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PubMed2001

Urinary 11-dehydro-thromboxane B(2) and coagulation activation markers measured within 24 h of human acute ischemic stroke.

The aim of this study was to determine the extent of change in platelet and coagulation markers in the acute phase of ischemic stroke and to assess the utility of marker measurement in stroke subtype classification. Urinary 11-dehydro-thromboxane B(2) (11-dTXB2), a marker of in vivo platelet activation, and markers of coagulation activation, including prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), and fibrinogen, were measured in 25 patients with ischemic stroke within 24 h of onset of symptoms. Marker levels in patients with ischemic stroke were compared with those in 19 age-matched controls who had not taken aspirin for at least 2 weeks before sampling and 25 healthy controls. Median marker levels were significantly increased in stroke over those in age-matched controls for fibrinogen (344 vs. 289 mg/dl; P=0.030), F1+2 (1.40 vs. 0.80 nmol/l; P=0.003), and TAT (6.65 vs. 2.20 microg/l; P<0.0001). Median marker levels for seven patients with cardioembolic stroke and 18 with non-cardioembolic stroke were not significantly different for any marker test. Eight patients taking aspirin at the time of the stroke had significantly lower 11-dTXB2 values than patients not taking aspirin (964 vs. 4,314 pg/mg of creatinine; P=0.007). Stroke patients not taking aspirin had significantly higher 11-dTXB2 concentration than age-matched controls (4,314 vs. 1,788 pg/mg of creatinine; P=0.006). Coagulation and platelet activation markers are increased in the acute phase of stroke regardless of the clinical mechanism. This finding suggests that the markers may not be useful for predicting clinical subtype of ischemic stroke in the acute phase.

Acute Disease↗

PubMed2002

Effects of hormone replacement therapy and estrogen receptor modulators on markers of inflammation and coagulation.

The lipid-lowering effects of hormone replacement therapy (HRT) can only partly explain the possible decrease in cardiovascular risk noted in observational studies with hormone use in postmenopausal women. Other possible mechanisms have been explored, including the role of inflammation and coagulation factors. There is mounting evidence that inflammation plays a critical role in the pathogenesis of atherosclerosis, and it has been demonstrated that higher levels of circulating proinflammatory factors are predictive of cardiovascular events. Thus, the effects of hormones and other agents on these factors are of considerable interest. In this article, the effects of various types of HRT and estrogen receptor modulators on inflammation and coagulation markers are reviewed, and their potential impact on clinical outcomes is considered.

C-Reactive Protein↗

PubMed2001

Coagulation activation markers do not correlate with the clinical risk of thrombosis in pregnant women.

OBJECTIVE: Because coagulation activation markers have been shown to indicate an increased risk of thrombosis, we tested whether thrombin-antithrombin III complexes and D-dimers correlated with the risk assessment in pregnant women on the basis of clinical data. STUDY DESIGN: We divided a group of 261 pregnant women (305 pregnancies) into low- and high-risk groups according to the personal and family histories of thrombosis and the presence of a hereditary or an acquired thrombophilia. Women with a thrombotic event in the current pregnancy formed a separate group. All pregnancies with or without heparin therapy were closely monitored with thrombin-antithrombin III and D-dimer values for the entire course of the pregnancy. Retrospectively, the data were then correlated with the different groups and subgroups. RESULTS: The course of the mean thrombin-antithrombin III values of all 305 pregnancies was close to or slightly above the upper cutoff line, whereas the D-dimer values were well within the normal range. Independent of heparin, there was no difference in the course of the thrombin-antithrombin III and D-dimer values between the low- and high-risk groups. Only women with ongoing thrombosis during pregnancy had significantly higher thrombin-antithrombin III and D-dimer values with or without heparin therapy. Among those individuals with elevated thrombin-antithrombin III or D-dimer values, there were no specific, recognizable patients who had elevated markers more often than others. CONCLUSIONS: Thrombin-antithrombin III and D-dimer values do not correlate with a risk stratification assessed by clinical criteria. There are many women at low clinical risk who have elevated markers, and there are many women at very high clinical risk who have normal markers. Thus thromboprophylaxis would often be used inadequately if the indication were based on coagulation markers.

Adolescent↗

PubMed2001

[Markers of coagulation and fibrinolysis in peripheral blood and in blood collected pouch of Douglas in patients with ectopic pregnancy].

