markers of VTE gives further support to the findings of the most recent epidemiological studies, which have not found any difference in the risk of VTE between third- and second-generation OCs.

Causality↗
PubMed1982

The hemostatic system in children undergoing intensive plasma exchange.

We report the effects on the hemostatic system of intensive plasma exchange therapy using replacement fluids devoid of plasma coagulation proteins. Five children were studied during ten exchanges. There were no hemorrhagic episodes clearly attributable to the plasma exchange, but one patient developed recurrent thrombosis of the vascular access used for the procedure. Plasma values of the various coagulation factors (II to XII) were decreased by 35 to 67% immediately following the plasmapheresis. The mean decrease in levels of antithrombin III antigen and activity and of plasminogen were 58, 60, and 66%, respectively. The recurrent thrombosis of the vascular access in one of the patients, and the decrease in antithrombin III and plasminogen values in plasma following plasmapheresis in all patients, suggest that there is increased potential for thrombosis in patients undergoing intensive plasmapheresis, despite the depletion of coagulation factors. At 24 hours following plasmapheresis the values for all factors were within normal limits, attesting to the ability of the synthetic mechanisms in children to replenish hemostatic factors rapidly.

Adolescent↗
PubMed1995

Hemostatic function of aspirin-treated platelets vulnerable to cardiopulmonary bypass. Altered shear-induced pathway.

The impaired hemostasis of aspirin-treated patients is an annoying problem during and after cardiopulmonary bypass. The hemostatic function of platelets comprises two mechanisms: the shear-induced and the cyclooxygenase pathways. Because the latter is inhibited in aspirin-treated patients, the hemostatic function depends mainly on the former pathway. To investigate the effect of cardiopulmonary bypass on the shear-induced pathway, a double-blind study of preoperative aspirin treatment (325 mg) and placebo was conducted in 40 patients undergoing coronary artery bypass grafting. Postoperative blood loss was higher in the aspirin-treated patients than in the placebo-treated patients (p < 0.05). The shear-induced hemostasis was monitored by the in vitro bleeding test (Thrombostat), which mimics bleeding through an injured arteriole. The shear-induced pathway of aspirin-treated platelets was not affected before cardiopulmonary bypass, but it was impaired more during the operation (p < 0.01) and remained worse afterward (p < 0.05), compared with that of placebo-treated platelets. The inhibitory effects of aspirin on thromboxane production and on collagen-induced platelet aggregation remained throughout the operation. In aspirin-treated platelets, the aggregation capacity induced by adenosine diphosphate was inhibited before the operation (p < 0.05) and showed substantial recovery during the operation (p < 0.05). These results suggest that the shear-induced pathway of aspirin-treated platelets is more vulnerable to cardiopulmonary bypass than the pathway in normal platelets and causes severe impairment of hemostasis afterward.

Adenosine Diphosphate↗
PubMed1999

Effects of a novel Mac-1 inhibitor, NPC 15669, on hemostatic parameters during preconditioned myocardial infarction.

NPC 15669, a member of the leumedins family, inhibits leukocyte adhesion to the endothelium by blockage of upregulation of a member of beta2 integrin family Mac-1 (CD11b/CD18). Inhibition of neutrophil-endothelial interactions may alter the course of myocardial reperfusion injury. However, the effects of NPC 15669 supplementation on the hemostatic profile during ischemia-reperfusion are unknown. The aim of the present study was to define changes in the certain hemostatic factors in the natural course of preconditioned myocardial infarction. Twelve consecutive Yorkshire swine underwent myocardial stunning (8 min. left anterior descending artery occlusion followed by 90 min. of reperfusion) and then preconditioned myocardial infarction (50 min. occlusion followed by 3 hours of reperfusion) experiments. NPC 15669 (10 mg/kg loading dose followed by constant infusion at 6 mg x kg(-1) x h(-1)) was administered in 6 animals; another 6 swine received saline and served as controls. Blood samples were obtained at baseline, twice during occlusion; and three times during reperfusion. The levels of antithrombin-III, Protein C, total Protein S, fibronectin, endothelin-1, as well as the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1a), were determined. NPC 15669 treatment was associated with diminished endothelin-1, TxB2 levels and increased fibronectin, 6-keto-PGF1a, Protein C and total Protein S concentrations in the setting of preconditioned myocardial infarction. There were no changes in the plasma concentrations of antithrombin-III in NPC 15669 group when compared with controls. The increase in Protein C, total Protein S, and 6-keto-PGF1a (favoring antithrombosis), and decrease in endothelin-1 and TxB2 levels (favoring vasodilatation), following NPC 15669 may explain the reduction in infarct size previously reported with this agent.

