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PubMed2001

Changes in hemostasis during treatment of hypertriglyceridemia with a diet rich in monounsaturated and n-3 polyunsaturated fatty acids in comparison with a low-fat diet.

High levels of fibrinogen, factor (F) VIIc, plasminogen activator inhibitor-1 (PAI-1), and plasma viscosity are associated with an increased coronary risk. As positive correlations of these parameters with triglycerides have been shown, the increased coronary risk associated with high levels of triglycerides may be assumed to be due to alterations within the hemostatic system. To reduce the coronary risk to which hypertriglyceridemic patients are exposed, dietary treatment is recommended; the optimal composition of such a diet is, however, a matter of debate. With regard to the effects on hemostasis, we compared in a sequential approach two diets for treatment of 25 nonobese male patients (age, mean+/-S.D., 40.4+/-8.7 years) with fasting triglycerides >2.3 mmol/l. The first diet (high fat) was rich in monounsaturated fatty acids (MUFA) and marine n-3 polyunsaturated fatty acids (PUFA), whereas the second diet (low-fat) was rich in complex carbohydrates and dietary fiber. The high-fat diet induced a significant lowering of FIIc, FIXc, FXc, FVIIc, FVIIa, FXIIa, PAI-1, plasma viscosity, and platelet activity, but led to an increase in fibrinogen, whereas the low-fat diet lowered FXIIc values and induced a nonsignificant decrease in fibrinogen. Probands on this diet had a slightly higher FVIIa and platelet activity than those on the high-fat diet. However, as all changes appeared to be within the normal range of each hemostatic parameter, it remains to be clarified whether the likely beneficial effects of the high-fat diet on most hemostatic factors are outweighed by the small increase in fibrinogen levels.

Adult↗

PubMed1998

Mechanical factors affecting hemostasis and thrombosis.

Both physical and chemical factors can influence the activity of platelets and coagulation factors responsible for the formation of thrombotic and hemostatic masses in the vicinity of an injured vessel wall. Studies performed in controlled shear devices (viscometers) have indicated that physical factors alone can induce platelet aggregation, even in the absence of exogenous chemical factors. The physical considerations which appear to be important for the local activation of hemostatic/thrombotic mechanisms appear to be related to the magnitude of the shear rate/stress, the duration of the applied physical force and the local geometry. Blood flow alone has multiple influences on platelet and coagulative mechanisms. It has been well established that at physiologically encountered shear conditions, increases in the local shear rate enhance the attachment of platelets to the vessel wall and the growth of platelet aggregates on adherent platelets. In contrast, increases in local shear conditions inhibit the production of fibrin formation on surfaces where tissue factor (TF) is exposed. At levels of shear rate/stress high as compared to normal physiological conditions, but comparable to those observed at the apex of severely stenosed vessels, platelet aggregate formation is dependent on the duration of the exposure time. Considerable advances in our understanding of flow-related mechanisms have evolved from the use of well-defined perfusion chambers employing parallel flow streamlines. However, processes leading to hemostasis and thrombosis generally occur in more complicated flow situations where flow streamlines are not parallel and in which abnormally high, as well as abnormally low, shear rates and shear stress levels may be encountered in close proximity to each other.

Animals↗

PubMed1998

Applications of a hollow fiber device to monitor hemostasis.

A global assessment of hemostasis can be determined by the perfusion of unanti-coagulated whole blood through a hollow fiber at a nominal shear rate of 300 sec(-1). Once the pressure across the hollow fiber is stable, uniform holes are punched through the top and bottom of the fiber, resulting in an optically detectable leakage of blood from the hollow fiber and a pressure drop throughout the system. Changes in the shear rate and flow profile at the puncture site are sufficient to activate platelets mechanically, resulting in a platelet plug observable by electron microscopy. Fibrin is the principal component of the luminal surface adjacent to the puncture site and a prominent fibrin tail extends downstream from this site. The time from the introduction of the punch site to 90% recovery of the baseline pressure defines the in vitro bleeding time (IVBT). The rate of the pressure recovery appears to be related to the efficiency of the thrombin-mediated recruitment of additional platelets to the plug. Pressure recovery can be delayed by either platelet or thrombin inhibitors.

