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PubMed2001

Hyperinsulinemia and hemostatic abnormalities are associated with silent lacunar cerebral infarcts in elderly hypertensive subjects.

OBJECTIVES: We sought to study the association of the silent cerebral infarct (SCI), a predisposing condition of stroke, with hyperinsulinemia and hemostatic abnormalities in older hypertensive subjects. BACKGROUND: Hypertension is a powerful risk factor for stroke. However, the role of other risk factors for stroke in hypertensive subjects remains incompletely understood. METHODS: We performed brain magnetic resonance imaging and measured cardiovascular risk factors, by administering the 75-g oral glucose tolerance test and measuring plasma insulin and hemostatic variables, in 123 asymptomatic hypertensive subjects (mean age 69 years). RESULTS: At least one SCI was detected in 80 subjects (65%), and multiple SCIs were found in 48 subjects (39%). The presence of SCIs was associated with older age, higher levels of 24-h systolic blood pressure, 2-h insulin, thrombin-generation markers (prothrombin fragment 1+2 and thrombin-antithrombin complexes), plasminogen activator inhibitor-1 (PAI-1), D-dimer and von Willebrand factor (vWF), but not with plasmin-alpha2-plasmin complex (PIC) levels. The 2-h insulin area under the curve (AUC) was positively correlated with PAI-1 and vWF levels (p < 0.01), and the PAI-1 level was negatively correlated with the PIC level (p < 0.02). Multiple logistic regression analysis revealed that age and the 2-h insulin AUC were significantly associated with SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities were significantly associated with the presence of multiple SCIs, particularly those located in the basal ganglia. CONCLUSIONS: In older asymptomatic hypertensive subjects, hyperinsulinemia appears to be associated with lacunar-type SCIs, particularly those located in the subcortical white matter, and hemostatic abnormalities show an association with the presence of multiple SCIs, particularly those located in the basal ganglia.

Aged↗
PubMed1997

Percutaneous interventions alter the hemostatic profile of patients with unstable versus stable angina.

OBJECTIVES: The objectives of this study were to define the hemostatic profiles of patients with unstable angina compared with patients with stable angina and to investigate the effect of percutaneous interventions on the follow-up hemostatic profiles of these patients. BACKGROUND: Disturbances in hemostatic factors have been shown to be present in various clinical syndromes involving coronary artery disease. However, their role in stable angina versus unstable angina is less well defined. METHODS: We studied 61 patients with either stable or unstable angina undergoing percutaneous coronary interventions. Blood samples were drawn immediately before the intervention and at 1-month follow-up. Plasma levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1) and von Willebrand factor (vWF) were measured by enzyme-linked immunosorbent assays. RESULTS: Patients with unstable angina had significantly higher t-PA levels (mean [+/-SE] 23.7 +/- 3.4 vs. 14.3 +/- 1.4 ng/ml, respectively, p = 0.02) and vWF antigen concentrations (2,231 +/- 157 vs. 1,792 +/- 108 mU/ml, respectively, p = 0.03) than patients with stable angina. No statistically significant differences were observed in the PAI-1 levels between the two groups (27.9 +/- 5.5 vs. 21.4 +/- 2.5 ng/ml, respectively, p = 0.25). At 1-month follow-up, there were no longer any significant differences in the t-PA or vWF levels between the two groups (15.7 +/- 1.2 vs. 13.6 +/- 0.6 ng/ml, p = 0.13; 1,962 +/- 170 vs. 1,809 +/- 88 mU/ml, p = 0.39, respectively). There were no significant differences between the hemostatic profiles of patients undergoing percutaneous transluminal coronary angioplasty or coronary stenting initially and at 1-month follow-up. CONCLUSIONS: These data suggest that elevated plasma levels of t-PA and vWF may correlate with instability of atheromatous plaques, and that their decrease after coronary interventions may reflect plaque reendothelialization and stabilization.