Animals↗
PubMed1987

Hemostatic evaluation of patients undergoing liver transplantation.

A detailed coagulation and thromboelastographic study was done on the first 50 liver transplantation procedures performed at the Mayo Clinic between March 1985 and June 1986. Most of the patients suffered from primary sclerosing cholangitis, primary biliary cirrhosis, or chronic active hepatitis. Seven patients required a second liver transplantation, and six patients died, none intraoperatively. Most of the patients had distorted hemostatic mechanisms preoperatively, as would be expected because the liver generates most of the clotting factors. The outstanding exception was factor VIII, which was usually in the high-normal range or even more elevated. Substantial deterioration of coagulation factors occurred regularly during reperfusion of the donor liver. In some instances, this trend was corrected within 1 hour, but platelet counts continued to decrease, and some coagulation factors rebounded only partially. Because thromboelastographic tracings are quickly available to the liver transplant team and because they tend to forewarn of impending hemostatic problems, we believe that thromboelastography is a reasonably effective procedure for monitoring coagulation during liver transplantation.

Blood Coagulation Factors↗
PubMed1997

Effects of heparin treatment on hemostatic abnormalities in obese non-insulin-dependent diabetic patients.

This study was conducted to identify the mechanisms responsible for coagulative and fibrinolytic alterations and to study the effects of a short-term treatment with low-dose heparin on hemostatic abnormalities in obese non-insulin-dependent diabetes mellitus (NIDDM) patients. Four groups of age- and sex-matched patients were studied: (1) lean nondiabetic subjects (n = 30) with a body mass index (BMI) less than 25 kg/m2 (lean control subjects), (2) obese nondiabetic subjects (n = 30) with a BMI greater than 30 kg/m2 (obese control subjects), (3) lean NIDDM patients (n = 30), and (4) obese NIDDM patients (n = 30). All subjects were tested on the following parameters: fibrinogen, factor VII, prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), tissue plasminogen activator (t-PA) antigen (Ag) before and after venous occlusion (VO), and plasminogen activator inhibitor type-1 (PAI-1) activity pre- and post-VO. In addition, all these parameters were evaluated in obese NIDDM patients after 10 days of treatment with a single dose of 12,500-U/d subcutaneous calcium heparin and after a 10-day washout period. At baseline, obese nondiabetic subjects, lean NIDDM patients, and especially obese NIDDM patients displayed significantly (P < .01) higher levels of fibrinogen, factor VII, F1 + 2, TAT, t-PA(Ag) pre-VO, and PAI-1 pre- and post-VO and significantly (P < .01) lower levels of t-PA(Ag) post-VO. In obese NIDDM patients treated with heparin fibrinogen, factor VII, F1 + 2, TAT, t-PA(Ag) pre-VO, and PAI-1 pre- and post-VO levels significantly (P < .01) decreased and t-PA(Ag) post-VO levels significantly (P < .01) increased at the end of treatment. Our findings demonstrate in obese nondiabetic subjects, lean NIDDM patients, and especially obese NIDDM patients the hemostatic abnormalities contributing to an enhanced risk of thrombotic complications. We conclude that in obese NIDDM patients, short-term treatment with heparin may reduce this thrombophilic state and have a potential benefit in the progression of diabetic microvascular and macrovascular disease and needs further investigation.

Anticoagulants↗
PubMed2000

Hemostatic suturing technique for uterine bleeding during cesarean delivery.

BACKGROUND: If medical management is unsuccessful in controlling postpartum hemorrhage, conservative surgical intervention or cesarean hysterectomy is required. TECHNIQUE: Hemostatic multiple square suturing using a straight number 7 or number 8 needle and number 1 chromic catgut is a new surgical technique to approximate anterior and posterior uterine walls, especially in areas where there is heavy bleeding. It controls postpartum hemorrhage by attachment and compression of the hemorrhage site of the endometrium or myometrium. EXPERIENCE: We used this technique in 23 women with postpartum hemorrhages at cesarean who did not respond to conservative treatment. In all 23 cases, bleeding decreased markedly and hysterectomy was avoided. All resumed normal menstrual flow after surgery. In four cases, further pregnancy was achieved after this method was used. CONCLUSION: Hemostatic multiple square suturing is an easy, safe, conservative surgical alternative to hysterectomy for treating uncontrollable postpartum hemorrhage.

Cesarean Section↗
PubMed2002

Pyometria after hemostatic square suture technique.