Biological Assay↗

PubMed2003

Modified Denis technique: a simple solution for maximal hemostasis in suprapubic prostatectomy.

OBJECTIVES: To describe our experience with a modified Denis technique for hemostasis in suprapubic prostatectomy. METHODS: We reviewed the charts of 78 patients who underwent suprapubic prostatectomy using a modified Denis technique between September 1996 and June 2001. After adenomectomy, we performed a bladder neck removable partition purse-string suture, and the prostatic fossa was drained. Patients were followed up for hemorrhagic complications and bladder neck strictures for 12 months. RESULTS: The mean intraoperative hemorrhage amount was 264 mL (range 160 to 510). The postoperative irrigating fluid volume was 2000 mL (range 500 to 4500), and the bladder irrigation duration was 24 hours in 70 patients (89.8%) and 48 hours in 8 patients (10.2%). Postoperative hemorrhage, measured by the prostatic fossa drain, was 0 mL in 48 patients and had a mean value of 55 mL (range 10 to 90) in 30 patients. No hemorrhagic complication was noted. None of our patients had transfusion, bladder clot formation, or late hemorrhage. One case (1.3%) of bladder neck stricture developed. CONCLUSIONS: This modified Denis technique is very effective and easy to perform and to learn. It has solved all our hemorrhagic problems in suprapubic prostatectomy.

Aged↗

PubMed1997

Could coenzyme Q10 affect hemostasis by inhibiting platelet vitronectin (CD51/CD61) receptor?

Improved cardiovascular morbidity and mortality have been observed in several clinical studies of dietary supplementation with coenzyme Q10 (CoQ10, ubiquinone). Several mechanisms have been proposed to explain the effects of CoQ10. One attractive theory links ubiquinone with the inhibition of platelets. The effect of CoQ10 intake on platelet surface antigens, and certain hemostatic parameters was examined in 15 humans and 10 swine. Study participants received 100 mg of CoQ10 twice daily in addition to their usual diet for 20 days resulting in a three-fold increase of total serum CoQ10 level. We observed a decline in plasma fibronectin (-20.2%), thromboxane B2 (-20.6%), prostacyclin (-23.2%), and endothelin-1 (-17.9%) level. Significant inhibition of vitronectin receptor expression was observed consistently throughout ubiquinone treatment. Inhibition of the platelet vitronectin receptor is a direct evidence of a link between dietary CoQ10 intake, platelets, and hemostasis. These findings may contribute to the observed clinical benefits by a diminished incidence of thrombotic complications in such patients.

Animals↗

PubMed1993

Ferric sulfate hemostasis: effect on osseous wound healing. II. With curettage and irrigation.

Hemorrhage control is often a problem for the clinician during osseous surgery. Ferric sulfate is an effective hemostatic agent, but with prolonged application to an osseous defect can cause persistent inflammation and delayed healing. The purpose of this investigation was to evaluate the effectiveness of ferric sulfate as a hemostatic agent and to determine its effect on healing after thorough curettage and irrigation from osseous surgical wounds. Standard size osseous defects were created bilaterally in the mandibles of rabbits. Ferric sulfate was placed in one defect until hemostasis was obtained; the contralateral defect was allowed to fill with blood and clot. After 5 min both defects were curetted and irrigated. The repair of the defects was evaluated histologically at 18 and 46 days. There were no significant differences between the ferric sulfate-treated defects and the untreated controls. When adequately curetted and irrigated from the surgical site prior to closure, ferric sulfate did not cause persistent inflammation or delay osseous repair in comparison to controls.

Alveolar Process↗

PubMed1997

The relevance of developmental hemostasis to hemorrhagic disorders of newborns.