In cases of ectopic pregnancy a blood collected in a pouch of Douglas is a nonclotting one. It contains no fibrinogen, prothrombin, factor V and VII, plasminogen and monomers of fibrin, however concentration of D-dimers is very high. Is this solely an effect of independently occurring fibrinolysis or does coagulation accompany this process? The definite answer can not be given. Coagulation and fibrinolysis markers obtained at the same time from peripheral veins were normal.

Adult↗

PubMed1999

The effects of in vitro hemodilution with gelatin, hydroxyethyl starch, and lactated Ringer's solution on markers of coagulation: an analysis using SONOCLOT.

UNLABELLED: Blood-saving strategies have recently been established to avoid allogeneic transfusion during surgery or after trauma. This includes an expanding use of crystalloids and colloids. These solutions interfere with coagulation systems, but quantitative measurements are still lacking. The SONOCLOT (Sienco Company, Morrison, CO) analysis (SCT), a viscoelastic test, measures clot formation and includes information on the cellular, as well as the plasmatic coagulation, system. To quantify hemodilutional effects on in vitro coagulation, we studied gelatin (G), hydroxyethyl starch 6% (HES; molecular weight 450,000), and lactated Ringer's solution (RL) in 33% and 66% dilutions measuring routines laboratory and SCT variables. Hemodilution with RL tended to increase in vitro coagulability. Among the tested colloids, G had the least impact on markers of coagulation. G33% did not differ significantly from the undiluted control group. HES had the largest impact on markers of coagulation compared with G and RL. In conclusion, SCT provides a fast and easy to perform bedside test to quantify in vitro hemodilution. IMPLICATIONS: The effects of progressive hemodilution on coagulation are difficult to measure. SONOCLOT analyses provide an easy to perform test with fast information on cellular and plasmatic coagulation properties. Among colloids, hydroxyethyl starch has the largest impact on markers of coagulation compared with gelatin or lactated Ringer's solution.

Adult↗

PubMed1994

Coagulation factors and markers of activation of coagulation in homocystinuria (HOCY): a study in two siblings.

Homocystinuria due to cystathionine-beta-synthase deficiency (CBS-def-HOCY) initially often present with thromboembolic events. In most cases in which coagulation factors have been analysed, a deficiency of AT-IIIc and factor VIIc has been reported, the cause of which has not been elucidated. Activation of coagulation with consumption of coagulation factors has been postulated as the mechanism. This paper reports a longitudinal study of two patients: patient 1 with thromboembolic disease and his asymptomatic sister, patient 2. Before start of therapy in patient 1, a reduction of FVIIc, other coagulation factors, and AT-IIIc was found. Markers of activation of coagulation (F1 + 2, TAT, FM, D-dimers) were elevated only in patient 1, and only at the time of thrombotic complications. In patient 2 reduced levels of FVIIc and other coagulation proteins, and a low borderline AT-IIIc level was found. Thus, in the two patients, sustained activation of coagulation can be reasonably excluded to be the cause of low levels of coagulation proteins. Vitamin therapy with 15 mg folate and 600 mg pyridoxine per day led to almost complete normalization of amino acids in urine and plasma. Thrombosis has not recurred to date. FVIIc and the other coagulation proteins and AT-IIIc increased in parallel with the biochemical remission. Direct inhibition of the activity of AT-III and coagulation factor VIII and other factors by homocysteine was attempted in vitro but could not be shown at HC concentrations known to occur in the plasma of HOCY patients. Therefore, in these patients, deficient synthesis of coagulation factors and AT-III due to a disturbance of amino acid metabolism is still the most probable explanation for the observed low levels.

Adult↗

PubMedDate not supplied

Pre-analytical variation in the measurements of sensitive markers of coagulation and fibrinolysis: the influence of venipuncture and mixing of blood.

The techniques adopted for venipuncture and the mixing of aspirated blood with anticoagulant were evaluated for their possible contribution in pre-analytical variation in estimating plasma prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), soluble fibrin and total fibrin(ogen) degradation products. Antecubital vein blood samples were simultaneously collected in 20 subjects from either arm by technologists with high and less blood sampling experience employing a crossover design. F1+2 and TAT were significantly higher in plasma obtained by a less experienced technologist. Three different mixing procedures of blood with anticoagulants did not influence the levels of the markers. The results emphasize that experienced technologists should preferably be selected for collecting blood for analysis of coagulation markers.