BACKGROUND: The square suture technique to achieve hemostasis for postpartum hemorrhage has been described in the medical literature. In a prior report of 23 cases, there were no complications from the technique. CASE: A young woman with an gravida 1 para 0 with an uncomplicated prenatal course presented at 40 weeks' estimated gestational age in active labor. Cesarean delivery was performed for arrest of dilatation and was complicated by postpartum hemorrhage unresponsive to medical therapy and uterine artery ligation. Several hemostatic square sutures were placed, obtaining hemostasis. The patient presented 4 weeks postpartum with pain and mucopurulent discharge. Pyometrium was discovered at the time of dilation and curettage. CONCLUSION: Pyometrium may result from the use of hemostatic square suture technique for control of postpartum hemorrhage.

Female↗
PubMed1997

Persistence of hemostatic alterations in patients affected by Crohn's disease after bowel surgery.

In Crohn's disease (CD) a condition of hypercoagulability with increased risk for thrombotic events has been reported. In this study we have investigated hemostatic parameters in thirty-one patients affected by CD before, 3 and 12 months after bowel operation, and in thirty healthy controls. Before surgery platelet number (PLT), fibrinogen (Fbg), prothrombin fragment F1 + 2 (F1 + 2), PAI and whole blood-spontaneous platelet aggregation (WB-SPA) were significantly higher (p at least < 0.0005) in patients than in controls, while factor XIII (F XIII) was significantly lower (p at least < 0.005). Three and twelve months after surgery PLT, FBG and WB-SPA significantly decreased in comparison to pre-surgery values (respectively p at least < 0.05 and p < 0.01), but PLT and Fbg were still significantly higher than in controls at 3 and 12 months (p < 0.01). At three and 12 months after operation F XIII was significantly higher in comparison with pre-surgery values (p at least < 0.05). The presence of antiphospholipid antibodies (aPL) was not different between CD patients and controls before surgery, whereas it significantly increased 12 months after surgery (p < 0.05). Our results suggest that in CD hemostatic changes are only in part influenced by local flogistic processes and that an inflammatory systemic condition may provoke both the bowel and extraintestinal manifestations of CD.

Adolescent↗
PubMed1997

The molecular markers of hemostatic activation on coronary artery disease.

Endothelial cells, circulating platelets, and proteins of the coagulation and fibrinolytic systems are known to contribute to the hemostatic processes. Various molecular markers of hemostatic alteration are found in increased amounts in the circulation during the activation of this process. In this study, we investigated serum lipoprotein (a) and plasma platelet factor 4, beta-thromboglobulin, thrombin-anthithrombin complex, fibrinopeptid A, D-dimer, tissue plasminogen activator, tissue plasminogen activator inhibitor, and fibronectin levels in patients with coronary artery disease. The levels of all these markers were found to be significantly higher as compared to the control group. Our findings suggest that patients with coronary artery disease have greater blood coagulability than controls, and the use of molecular markers has become greatly important in clinical practice.

Adult↗
PubMed1997

Endothelial cell markers in chronic uremia: relationship with hemostatic defects and severity of renal failure.

Plasma von Willebrand factor antigen, soluble thrombomodulin, and tissue factor were increased in 31 patients with severe chronic renal failure (creatinine clearance <20 ml/min) under conservative treatment, whereas plasminogen activator inhibitor antigen did not differ significantly from healthy controls. No correlation among plasma levels of these proteins was found. Three patterns of relationship between endothelial cell markers and hemostatic defects were identified: 1) Plasma thrombomodulin, a marker of endothelium damage, was found an independent predictor of bleeding time and platelet aggregation, and secretion defects, and was also related to the severity of renal failure; 2) von Willebrand factor antigen, an index of endothelial cell activation and secretion, was significantly correlated with intravascular markers of thrombin and plasmin generation and with platelet adenosine triphosphate content, but not with plasma creatinine levels; and 3) tissue factor and plasminogen activator inhibitor antigen levels were not statistically correlated with the diverse hemostatic defects. Activation of coagulation and fibrinolysis, secondary to endothelial cell activation, appearing early during the evolution of chronic renal failure, is pathogenically related to the platelet dysfunction, and probably to development of atherosclerosis and thrombotic events in this disease. The progression of chronic renal failure, through endothelial cell damage, would lead to aggravation of the platelet functional defect potentiating the hemorrhagic risk.

Antigens↗
PubMed1999

Hemostatic markers in ischemic stroke of undetermined etiology.