Aged↗
PubMed1998

Survival in Acute Myocardial Infarction Induced by Coronary Ligation: Prognostic Relevance of Certain Hemostatic Factors During the Occlusion Phase.

Alterations in various hemostatic factor have been identified as risk factors for survival after acute myocardial infarction (AMI). However, these clinical data are primarily limited to observations made during the postinfarct stage. We assessed the effects of 50 minutes of left anterior descending artery occlusion on several hemostatic factors and analyzed their changes with outcome in 18 Yorkshire swine. Blood samples were obtained from the systemic circulation at base-line and at 25 and 50 minutes of occlusion. Platelet aggregability and plasma antithrombin-III protein C, protein S, fibronectin, endothelin-1, as well as the metabolites of thromboxane and prostacyclin were measured. Of the 18 swine, 7 survived the infarct and 11 animals developed fatal ventricular fibrillation. Both groups demonstrated significant decreases in platelet aggregation, and a decline in plasma protein S when compared with baseline. Thromboxane, prostacyclin, and ondothelin-1 plasma concentrations were also markedly reduced at the end of occlusion. There were significant changes in antithrombin-III, protein C, and fibronectin levels between surviving animals and those that died of ventricular fibrillation. Acute coronary artery occlusion is associated with substantial changes in the hemostatic factors in swine. Plasma levels of fibronectin, antithrombin-111, and protein C differed between survivors and nonsurvivors and thus might serve as predictors of mortality due to fatal ventricular fibrillation during AMI. The mechanisms of these changes during the acute phase of AMI are unclear. Immediately AMI prognosis may be related to hemostatic changes not only after thrombolysis or spontaneous reperfusion, but also during the occlusion phase as well.

Journal Article↗
PubMedDate not supplied

The hemostatic system and angiogenesis in malignancy.

Coagulopathy and angiogenesis are among the most consistent host responses associated with cancer. These two respective processes, hitherto viewed as distinct, may in fact be functionally inseparable as blood coagulation and fibrinolysis, in their own right, influence tumor angiogenesis and thereby contribute to malignant growth. In addition, tumor angiogenesis appears to be controlled through both standard and non-standard functions of such elements of the hemostatic system as tissue factor, thrombin, fibrin, plasminogen activators, plasminogen, and platelets. "Cryptic" domains can be released from hemostatic proteins through proteolytic cleavage, and act systemically as angiogenesis inhibitors (e.g., angiostatin, antiangiogenic antithrombin III aaATIII). Various components of the hemostatic system either promote or inhibit angiogenesis and likely act by changing the net angiogenic balance. However, their complex influences are far from being fully understood. Targeted pharmacological and/or genetic inhibition of pro-angiogenic activities of the hemostatic system and exploitation of endogenous angiogenesis inhibitors of the angiostatin and aaATIII variety are under study as prospective anti-cancer treatments.

Animals↗
PubMed2000

Study of cardiovascular risk factors and hemostatic molecular markers in elderly persons.

In this study, plasma concentrations of hemostatic molecular markers were investigated in 118 elderly persons with normal renal function (aged 65 to 97 years) who could manage their activities of daily living (ADL) by themselves, to find a strategy for conservation or elevation of ADL and quality of life (QOL). In all subjects, the frequency by which hemostatic markers exceeded their upper limit of normal range was 35.9% for thrombin-antithrombin HI complex (> or = 3.7 ng/ml), 38.3% for soluble fibrin monomer (> or = 4.0 microg/ml), 41.8% for D-dimer (> or = 1.0 microg/ml), 49.0% for plasmin-alpha2 plasmin inhibitor complex (> or = 1.0 microg/ml), and 53.7% for thrombomodulin (> or = 20 ng/ml). The mean plasma levels of these markers were slightly higher than the upper limit of their normal range. These markers were also investigated in samples of patients with and without cardiovascular risk factors and with and without cardiovascular diseases (ischemic heart disease and/or cerebral infarction). Furthermore, the results were analyzed in relationships between cardiovascular disease and cardiovascular risk factor or aging. The findings suggest that aging exerts a stronger influence on plasma levels of these hemostatic molecular markers than the presence of cardiovascular risk factors and cardiovascular diseases. From the viewpoint for conservation or elevation of ADL and QOL in elderly persons, also other factor, such as drug intake, lifestyle, aging, and so on, must be considered to clarify the relationship between the plasma levels of the hemostatic molecular markers and cardiovascular risk factors or cardiovascular diseases.