Antithrombin III↗

PubMed1994

Influence of conditions of blood sampling on coagulation activation markers (prothrombin fragment 1 + 2, thrombin-antithrombin complexes and D-dimers) measurements.

In this study, we evaluated the effects of anticoagulants used in blood sampling on the measurements of coagulation activation markers F1 + 2, TAT, D-Dimers by Elisa methods. The study was carried out on normal subjects and patients with inherited deficiency of coagulation inhibitors, antithrombin III (ATIII) protein C (PC) and protein S (PS). Three different anticoagulant solutions were compared: 1) ACD/EDTA/adenosine/heparin, 2) EDTA/aprotinin/a synthetic thrombin inhibitor and 3) sodium citrate. The results showed that sodium citrate, commonly used in coagulation laboratories, is a suitable anticoagulant for the study of coagulation activation markers. In addition, the type of tubes (plastic tubes vs glass Vacutainer R tubes) used for blood sampling as well as the order of sampling (early or late after the phlebotomy procedure) did not influence the results. We concluded that assays of coagulation activation markers F1 + 2 and D-Dimers can be performed in samples collected routinely by haemostasis laboratory staff using Vacutainer R tubes with sodium citrate. Further investigations are needed to understand why TAT measurements gave a pattern of results quite different from F1 + 2 or D-Di measurements.

Anticoagulants↗

PubMed1996

Short-time stability of markers of coagulation and fibrinolysis in frozen plasma.

We studied the stability of three markers of coagulation (prothrombin fragment 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), and soluble fibrin (SF)) in stored frozen plasma, in addition to one marker of fibrinolysis (total fibrinogen degradation products and fibrin degradation products (TDP)). All markers were measured using enzyme linked immunosorbent assays (ELISA). None of the markers changed significantly after initial freezing. F1 + 2 in plasma was stable following storage at -80 degrees C for 3 months. In plasma containing high SF levels stored at -80 degrees C, an insignificant time dependent trend towards decreasing plasma values was observed. TAT levels in plasma decreased significantly following 3 months at -80 degrees C. TDP levels in plasma showed some fluctuation when stored in freezer. Our results suggest that careful observation of the long time storage stability of protein components is demanded in clinical research.

Adult↗

PubMed2002

Clopidogrel does not suppress blood markers of coagulation activation in aspirin-treated patients with non-ST-elevation acute coronary syndromes.

AIMS: The Clopidogrel in Unstable angina to prevent Recurrent Events (CURE) Study demonstrated that clopidogrel plus aspirin was superior to aspirin alone for prevention of recurrent vascular events in patients with acute coronary syndromes. The aim of this study was to compare the effect of these two regimens on biochemical markers of platelet and coagulation activation. METHODS AND RESULTS: We studied 485 patients with non-ST-elevation acute coronary syndrome who were randomized to clopidogrel (300 mg loading dose followed by 75 mg daily) or placebo for a period of 3-12 months. All patients also received aspirin (recommended dose 75-325 mg daily). Blood levels of P-selectin, prothrombin fragment F1.2, D-dimer, and von Willebrand factor were measured at baseline, day 7 (or hospital discharge), and at day 30 after randomization. Patients receiving clopidogrel plus aspirin compared with aspirin alone had similar baseline geometric mean plasma levels of P-selectin (50.2 vs 51.7 ng.ml(-1), P=0.45), prothrombin fragment F1.2 (1.13 vs 1.12 nmol.l(-1), P=0.94), D-dimer (467 vs 460 ng.ml(-1), P=0.85), and von Willebrand factor levels (1.89 vs 1.85 U.ml(-1), P=0.59) and there also were no significant differences at day 7, or day 30. However, compared with baseline, there was a significant rise in prothrombin fragment F1.2 at day 7 (from 1.12 to 1.39 nmol.l(-1), P<0.0001) and day 30 (from 1.12 to 1.44 nmol.l(-1), P<0.0001), and D-dimer at day 7 (from 464 to 539 nmol.l(-1), P<0.0001) and day 30 (from 464 to 576 nmol.l(-1), P<0.0001). The magnitude of this rise appeared to be greatest in patients who experienced the primary outcome, a composite of cardiovascular death, myocardial infarction, stroke, or refractory ischaemia by the end of the study. P-selectin levels were not elevated at any time point but von Willebrand factor values were elevated at baseline and remained elevated at days 7 and 30. CONCLUSION: Our results indicate that the clinical benefits of clopidogrel are not associated with a parallel reduction in markers of coagulation activation. Early suppression of coagulation markers most likely reflects the effects of heparin. The persistence of thrombin generation despite long-term clopidogrel and aspirin therapy suggests that even more intensive antithrombotic therapy may be required in these patients.