To evaluate the role of the coagulation and fibrinolysis abnormalities in the pathogenesis of ischemic stroke of undetermined etiology, we assayed plasma concentration of fibrinopeptide-A and thrombin-antithrombin III complex, both sensitive markers for thrombin activation and fibrin formation, and D-dimer, a marker of plasmin activity and fibrinolysis. Hemostatic markers were measured in 32 patients with acute stroke and 20 patients with chronic stroke, and compared with 21 normal subjects. Fibrinopeptide-A and thrombin-antithrombin III complex levels were not elevated significantly, whereas the D-dimer level was markedly raised in acute (p<0.001) and chronic (p<0.05) phases of ischemic stroke in comparison with the control group. Prolonged elevation of D-dimer concentration suggests that hemostatic abnormalities have a primary role in the pathogenesis of ischemic stroke. The measurement of D-dimer concentration may help to better decide the indications for therapy of the patients with ischemic stroke of undetermined etiology.

Acute Disease↗
PubMed1999

Whole body hyperthermia: effects upon canine immune and hemostatic functions.

In this study, the effects of induced whole body hyperthermia (WBH; 42.3 degrees C for 90 min) on peripheral blood mononuclear cell (PBMC) phenotype distribution, in vitro blastogenic responsiveness and selected parameters of hemostasis were determined in dogs. Hyperthermia was induced by heating venous blood during extracorporeal circulation (EC); induction of WBH by peritoneal lavage (PL) and perfusion without heating (i.e. euthermic EC and euthermic PL) were used as controls. Whole body hyperthermia was associated with lymphopenia and thrombocytopenia that persisted throughout the eight-day post-treatment observation interval. The lymphopenia was selective in that CD5-positive T lymphocytes were more sensitive than were sIg-positive B cells and, within the T-cell compartment, suppressor (CD8-positive) cells were more sensitive to hyperthermic stress than helper (CD4 positive) lymphocytes. Lymphopenia was also observed in EC and PL euthermic controls, although that lymphopenia was transient and nonselective. Persistent suppression of T-cell phytomitogen-induced blastogenesis was induced by WBH in contrast to transient suppression in euthermic controls. For all treatment groups, lymphopenia and suppressed blastogenesis were correlated to elevated plasma cortisol levels. Induction of WBH by EC resulted in coagulopathy characterized by thrombocytopenia, increased plasma fibrin degradation products, prolonged clotting times, and evidence of spontaneous bleeding. These hemostatic alterations were correlated temporally to increased serum levels of liver enzymes. However, there was no evidence of hepatic injury when WBH was induced by PL, where transient thrombocytopenia was the only significant hemostatic alteration. These results indicate that 42.3 degrees C whole body hyperthermia can be well-tolerated and, although associated with suppression of general indexes of immunocompetence, is not associated with opportunistic infections.

Animals↗
PubMed1997

Effects of intracoronary diltiazem on certain hemostatic parameters during acute myocardial infarction in swine.

Controversy currently exists regarding the use of diltiazem in the treatment of acute myocardial infarction (AMI). due to conflicting results from clinical trials and animal studies. The purpose of this project was to evaluate the changes in the hemostatic profile during AMI following low dose intracoronary diltiazem infusion. Fourteen Yorkshire swine underwent thoracotomy and 50 min LAD occlusion, followed by 3 h of reperfusion. The first group (n = 8) received 2.5 mg of diltiazem intracoronary at a rate of 5.6 micrograms kg min-1 at the onset of reperfusion. The second group (n = 6) received 0.9% saline intracoronary at the onset of reperfusion and served as the control. The dynamics of plasma antithrombin-III (AT-III), Protein C, total Protein S, fibronectin, endothelin-1 (ET-1), and the stable metabolites of thromboxane (TxB2) and prostacyclin (6-keto-PGF1a) were determined at baseline, then twice during occlusion and finally three times during reperfusion. Diltiazem infusion resulted in diminished ET-1 (34.5%), fibronectin (23.2%), and TxB2 (35.6%); and elevated Protein C (29.3%) when compared with controls. We conclude that intracoronary diltiazem favorable influences hemostasis during AMI in swine. The cardioprotective effects of diltiazem during AMI may be related to the improved hemostatic profile and the reduced incidence of thrombotic complications in such patients.

Animals↗
PubMed2003

Argon plasma coagulation (APC) for endo-urological procedures: ex-vivo evaluations of hemostatic properties.