Aged↗
PubMed2002

Hemostatic and rheological variables and risk of cardiovascular disease.

Increasing blood levels of hemostatic variables may increase the risk of thrombosis, while increasing levels of rheological variables which reduce blood flow may increase the risk of ischemic events. Systematic reviews of prospective cohort studies of hemostatic and rheological variables suggest that increasing blood levels of fibrinogen, von Willebrand factor, tissue plasminogen activator antigen, fibrin D-dimer, hematocrit, viscosity, and erythrocyte sedimentation rate may be predictors of risk of coronary heart disease (CHD), but their causal relevance is unknown. At present, data for the associations of other hemostatic variables with CHD, and for the associations of hemostatic variables with stroke, venous thromboembolism, and mortality, is relatively sparse and inconclusive. More detailed syntheses of existing prospective data (such as the Fibrinogen Studies Collaboration), observational studies of CHD and the genetic determinants of these plasma components, as well as large-scale randomized trials should help to determine whether or not these associations are (1) useful in prediction of cardiovascular risk and/or (2) of causal significance.

Blood Coagulation↗
PubMed2004

Contribution of the hemostatic system to angiogenesis in cancer.

It is now recognized that the hemostatic system plays an important role in cancer growth and dissemination, processes known to be vitally dependent on new tumor blood vessel formation (angiogenesis). There is also an increasing body of evidence supporting the link between the various components of the coagulation/fibrinolysis systems and angiogenic activity in cancer patients. Tissue factor (TF), thrombin, fibrinogen, fibrin, and plasminogen activation system, as well as platelets, all are able to promote angiogenesis. On the other hand, coagulation inhibitors, as well as cryptic (proteolytically released) domains of hemostatic proteins, are also known to act as angiogenesis inhibitors. Indeed, modulation (stimulation or inhibition) of angiogenesis may result from either classical functions of various molecular components of the hemostatic cascade, their less studied "alternative" activities, or both. Although much remains to be understood about this complex circuitry these considerations support the judicious use of anticoagulants in patients with malignancy as well as encourage the search for novel antiangiogenic activities that may reside within molecular and cellular components of the hemostatic system.

Blood Coagulation Factors↗
PubMedDate not supplied

Effect of glucocorticoids, E. coli- and Erwinia L-asparaginase on hemostatic proteins in children with acute lymphoblastic leukemia.

BACKGROUND: The concentrations of plasma hemostatic proteins were analyzed prospectively in 42 children with acute lymphoblastic leukemia (ALL), treated according to the protocol ALL-BFM-90. PROCEDURE: Treatment included glucocorticosteroids (GC), E. coli L-asparaginase (Asparaginase, Medac) or Erwinia L-asparaginase (Erwinase, Speywood), vincristine, anthracyclines and intrathecal methotrexate. The analysis of hemostatic proteins was performed during induction and re-induction therapy. RESULTS: At diagnosis, the plasma concentrations of fibrinogen, antithrombin III (AT), plasminogen and protein C were within normal limits, whereas the von Willebrand factor antigen (vWF:Ag) was elevated. After eight days of mono-therapy with GC the concentration of fibrinogen decreased to 59%, vWF:Ag decreased to 67%, AT increased to 124%, protein C increased to 201% of the initial value (mean all p < or = 0.01), while the concentration of plasminogen remained unchanged. During the re-induction phase, the concentrations of the hemostatic proteins, with exception of vWF:Ag, altered in a similar way in response to GC as observed during the induction phase. Administration of two doses of E. coli L-asparaginase (10,000 U/m2) during the induction therapy led to a significant decrease of AT (123 +/- 24 to 63 +/- 15%/mL), protein C (168 +/- 34 to 87 +/- 19%/mL), plasminogen (94 +/- 21 to 41 +/- 12%/mL) and fibrinogen (148 +/- 59 to 79 +/- 30 mg/dL, p < or = 0.01 for all parameters). In contrast, administration of two doses of Erwinia L-asparaginase (10,000 U/m2) during re-induction therapy did not lead to change in the concentration of AT, protein C or plasminogen, and the decrease in fibrinogen (162 +/- 17 to 121 +/- 24 mg/dL) was less pronounced. CONCLUSIONS: Our results indicate that GC and E. coli L-asparaginase, in particular, induce hemostatic alterations which have implications on our understanding of thrombotic and hemorrhagic events during the treatment of ALL in children.