The hemostatic system is a dynamic evolving process that is age-dependent. Components of the hemostatic system are synthesized in early fetal life and do not cross the placenta from mother to fetus. However, plasma concentrations of proteins involved in hemostasis significantly differ from adults. Physiological reference ranges are available for premature infants, full-term infants and children from ages 1 to 16 years. In the coagulation system, plasma concentrations of the vitamin K-dependent and contact factors are decreased at birth, whereas other factors such as fibrinogen, FV, FVIII, and FXIII are similar or increased compared with adults at birth. In the fibrinolytic system, plasma concentrations of plasminogen are decreased at birth, whereas tissue plasminogen activator and plasminogen activator inhibitor are increased. Clinically, the hemostatic system of the young is effective and healthy infants do not suffer from spontaneous hemorrhagic complications. However, infants are more vulnerable, compared with older patients, for bleeding in the presence of either congenital or acquired haemostatic defects. Severe congenital bleeding disorders, although rare, frequently present in the newborn period. The most common acquired causes of bleeding newborns include disseminated intravascular coagulation, vitamin K deficiency, and liver disease. A description of these disorders and treatment guidelines are provided.

Blood Coagulation↗

PubMedDate not supplied

Effect of nabumetone on hemostasis during arthroscopic knee surgery.

The known effects of commonly used nonsteroidal anti-inflammatory drugs (NSAIDs) on hemostatic parameters have led to concern over their use in the perioperative period. Nabumetone, unlike other NSAIDs, has little effect on collagen-induced platelet aggregation. To evaluate the effect of nabumetone 2000 mg daily on other hemostatic parameters (e.g., bleeding time, prothrombin time, and partial thromboplastin time) in the clinical setting, this double-masked study was conducted in patients with osteoarthritis undergoing arthroscopic knee surgery. After a 1-week placebo washout period, 58 patients were randomized to receive nabumetone and 53 were randomized to receive placebo. They were assessed before surgery (after 1 to 2 weeks of treatment) and again after surgery (after an additional 3 weeks of treatment). The study was designed to have 90% power to show equivalence in bleeding time to within 1.5 minutes, a difference assumed to be of no clinical importance. No meaningful differences were observed between the groups in any of the measured hemostatic parameters. Before surgery, the bleeding time increased by only 0.3 minutes with nabumetone and decreased by 0.2 minutes with placebo. The mean (+/- SD) difference between the groups in change from baseline was 0.5 +/- 0.3 minutes. After surgery, the changes were 0.1 minutes and 0.0 minutes, respectively, and the difference between groups was 0.2 +/- 0.3 minutes. These differences were neither statistically nor clinically significant, and maximum individual increases were similar in each group. Furthermore, there were no reports of abnormal bleeding in the operative knees. The results of this study show that nabumetone had little or no effect on hemostasis and suggest that this drug can be used safely in the perioperative period.

Adult↗

PubMed1998

Effect of reteplase on hemostasis variables: analysis of fibrin specificity, relation to bleeding complications and coronary patency.

UNLABELLED: The first aim of the present study was to characterize the systemic and fibrin-specific lytic effect of reteplase in the treatment of patients with acute myocardial infarction. The second aim was to investigate the relation of hemostasis variables to risk of bleeding complications and to coronary patency. The present study is a hemostatic substudy of the German Recombinant Activator Study. Forty two patients have been treated with 10 MU of reteplase (Group A) and 100 patients with 15 MU of reteplase (Group B), given as a single bolus. Blood samples for assessment of fibrinogen, plasminogen, alpha-2-antiplasmin, fibrinogen degradation products (FDP) and D-dimers were obtained before and at 2, 4, 8, and 24 h after thrombolytic therapy. The median fibrinogen concentration was decreased from 279 to 169 mg/dl in Group A and from 254 to 92 mg/dl in Group B four hours after administration of reteplase. The decrease in fibrinogen was significantly more pronounced in Group B (P=0.0004). The median plasminogen concentration was decreased to 53% in Group A and to 33% in Group B two hours after administration of reteplase (P=0.0001). Alpha-2-antiplasmin was reduced to 27% and 17,5%, respectively (P=0.0007). D-Dimer levels were increased to 5.2 microg/ml in Group A and 11,6 microg/ml in Group B (P=0.02) and FDP levels to 3.0 microg/ml in Group A and 12,6 microg/ml in Group B (P=0.04). Patients with bleeding complications revealed significant lower nadir levels of fibrinogen than patients without bleeding complications (54 mg/dl versus 125.5 mg/dl, P=0.02). There was no significant difference in any hemostatic parameter between patients with patent and nonpatent infarct related arteries. CONCLUSIONS: Reteplase causes a moderate systemic lytic effect comparable with other relative fibrin specific thrombolytic agents. An increase in the dose from 10 to 15 MU is associated with a marked increase in both fibrin specific and systemic lytic effect. Patients with bleeding complications reveal significant lower nadir levels of fibrinogen than patients without bleeding complications. Determination of any hemostatic parameter seems to be no useful method to predict efficacy of thrombolysis in terms of coronary patency in the individual patient.