OBJECTIVES: Argon plasma coagulation (APC) is an innovative therapeutic modality of non-contact electrocoagulation, which applies high-frequency current via ionized argon plasma. After several years of successful use in open surgery, endoscopic techniques have been established in various surgical fields. The aim of this study was to evaluate the hemostatic properties of this technique in a fluid medium with regard to endourological procedures. METHODS: Isolated blood-perfused porcine kidneys were used to determine hemostatic efficacy of APC following TURP-like tissue ablation with a conventional loop electrode, compared to standard electrocoagulation with a ball electrode after tissue resection. Blood loss was quantified, specimens were evaluated histologically for coagulation zones. RESULTS: APC following tissue resection significantly (p<0.001) reduced bleeding compared to conventional contact electrocoagulation subsequent to tissue resection for an ablation volume of 4 cm(3) of perfused kidney tissue (2.1 ml/min vs. 5.6 ml/min). The depths of the coagulation zones were significantly larger (2.4 mm vs. 0.8 mm) and remarkably uniform for the groups treated with APC following tissue resection. CONCLUSIONS: APC performed in a fluid medium is feasible. APC following conventional TURP-like tissue resection creates significantly better hemostasis compared to standard contact coagulation after tissue resection. These findings justify further investigations to elucidate the value of APC in endourological procedures.

Animals↗
PubMed2004

Effects of perindopril treatment on hemostatic function in patients with essential hypertension in relation to angiotensin converting enzyme (ACE) and plasminogen activator inhibitor-1 (PAI-1) gene polymorphisms.

BACKGROUND AND AIM: An imbalance in the hemostatic system is a frequent finding in untreated essential hypertension (HT), and it has been shown that treatment with angiotensin converting entyme (ACE) inhibitors improves hemostatic function. In order to elucidate the role of genetic factors, we studied hemostasis in patients with untreated and treated HT and correlated the results with ACE I/D and plasminogen activator enhibitor-1 (PAI-1) 4G/5G gene polymorphisms. METHODS AND RESULTS: Forty-three males with HT (mean age 31.7 +/- 6.8 years) were compared with 34 age and gender-matched controls. All of the patients were treated with perindopril (4 mg/day) and, after one and six months of therapy, their levels of plasma fibrinogen (Fb), t-PA antigen, PAI-1 antigen, von Willebrand factor (vWF), ACE activity and blood pressure were measured. ACE and PAI-1 genotypes were identified by means of the polymerase chain reaction on DNA isolated from peripheral blood lymphocytes. Untreated patients had significantly higher levels of Fb, PAI-1 (p < 0.01) and t-PA (p < 0.05) regardless of their ACE or PAI-1 genotypes. Perindopril reduced blood pressure regardless of ACE or PAI-1 genotype (p < 0.001). ACE II homozygotes showed the greatest decrease in ACE activity (p < 0.01) and a significant reduction in Fb levels (p < 0.05) after just one month of treatment. Analysis of the group as a whole revealed an increase in t-PA antigen levels after six months of treatment, regardless of ACE or PAI-1 genotype (p < 0.01). CONCLUSIONS: Our results show that essential hypertension predisposes to the procoagulant state characterized by hyperfibrinogenemia and hypofibrinolysis. Perindopril reduced fibrinogen levels in ACE II homozygotes due to its more potent inhibitory action on the renin-angiotensin system in such patients. It improved fibrinolysis by increasing t-PA levels regardless of ACE and PAI-1 genotype.

Adult↗
PubMed1997

Hemostatic factors and platelet aggregation after a fish-enriched diet or fish oil or docosahexaenoic acid supplementation.

The effects of a fish-enriched diet or dietary supplements consisting of either fish oil or a docosahexaenoic acid-rich oil (DHA-oil) on platelet aggregation and hemostatic factors were studied in healthy male students. After an experimental period of 15 weeks, the levels of tissue factor pathway inhibitor, prothrombin fragment 1+2 and fibrinogen as well as factor VII activity were not changed. Factor X activity was slightly decreased by the fish diet (P < 0.05). Collagen but not ADP-induced maximum platelet aggregation decreased in the fish diet and the fish oil groups (P < 0.05 in both). In the DHA-oil group there was a slight, statistically insignificant, increase of platelet aggregation which correlated significantly with the decrease of plasma triglycerides. Platelet aggregation measured 4 h after a standardized fat meal was lower than in the fasting state and this decrease correlated with the increase of plasma triglycerides. These results show that a fish diet and fish oil, but not DHA-oil, inhibit in vitro platelet aggregation and that hemostatic factors are not affected by moderate n-3 fatty acid supplementation.

Adolescent↗