Adolescent↗
PubMed1997

Epidemiology of thrombotic-hemostatic factors and their associations with cardiovascular disease.

Abundant evidence proves that thrombosis is involved in the acute presentation of coronary, cerebrovascular, and peripheral vascular diseases. However, the role of thrombotic factors in the development of the atherosclerotic lesions themselves has been more difficult to prove. This difficulty has been due, at least in part, to several methodologic issues in the study of hemostatic factors and cardiovascular disease (CVD). These include the possibility that associations between CVD and hemostatic factors may not be causal but rather due to confounding by other factors, acting as part of an extended causal pathway or requiring interaction with other risk factors or atherosclerotic disease, or may result from disease rather than causing the disease. In addition, several challenges remain in the measurement of hemostatic factors. Nonetheless, a growing number of studies have examined the association of CVD with coagulation factors (fibrinogen, factor VII, factor VIII, and platelet aggregability) and fibrinolytic factors [tissue plasminogen activator, plasminogen activator inhibitor 1, lipoprotein(a), and plasminogen or global fibrinolytic activity]. Of these, only for fibrinogen is there significant, strong, and consistent evidence of a causal association. Given the preliminary nature of these associations, any association between dietary factors and hemostatic factors other than fibrinogen is difficult to invoke as evidence for a deleterious effect of diet on CVD risk via thrombogenic mechanisms.

Blood Coagulation↗
PubMed2003

Hemostatic regulators of tumor angiogenesis: a source of antiangiogenic agents for cancer treatment?

The maintenance of vascular integrity and control of blood loss are regulated by a sophisticated system of circulating and cell-associated hemostatic factors. These factors control local platelet aggregation, the conversion of soluble fibrinogen to an insoluble fibrin polymer, and the dissolution of fibrin. However, hemostatic factors are also involved in a number of physiologic processes, including development, tissue remodeling, wound repair, reproduction, inflammation, and angiogenesis. In this review, we outline ways in which angiogenesis is coordinated with and regulated by hemostasis. We focus on inhibitors of angiogenesis contained within platelets or harbored as cryptic fragments of hemostatic proteins and assess the experimental and preclinical evidence for their ability to inhibit tumor angiogenesis and, thus, their potential to be anticancer agents. Finally, we review the results of recent clinical trials involving angiogenesis inhibitors and the evidence that antiangiogenic therapy may be associated with hemostatic complications.

Angiogenesis Inhibitors↗
PubMed1994

Characterization of prothrombin activation during cardiac surgery by hemostatic molecular markers.