Clinical Trials, Phase II as Topic↗

PubMed1988

An overview of hemostasis.

The normal hemostatic system is complex yet exquisitely well regulated. Interrelationships exist between responses of the vasculature, circulating platelets, coagulation proteins, and fibrinolytic mechanism. These relationships serve to limit blood loss, preserve tissue perfusion, and stimulate local repair processes. Natural inhibitors of coagulation and fibrinolysis modulate these systems to prevent uncontrolled thrombosis or hemorrhage following pathologic stimuli. Vascular endothelial cells play an important role in the maintenance of a thromboresistant luminal interface with circulating cells and proteins. Normal hemostasis also requires the synthetic, metabolic, and repair processes of the vascular endothelium. The initial vascular response to injury produces brief vasoconstriction and exposes subendothelial substances that attract circulating platelets and activate coagulation proteins. Platelets respond by adherence and aggregation at the site of injury, with subsequent release of substances that mitigate blood loss. Platelet adherence to collagen requires von Willebrand's factor, fibrinogen, fibronectin, and specific glycoprotein receptors on platelet surfaces. Platelet-to-platelet interactions (aggregation) recruit additional platelets to the primary hemostatic plug. Aggregation requires fibrinogen, energy, and calcium. Release of ADP, serotonin, and the contents of intracellular granules as well as generation of prostaglandins prepares platelet surfaces for reactions with the coagulation proteins. Activation of the intrinsic or extrinsic coagulation pathway, or of both, causes formation of fibrin from fibrinogen by means of an elaborate and intricate system that also entraps platelets and activated coagulation proteins. The intrinsic system is activated by the contact of factor XII with a negatively charged surface, most likely collagen. Through a series of reactions with prekallikrein, HMWK, and factors XI, IX, and VIII, the common coagulation pathway is propagated. The extrinsic, or tissue factor, system stimulates both the common pathway and factor IX the intrinsic pathway. Discovery of this stimulation of the intrinsic pathway by factor VII in the extrinsic pathway has stimulated reassessment of the biologic importance of the extrinsic system. The common pathway includes factors X and V and causes thrombin to convert fibrinogen to fibrin. Calcium and platelet phospholipids are substances that have important roles in steps in the coagulation scheme. Once fibrin is formed, factor XIII interacts with the substance, providing a stabilizing effect.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2000

[Aspirin and hemostasis].

Aspirin is one hundred years old, though its use has clearly evolved during the last 25 years. Identifying its action mechanism has allowed us to better understand the antithrombotic impact. Prostaglandin H synthetase (PGHS) is a bifunctional enzyme with cyclooxygenase and peroxydase activities. There are two isoforms: constitutive PGHS-1 and inducible PGHS-2. Aspirin irreversive acetylates the platelet cyclooxygenase involved in the formation of thromboxane A2, a powerful proaggregating agent and vasoconstrictor. More than 95% of inhibition of this synthesis takes place in two to three days using very weak doses of aspirin, on the order of 30 to 50 mg per day. Under some circumstances, this inhibition requires higher dosages. Certain clinical and biological circumstances could lead to a resistance to aspirin, making a readjustment of doses and sometimes complementary explorations necessary. The ISIS 2 study showed in an apparently irrefutable way the entry of aspirin into the antithrombotics arsenal, with a significant risk reduction of vascular death and recurrence of infarctus. Numerous studies have confirmed this efficacy. Consensus studies are based on information showing total coherence between the dose necessary to acetylate the enzyme to inhibit thromboxane A2 platelet production and the clinical antithrombotic effect. Aspirin seems to have a secure place, and it begins the third millennium in relative peace with new extra-platelet potentialities outside the framework of hemostasis and thrombosis.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMed1983

[Parameters of hemostasis in Behçet's disease].