Antigens↗

PubMed2001

Correlation between quantitative left atrial spontaneous echocardiographic contrast and intact fibrinogen levels in mitral stenosis.

An association between left atrial spontaneous echocardiographic contrast (LASEC) and thromboembolic events has been recognized. However, the appearance of LASEC and the assessment of its intensity are gain dependent. To evaluate the relation between LASEC intensity and coagulation activity, 11 patients with mitral stenosis underwent transesophageal echocardiography with quantitative integrated backscatter assessment of LASEC. Right and left atrial blood samples were evaluated for concentrations of coagulation markers, including intact fibrinogen, fibrinopeptide A, D-dimer, prothrombin fragment 1+2, and thrombin-antithrombin III complex. The patients were found to have significantly higher mean left atrial concentrations compared with right atrial concentrations of thrombin-antithrombin III (28.46 +/- 21.05 versus 3.21 +/- 7.16 ng/mL, respectively; P =.001) and fibrinopeptide A (32.78 +/- 17.54 versus 7.42 +/- 8.27 nmol/L, respectively; P <.001). Intact fibrinogen levels were similar in both atria, and a strong, direct correlation existed between left and right atrial intact fibrinogen levels (r = 0.78, P =.005). Quantitative integrated backscatter of LASEC correlated directly with left atrial fibrinogen level (r = 0.78, P =.013) but not with markers of thrombin generation (thrombin-antithrombin III) or activity (fibrinopeptide A). Our results confirm that patients with mitral stenosis have evidence of a regional hypercoagulable state in the left atrium. However, the intensity of LASEC assessed by quantitative integrated backscatter correlates with both right and left atrial intact fibrinogen level, a systemic marker of coagulation.

Adult↗

PubMed2006

The resuscitative fluid you choose may potentiate bleeding.

BACKGROUND: Trauma is the leading cause of death in the younger population in the United States, frequently from the development of hemorrhagic shock. Controversy exists over the type of volume resuscitation for restoring hemodynamic stability that should be used in hemorrhagic shock. Little is known about how various resuscitative paradigms affect the coagulation cascade, which is essential to controlling hemorrhagic shock. METHODS: We studied the effect of various resuscitative formulas on blood coagulation using a new model of whole blood in a controlled setting with corn trypsin inhibitor and a 5-pM stimulus of tissue factor. We investigated thrombin generation, fibrin formation, and platelet activation with four diluents: 0.9% NaCl (NS), lactated Ringer's solution (LR), 6% hydroxyethyl starch (HES), and 3% NaCl (HS), each from 0% to 75% blood dilution. Thrombin generation was measured periodically during a time course of 20 minutes in its complex with antithrombin III. Platelet activation and fibrinopeptide A (FPA) release were monitored in serum at a 20-minute time point. Fibrin clots were collected and weighed. RESULTS: The coagulation markers (thrombin generation, platelet activation, and FPA release) were significantly different by dilution (p < 0.001 in all) and diluent by dilution (p < 0.001 in all). Thrombin generation, platelet activation, and FPA release decreased the least with the diluents NS and LR. LR caused the least amount of variation in thrombin generation over the dilution course. HS produced the most dramatic change in all of the markers; no coagulation was seen between 30% to 75% dilution (p < 0.05). HES produced greater decreases in thrombin generation and FPA release than NS and LR. Fibrin clot mass decreased with a 10% to 20% dilution for NS and LR, whereas stable fibrin mass did not decrease with the diluents HES and HS at 10% to 20% dilutions. At >30% dilutions, HS produced no stable clots and HES dramatically decreased clot formation by 61% and maintained this level. CONCLUSIONS: LR and NS had the least effect on thrombin generation, clot formation, and platelet activation at various concentrations compared with HES and HS. This observational data suggests that volume expanders such as HES and HS may be detrimental in treatment of hemorrhagic shock.

Adult↗

PubMed1994

The reliability of Hickman catheter blood for the assessment of activation markers of coagulation and fibrinolysis in patients with hematological malignancies.