BACKGROUND: Prothrombin activation represents the key regulatory step in the hemostatic process. Once formed, thrombin contributes to the generation of fibrin as well as the activation of platelets and fibrinolysis. Failure to suppress thrombin formation during cardiac surgery could result in disorders of hemostasis and thrombosis in the perioperative period. The aim of this study was to determine the time course for prothrombin activation during the perioperative period associated with cardiac surgery. METHODS: We measured prothrombin activation during the perioperative period in 19 adult patients undergoing primary cardiac surgery using enzyme-linked immunosorbent assays for the detection of thrombin formation (prothrombin fragment 1.2 and thrombin-antithrombin III complex) and thrombin activity (fibrinopeptide A and fibrin monomer). Blood samples were obtained preoperatively; at 30-min intervals during cardiopulmonary bypass (CPB); and 1, 3, and 20 h after completion of CPB. RESULTS: Despite anticoagulation with heparin, plasma concentrations of prothrombin fragment 1.2, thrombin-antithrombin III complex, and fibrin monomer increased throughout CPB. Peak concentrations for all hemostatic markers occurred in the samples obtained 3 h after completion of CPB. By the morning after surgery, plasma prothrombin fragment 1.2 returned to preoperative concentrations; however, fibrinopeptide A and fibrin monomer concentrations remained significantly increased (P < 0.05) compared to preoperative values. CONCLUSIONS: These data clearly demonstrate the occurrence of prothrombin activation and thrombin activity during CPB despite heparin concentrations adequate to maintain the activated clotting time greater than 400 s. Hemostatic markers for the activation of prothrombin demonstrated peak concentrations 3 h after completion of CPB with a return to baseline concentrations by the morning after surgery. Markers for thrombin activity, however, suggest the presence of active thrombin through the morning after surgery. Further investigations will be necessary to determine the role of hemostatic activation in thrombotic complications after cardiac surgery.

Aged↗
PubMed1995

Hemostatic competency and elastase-alpha 1-proteinase inhibitor levels in surgery, trauma, and sepsis.

Previous studies investigated the effects of neutrophil elastase on isolated factors in the hemostatic process. Some of these reported effects are, however, procoagulative and others anticoagulative. The aim of this study was to ascertain the effect of elastase on the in vivo hemostatic competency. The effect of elastase activity on the hemostatic competency was determined in a group of 50 surgical intensive care unit patients and 23 control subjects. Surgical intensive care unit patients were subgrouped into a surgery, a trauma, and a sepsis-multiple organ failure group. Elastase activity was assessed by elastase-alpha 1-proteinase inhibitor levels and hemostatic competency by thromboelastography. Thromboelastography results showed a relatively normal coagulative ability in the surgery group, a varying degree of thromboelastographic hypocoagulability in the trauma group, and pronounced thromboelastographic instability in the sepsis-multiple organ failure group. Increases in elastase-alpha 1-proteinase inhibitor levels up to 200 micrograms/L were accompanied by a compromised coagulative ability as seen in a prolongation of both the first and second phases of the clotting time, as well as a decrease in the maximal clot elasticity.

Case-Control Studies↗
PubMedDate not supplied

Abnormal hemostatic profiles and gastric necrosis in canine gastric dilatation-volvulus.

Hemostatic profiles (prothrombin time, activated partial thromboplastin time, fibrinogen concentration, fibrin degradation product concentration, platelet count, and antithrombin III activity) were acquired prospectively in 20 dogs with a diagnosis of gastric dilatation-volvulus. Eighteen dogs had abnormal results of one or more hemostatic test, including eight dogs that had hemostatic profiles consistent with a diagnosis of disseminated intravascular coagulation. During surgery, or at necropsy, the dogs' stomachs were evaluated for gross abnormalities, and lesions were graded subjectively as mild, moderate, or severe. Eight dogs had mild gastric lesions, five had moderate lesions, and seven had severe changes indicating gastric necrosis. Seventy percent (7/10) of the dogs with two to six abnormal hemostatic test results had gastric necrosis, whereas none of the 10 dogs with no or one abnormality had gastric necrosis (p < .001). A multiple linear regression equation, based on fibrin degradation product concentration, activated partial thromboplastin time, and antithrombin III activity was derived to predict gastric necrosis. This equation correctly identified gastric necrosis with 86% sensitivity, 100% specificity, 100% positive predictive value, and 93% negative predictive value.

Animals↗
PubMed2006

Primary and secondary hemostatic functionalities of rehydrated, lyophilized platelets.