Venous thrombosis occurred frequently in Behçet's disease. In 12 patients with Behçet's disease of whom 6 have had leg venous thrombosis, some parameters of hemostasis or fibrinolysis have been studied. Platelet count, fibrinogen level, factor VIII coagulant activity, factor VIII antigen, plasminogen and antithrombin III level were in the normal range. Fibrinolytic capacity in response to venous occlusion of the arms was the same in patients and in healthy subjects, in the patients, there was no difference in regard to the occurrence of venous thrombosis. These parameters seemed therefore not able to detect the thrombotic tendency in this disease. These results are discussed with the other reports of the literature.

Adult↗

PubMedDate not supplied

Molecular interaction studies of hemostasis: fibrinogen ligand-human platelet receptor interactions.

The interactions between fibrinogen ligands and platelet receptor alpha(IIb)beta(3) were studied under physiological conditions by atomic force microscopy (AFM). Two linear peptide sequences in fibrinogen, RGD and HHLGGAKQAGDV, play central roles in the regulation of hemostasis and thrombosis by facilitating adhesion and aggregation of platelets. In order to measure the interactions (i.e., debonding force), oligopeptides, GSSSGaaa, where aaa is -RGDSPA or -HHLGGAKQAGDV, were synthesized and grafted on to the surface of AFM probe tips. The interaction forces between a peptide-modified AFM probe tip and platelet surface were determined from pN to nN levels using AFM force measurements. Our results show that the zero kinetic off-rate, K(off)(0), for RGDSPA is significantly smaller than that for HHLGGAKQAGDV, under the consideration of flexible receptor surfaces. From our analysis, the K(off)(0), the single molecular binding energy E(b), and the transition state x(b), were extracted from the data, and estimated to be 1.53s(-1), -2.64x10(-20)J and 1.03A for the RGD-alpha(IIb)beta(3) system, and 47.58s(-1), 2.67x10(-20), 1.09A for the HHLGGAKQAGDV-alpha(IIb)beta(3) system, respectively.

Amino Acid Sequence↗

PubMed1999

Changes of hemostasis, endogenous fibrinolysis, platelet activation and endothelins after percutaneous transluminal coronary angioplasty in patients with stable angina.

OBJECTIVES: This study investigated parameters of endogenous fibrinolysis, activation of coagulation and platelets, and endothelin levels before and after elective percutaneous transluminal coronary angioplasty (PTCA) in patients with stable coronary artery disease (CAD). BACKGROUND: Abrupt vessel closure is a serious short-term complication after PTCA and is often unforeseeable. Detailed insight into the effect of PTCA on hemostasis, platelets and the release of vasoconstrictive substances, which are among the mainly discussed mechanisms of abrupt vessel closure, is needed to enhance the safety of coronary intervention. METHODS: Plasma levels of markers of platelet activity, coagulation, endogenous fibrinolysis and endothelins were determined in 20 patients with stable CAD undergoing elective PTCA. The blood specimens were drawn before, immediately after, 1 h after intervention and on the next morning. RESULTS: All patients showed an initially uncomplicated PTCA. Regarding the efficacy of anticoagulation after receiving 15.000 IU heparin during PTCA, two groups were compared. In eight patients with ineffective anticoagulation production of thrombin and platelet activation directly after and 1 h after PTCA was significantly higher compared with 12 patients with effective anticoagulation. Despite the strong activation of coagulation, only a low fibrinolytic response could be observed. Endothelins rose significantly after PTCA in both groups but stayed longer on higher levels in patients with distinct thrombin generation. Three of the eight patients without sufficient heparin treatment suffered abrupt vessel closure. CONCLUSIONS: Initially uncomplicated dilation of coronary arteries leads to systemically measurable activation of coagulation and platelets in patients with ineffective doses of heparin and release of endothelins in all patients. Therefore, individual adjustment of anticoagulation and platelet inhibition in combination with effective antivasospastic substances are needed in every patient before, during and after initially uncomplicated PTCA to prevent this serious complication.