We studied the reliability of Hickman catheter (HC) blood for the determination of activation markers of coagulation and fibrinolysis in 14 patients with hematological malignancies. 10 of 22 HC samples were contaminated with heparin, probably as a consequence of our institutional antithrombotic catheter care, and withdrawn from statistical analysis. Prothrombin activation fragment F1.2, thrombin-antithrombin III complexes, soluble fibrin, degradation products of fibrinogen and fibrin, total degradation products, alpha 2-antiplasmin and antithrombin III levels withdrawn from Hickman catheters did not differ significantly from peripheral venous blood samples. Fibrinogen levels were slightly but significantly higher in peripheral venous blood samples. We conclude that Hickman catheter blood gives reliable results for the determination of activation markers of coagulation and fibrinolysis in patients with hematological malignancies, but may be less useful in clinical practice due to frequent heparin contamination.

Adolescent↗

PubMed2002

Activation markers of coagulation and fibrinolysis in twins: heritability of the prethrombotic state.

BACKGROUND: Activation markers of coagulation and fibrinolysis are increased in individuals at risk of coronary-artery disease and other thrombotic disorders--a condition defined as the prethrombotic state. We aimed to find out the extent to which the prethrombotic state is determined by genetic factors. METHODS: We analysed concentrations of prothrombin, prothrombin fragment 1+2, thrombin-antithrombin complex, crosslinked fibrin degradation product D-dimer, and thrombin-activatable fibrinolysis inhibitor by ELISA in 118 monozygotic and 112 dizygotic unselected female twins aged 21-73 years from the St Thomas' UK Adult Twin Registry. We used quantitative genetic-model fitting to estimate heritability. FINDINGS: We found significant heritabilities in concentrations of the activation markers in plasma. Genetic factors contributed 45, 40, and 65% of the variation in concentrations of fragment 1+2, thrombin-antithrombin complex, and D-dimer, respectively. Age was important only in fragment 1+2 concentrations, in which it accounted for 12% of the variation. The remaining variation could be attributed to unique environmental factors. Variation in concentrations of precursor prothrombin in plasma was determined by 57% heritability, and that of zymogen thrombin-activatable fibrinolysis inhibitor showed a very strong genetic component (82%). INTERPRETATION: The activation mechanisms of the coagulation and fibrinolytic systems, and therefore the prethrombotic state, are controlled to a substantial degree by genetic factors. Genes influencing activation of haemostasis are likely to be an important component of the overall thrombotic tendency in the general population.

Adult↗

PubMed2001

High plasma homocyst(e)ine levels in elderly Japanese patients are associated with increased cardiovascular disease risk independently from markers of coagulation activation and endothelial cell damage.

Elevated plasma homocyst(e)ine is a risk factor for cardiovascular disease (CVD) in many populations, but the relationship between homocyst(e)ine and CVD in Japanese subjects has been unclear. It has been hypothesized that the link between homocyst(e)ine and CVD may be mediated in part by activation of coagulation and endothelial cell injury in the elderly Japanese subjects. To further evaluate this hypothesis, the present cross-sectional study was designed to assess the relationships among plasma homocyst(e)ine concentrations, risk of CVD, and markers of coagulation (fibrinogen, FVII, F1+2, FVIIa and FXIIa) and endothelial cell damage (vWF and thrombomodulin) in 146 elderly Japanese subjects (79 healthy controls and 67 patients with CVD). The geometric mean (range) of plasma homocyst(e)ine concentrations was 10.2 (3.2--33) micromol/l in 79 Japanese healthy elderly subjects. As expected, healthy female and male elderly subjects had homocyst(e)ine levels that were 2.5 and 5.3 micromol/; higher, respectively, compared to healthy young control subjects (n=62). Healthy young and elderly men had homocyst(e)ine levels that were 1.7 and 4.5 micromol/l higher, respectively, compared to values in women. This higher plasma homocyst(e)ine levels in the elderly subjects were negatively correlated with levels of folic acid, albumin and total cholesterol, but were not significantly related to markers of coagulation or endothelial cell-damage. The results of multiple logistic regression analyses suggested that high homocyst(e)ine levels were independently related to CVD risk. In addition, levels of FVIIa, and F1+2 were significantly higher in elderly Japanese patients with CVD compared to elderly subjects without CVD, but were unrelated to plasma homocyst(e)ine concentrations. In summary, elevated plasma concentrations of homocyst(e)ine, FVIIa, and F1+2 were associated with increased risk of CVD in elderly male and female Japanese subjects, but the association between homocyst(e)ine and CVD was unrelated to abnormalities in markers of coagulation and endothelial cell damage in this population.