BACKGROUND: The rehydrated, lyophilized (RL) platelet (PLT) is being developed as a hemostatic infusion agent for the control of active bleeding. The key to the method for preparing RL PLTs is a mild aldehyde stabilization that allows for freezing and lyophilizing without cellular rupture. RL PLTs have been shown to be effective at rapidly controlling bleeding in animal models of cardiopulmonary bypass induced PLT dysfunction and washout thrombocytopenia, yet the rehydrated cells have proved to be safe with respect to induction of pathologic intravascular coagulation. STUDY DESIGN AND METHODS: In vitro and in vivo studies were performed to better understand the differential effect of the RL PLT manufacturing method on primary and secondary hemostatic processes. The functionality of the von Willebrand factor (VWF) receptor (glycoprotein Ib) complex, the PAR receptors, integrin-mediated aggregation (inside-out signaling), and surface membrane prothrombin to thrombin conversion systems were investigated. RESULTS: RL PLTs were found to retain native VWF-mediated adhesion and surface thrombin generation functions. In contrast, the coupling of thrombin receptors to integrin inside-out signaling was largely inhibited. CONCLUSION: These results suggest that RL PLTs may stop bleeding by forming primary hemostatic plugs and providing a localized source of thrombin for secondary hemostatic processes, yet do not build up occlusive pathologic clots possibly because integrin functions for forming PLT-PLT aggregates are partially inhibited.

Blood Coagulation↗
PubMed2004

Effects of lipids and lipid-lowering therapy on hemostatic factors in patients with myocardial infarction.

BACKGROUND: The risk of cardiovascular disease (CVD) is associated with specific hemostatic markers and lipid profiles, and evidence indicates that there are associations between lipid profiles and the levels of certain hemostatic factors. The disturbances in hemostasis and the risk of CVD can be ameliorated by lipid-lowering therapy. OBJECTIVE: We investigated the associations of lipid profiles with factor (F)VIIa, von Willebrand factor (VWF), D-dimer and plasminogen activator inhibitor-1 (PAI-1), and examined whether lipid-lowering statin therapy would affect the levels of these hemostatic markers. PATIENTS AND METHODS: This cross-sectional study analyzed 1045 postmyocardial infarction patients. RESULTS: In multivariate regression analyses (without adjusting for clinical covariates) HDL-cholesterol (HDL-C) and HDL size were independent and significant predictors of FVIIa; HDL size was a predictor of VWF; HDL size, HDL-C and LDL size were predictors of D-dimer; and triglyceride and HDL size were predictors of PAI-1. After adjusting for clinical covariates, HDL-C, lipoprotein (Lp)(a), apolipoprotein B (apoB) and warfarin were independent and significant predictors of FVIIa; HDL size, age, diabetes mellitus, insulin, race and warfarin were predictors of VWF; HDL-C, HDL size, LDL size, age, warfarin, hypertension and gender were predictors of D-dimer; and triglyceride, HDL size, body mass index, insulin and hypertension were predictors of PAI-1. Patients on statin therapy had significantly lower levels of D-dimer than those who were not on this therapy. CONCLUSION: There are significant associations of lipid profiles with hemostatic factors, the directions of which suggest novel pathways by which dyslipidemia may contribute to coronary heart disease.

Adult↗
PubMed2004

Hemostatic and hematological abnormalities in gain-of-function fps/fes transgenic mice are associated with the angiogenic phenotype.