Aged↗

PubMed1995

Does desmopressin improve hemostasis and reduce blood loss from aortic surgery? A randomized, double-blind study.

PURPOSE: The purpose of this study was to determine the effect of desmopressin acetate (DDAVP) on blood loss, transfusion requirements, and thromboembolic complications in patients undergoing elective aortic operations. METHODS: A randomized, double-blind trial was carried out during a 3-year period with patients receiving 20 micrograms DDAVP or identical-appearing placebo at the time of aortic cross-clamp placement. In addition to major bleeding and thromboembolic end points, bleeding times and platelet counts were monitored serially. RESULTS: Forty-three patients were randomized to receive DDAVP, and 48 were assigned to a placebo. An equivalent proportion of patients with aneurysm and patients with occlusive disease was in each group. In spite of mild prolongation in the postoperative bleeding times and moderate thrombocytopenia, DDAVP had no beneficial effect on blood loss or transfusion requirements. Total blood transfusion amount (mean +/- standard deviation) for patients receiving DDAVP was 3.1 +/- 3.0 U compared with 2.7 +/- 3.0 U for those receiving placebo. For all patients the period associated with the greatest blood loss was the time between heparin administration with cross-clamp application and reversal of heparin with protamine sulfate. The incidence of major thromboembolic complications was similar in both groups. CONCLUSION: Thrombocytopenia and mild platelet dysfunction are common after aortic operation, but DDAVP does not improve hemostasis or lessen transfusion requirements. This study does not rule out a beneficial effect of DDAVP in patients who are undergoing more complex aortic operations or who have major hemostatic aberrations.

Aged↗

PubMed1995

Hematology and hemostasis in the horse: normal functions and common abnormalities.

In diseased animals, laboratory evaluations of erythrocytes, leukocytes, and hemostasis provide important information that contributes to either narrowing the list of potential diagnoses or to determining a specific diagnosis. To adequately interpret the results of these evaluations, normal erythrocyte and leukocyte kinetics and normal hemostatic function must be understood. In addition, knowledge of common diseases resulting in abnormalities of these laboratory tests and of typical changes in these tests caused by these diseases is vital. This article has reviewed normal erythrocyte and leukocyte kinetics and normal hemostatic functions that are clinically significant and has described the laboratory abnormalities expected in common diseases affecting these functions.

Aging↗

PubMed2000

Simple method of hemostasis in implantation and explantation of HeartMate left ventricular assist device.

We described a simple method of hemostasis in implantation and explantation of HeartMate left ventricular assist device. Wrapping of the inflow cannula, outflow conduit and outflow graft with Vascutek tube graft can localize the bleeding due to patient's coagulopathy, imperfect coating and device defect. During explantation, bivalving the tube graft, leaving the graft in place and no-touch of the adhesion between graft and soft tissue can minimize the dissection and prevent the potential bleeding.

Adult↗

PubMed2003

Biological effects of off-pump vs. on-pump coronary artery surgery: focus on inflammation, hemostasis and oxidative stress.

Cardiopulmonary bypass (CPB) has been recognized as a cause of complex systemic inflammatory response, which significantly contributes to several adverse postoperative complications. In the last few years, off-pump coronary artery bypass grafting has gained widespread diffusion as an alternative technique to conventional on-pump coronary artery bypass grafting. Surgeons supporting off-pump surgery state that the avoidance of the CPB and myocardial ischemia-reperfusion significantly reduces the postoperative systemic inflammatory response and other biological derangements and, possibly, may improve the clinical outcomes. We review, here, the available evidence concerning possible differences between off-pump and on-pump procedures in terms of inflammation, hemostasis and oxidative stress. Consistent differences in the involvement of these systems are observed, but they are limited to the final steps of the surgical procedures and the early hours after. These findings suggest that the global surgical trauma may be as important, or even more, as the CPB in terms of systemic inflammatory and coagulation-fibrinolytic pathway activation. Further studies are needed in order to confirm this hypothesis.

Biomarkers↗