Aged↗

PubMed2005

The impact of two whole blood inline filters on markers of coagulation, complement and cell activation.

BACKGROUND AND OBJECTIVES: There exists a current lack of information about the impact of different inline filters, used for the leucoreduction of whole blood (WB), on the levels of clotting factors and markers of coagulation, complement and cell activation in plasma. Only a few small comparisons of different types of WB inline filters have been published to date. MATERIALS AND METHODS: This study compared two plasma types of 200 units each. Both study groups were derived from WB, inline-filtered and held for 2 h at 20 degrees between donation and filtration. Then, 200 units (Group A) were filtered using a positively charged polyester filter (Baxter RZ2000) and the other 200 units (Group B) were filtered using an uncharged polyester filter (Fresenius). After filtration, both groups were analysed for fibrinogen, factors V and VIII:C (FV and FVIII:C, respectively), immunoglobulin G (IgG), residual leucocytes and platelets, and markers of coagulation, complement and cell activation. Predonation plasma samples from CPDA1-anticoagulated blood were obtained from 100 different individuals and served as controls. RESULTS: WB inline filtration did not influence fibrinogen, FV, FVIII:C or IgG levels. Neither filter induced thrombin or fibrin formation. The charged filter caused substantial complement activation and neutrophil elastase and platelet factor 4 release. In contrast, the plasma filtered through the uncharged filter showed markedly lower levels of C3a-desArg, C5a, neutrophil elastase and platelet factor 4, and moderately reduced levels of prothrombin fragments 1+2 and D-dimer, compared with controls. CONCLUSIONS: Filter type has a significant impact on the quality of plasma derived from WB filtered through inline filtration systems. Some filters produce substantial coagulation and complement activation and cell release, while others appear to reduce the plasma levels of activation markers. The clinical significance of these findings remains to be determined.

Adolescent↗

PubMed2002

The use of coagulation activation markers (soluble fibrin polymer, TpP, prothrombin fragment 1.2, thrombin-antithrombin, and D-dimer) in the assessment of hypercoagulability in patients with inherited and acquired prothrombotic disorders.

A total of 260 consecutive patients, referred for hypercoagulable assessment, was included in this study. Four coagulation activation markers were utilized to assess these patients [enzyme-linked immunosorbent assays for soluble fibrin polymer (TpP), prothrombin fragment 1.2, thrombin-antithrombin complex, and D-dimer]. The mean levels of the activation markers directly correlated with the number of hypercoagulable abnormalities. The percentage of patients with increased TpP levels for each group was lower than the other activation markers. The findings indicate that activation markers reflect the number of underlying thrombophilic abnormalities. Our data suggest that there is a utility in performing a panel of coagulation activation markers to assess the thrombotic risk. The measurement of soluble fibrin polymer may be more reflective of an impending vascular event.

Activated Protein C Resistance↗

PubMed1998

Markers of coagulation and platelet activation during percutaneous mitral valvuloplasty.

The effect of percutaneous mitral valvuloplasty (PMV) on markers of coagulation and platelet activation was investigated to assess whether coagulation or platelet activation take place during and after PMV even under conditions of full heparinization. Before PMV, all the hemostatic parameters studied were in the normal range compared with those of a control group. Two hours after PMV the levels of prothrombin fragment F1 and 2 (F1+2) (1.6+/-0.6 nmol/l versus 0.8+/-0.3 nmol/l, P < 0.005), plasma thrombin-antithrombin III (TAT) complexes (5.4+/-3.2 ng/ml versus 2.2+/-0.9 ng/ml) and beta-thromboglobulin (119+/-70 ng/ml versus 42.2+/-41 ng/ml) had increased significantly compared with those measured at basal conditions. Activated partial thromboplastin time was significantly prolonged (152+/-40 s versus 21+/-5 s), reflecting full heparinization. Levels of fibrinogen, F1+2, TAT and beta-thromboglobulin remained increased 72 h after PMV. We conclude that patients with severe, symptomatic mitral stenosis undergoing PMV need a more specific antithrombotic therapy or a more prolonged and perhaps less intensive heparinization.

Adult↗