The Fps/Fes tyrosine kinase has been implicated in the regulation of hematopoiesis and inflammation. Mice expressing an activated variant of Fps/Fes (MFps) encoded by a gain-of-function mutant transgenic fps/fes allele (fps(MF)) exhibited hematological phenotypes, which suggested that Fps/Fes can direct hematopoietic lineage output. These mice also displayed marked hypervascularity and multifocal-hemangiomas which implicated this kinase in the regulation of angiogenesis. Here we explored the potential involvement of Fps/Fes in the regulation of hemostasis through effects on blood cells and the vascular endothelium. Hematological parameters of fps(MF) mice were characterized by peripheral blood analysis, histology, and transmission electron microscopy. Hemostasis parameters and platelet functions were assessed by flow cytometry and measurements of activated partial thromboplastin time, prothrombin time, thrombin clot time, platelet aggregation, bleeding times and in vitro fibrinolytic assays. Hematological and morphological analyses showed that fps(MF) mice displayed mild thrombocytopenia, anemia, red cell abnormalities and numerous hemostatic defects, including hypofibrinogenemia, hyper-fibrinolysis, impaired whole blood aggregation and a mild bleeding diathesis. fps(MF) mice displayed a complex array of hemostatic perturbations which are reminiscent of hemostatic disorders such as disseminated intravascular coagulation (DIC) and of hemangioma-associated pathologies such as Kasabach-Merritt phenomenon (KMS). These studies suggest that Fps/Fes influences both angiogenic and hemostatic function through regulatory effects on the endothelium.

Anemia↗
PubMed2006

Plasma hemostatic factors and endothelial markers in four racial/ethnic groups: the MESA study.

BACKGROUND: Hemostatic factors and endothelial markers may play some role in racial/ethnic differences in cardiovascular disease (CVD) rates. However, little information exists on hemostatic factors and endothelial markers across racial/ethnic groups. OBJECTIVES: To describe, in four American racial/ethnic groups (Caucasian, Black, Hispanic, and Chinese), mean levels of selected hemostatic factors and endothelial markers. PATIENTS AND METHODS: Multi-ethnic Study of Atherosclerosis baseline data were used (participant age: 45-84 years). Sex-specific analysis of covariance models, and t-tests for pairwise comparisons, were used to compare means of factors and markers. Adjustments were made for demographics and traditional CVD risk factors. Differences were significant at P < 0.05. RESULTS: Blacks had the highest levels of factor VIII, D-Dimer, plasmin-antiplasmin (PAP), and von Willebrand factor, among the highest levels of fibrinogen and E-selectin (women only), but among the lowest levels of intercellular adhesion molecule 1 (ICAM-1), and, in men, the lowest levels of plasminogen activator inhibitor-1 (PAI-1). Whites and Hispanics tended to have intermediate levels of factors and markers, although they had the highest levels of ICAM-1, and Hispanics had the highest mean levels of fibrinogen and E-selectin (women only). Chinese participants had among the highest levels of PAI-1, but the lowest, or among the lowest, of all other factors and markers. No soluble thrombomodulin differences were observed. CONCLUSIONS: In this large cohort, hemostatic factor and endothelial marker mean levels varied by race/ethnicity, even after adjustment for traditional CVD risk factors.

Aged↗
PubMed2004

Relationship of physical fitness, hormone replacement therapy, and hemostatic risk factors in postmenopausal women.

This cross-sectional study evaluated the relationship of physical fitness, hormone replacement therapy (HRT), and hemostatic profiles at rest and after an acute bout of maximal exercise in 48 healthy postmenopausal women. Subjects were categorized by fitness and HRT user status into four groups: unfit nonusers, fit nonusers, unfit users, and fit users. Fibrinolytic variables tissue plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1) activity, and antigen and prothrombin fragment 1 + 2, a molecular marker of in vivo thrombin generation, were measured before and after maximal exercise. Fibrinogen was also measured at rest. Higher tPA and lower PAI-1 activities (P <0.05) were seen in HRT users and fit groups. tPA and PAI-1 antigens were lower in HRT and fit groups (P <0.05) but not after correction for body mass index. Prothrombin fragment 1 + 2 was lower in the fit groups regardless of HRT status (P <0.05). Fibrinogen was similar in all groups. Favorable hemostatic profiles were observed in physically fit compared with unfit women, especially in HRT nonusers. Thus fitness is more strongly related to these hemostatic risk factors compared with HRT since HRT did not affect these hemostatic variables in fit postmenopausal women.

Cardiovascular Diseases↗