Levels Of Tissue Factor Procoagulant Activity Research Articles

Changes in Procoagulant Blood Biomarkers After Mechanical Thrombectomy

ObjectivesThere is limited knowledge of the relationship between mechanical thrombectomy (MT) and endothelial inflammation in large-vessel occlusion (LVO) acute ischemic stroke (AIS). Intimal arterial damage releases tissue factor, a precipitant of the clotting cascade and thrombosis. We report changes in blood coagulation markers after MT treated with and without tissue plasminogen activator for AIS. Materials and MethodsCases of LVO-AIS treated with MT were included. Blood coagulation marker levels were measured within 10 h of stroke onset as a baseline and then 48 h later. Assayed biomarkers included: tissue factor procoagulant activity (TFPCA), factor VII (FVII), activated factor VII (FVIIa), factor VIII (FVIII), d-dimer, thrombin-antithrombin complex (TAT), plasminogen activator inhibitor-1 (PAI-1), and tissue factor pathway inhibitor (TFPI). Biomarker levels of MT with tissue plasminogen activator (TPA) or without (non-TPA) are reported. ResultsBiomarker levels from five patients with LVO-AIS treated with MT (three non-TPA, two TPA) were included. In non-TPA cases, TFPCA and PAI-1 increased while FVII, FVIIa, TAT, d-dimer, and TFPI decreased from baseline to 48 h. In TPA cases, TFPCA, FVIIa, d-dimer, TFPI, and PAI-1 decreased while FVIII increased from baseline to 48 h. ConclusionsTFPCA increased after MT in non-TPA but decreased in TPA treated patients. This finding suggests that MT is associated with elevated inflammation and procoagulation which may be reduced with TPA treatment. With further validation, the increase in TFPCA levels could help guide anticoagulant management of patients with MT without TPA.

Abstract 1345: Mutant IDH1 and tissue factor in gliomas

Abstract Background: IDH1 mutations (IDH1mut) occur in 20-30% of gliomas, induce DNA hypermethylation, and are associated with a better prognosis than IDH1 wild-type (IDH1wt) gliomas, yet the basis for this remains unclear. Furthermore, venous thromboemboli (VTE) are a serious complication in glioma patients, and the mechanism for this is also unclear. We recently discovered that IDH1mut gliomas are much less likely to develop VTE compared to IDH1wt gliomas. Our data suggests that suppression of Tissue Factor (TF), the primary initiator of coagulation, is a key reason for this. TF also directly enhances tumor malignancy via protease-activated receptor 2 (PAR2). In this study, we further explored the significance of TF on malignancy and thrombosis in IDH1wt and IDH1mut gliomas. Methods: Assays were performed using 6 patient derived glioma cells, 3 IDH1wt (GBM6, GBM12, GBM43) and 3 IDH1mut (TB09, BT142, GBM164). DNA methylation was analyzed by Illumina Human 850K. TF procoagulant activity (PCA) was determined by FXa generation, using preoperative glioma patient arterial plasma, conditioned medium, or cells. In vivo models of cancer induced thrombosis were created via surgical stenosis of the inferior vena cava of mice engrafted with IDH1wt or IDH1mut gliomas. In vitro markers of malignancy were measured by BrdU incorporation for cell proliferation, serum gradient Matrigel-coated transwell inserts for invasion, soft agar colony formation for clonogenicity. Nude mice (N≥6/group) were orthotopically transplanted with IDH1wt glioma cells and monitored for growth using bioluminescence imaging. Results: The TF gene, F3, was significantly hypermethylated in IDH1mut cells compared to IDH1wt cells, and IDH1mut glioma cells had lower levels of TF protein and TF PCA compared to IDH1wt cells. Exogenous treatment with the product of IDH1mut enzyme, D-2-hydroxyglutarate, directly suppressed TF PCA by 38% in IDH1wt cells (P=0.03), as did transgene IDH1mut expression. Mice with IDH1mut glioma xenografts produced fewer and smaller IVC thrombi than mice with IDH1wt xenografts (0.9±0.9 vs 10.3±3.6 mg, P=0.02). Patients whose gliomas contained IDH1mut had lower TF PCA compared to IDH1wt (0.5±0.2 vs 1.2±0.2 pg/mL, P=0.04), and there was a strong link between levels of TF PCA and subsequent development of VTE (P=0.03). TF knockdown greatly reduced cell proliferation, invasion, and colony formation of IDH1wt cells. Likewise, the PAR2 antagonist, GB83, inhibited IDH1wt cell proliferation by 54% (P<0.001) and reduced cell invasion by 25% (P<0.05). TF knockdown also reduced in vivo growth of IDH1wt gliomas by 96% at 28 days post engraftment (P=0.03), and extended median survival of engrafted mice by 86% (P=0.001). Conclusions: IDH1mut mediated suppression of TF expression and PCA may be a critical component of the less thrombogenic, and less malignant, IDH1mut phenotype. Targeting TF-PAR2 signaling may therefore represent a novel therapeutic strategy to reduce IDH1wt glioma malignancy. Citation Format: Dusten Unruh, Snezana Mirkov, Charles D. James, Craig Horbinski. Mutant IDH1 and tissue factor in gliomas [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 1345. doi:10.1158/1538-7445.AM2017-1345

Δ(9)-Tetrahydrocannabinol (THC) enhances lipopolysaccharide-stimulated tissue factor in human monocytes and monocyte-derived microvesicles.

BackgroundImmunomodulatory effects in humans of Δ9−Tetrahydrocannabinol (THC), the psychoactive component of marijuana are controversial. Tissue factor (TF), the activator of the extrinsic coagulation cascade, is increased on circulating activated monocytes and is expressed on microvesicles released from activated monocytes during inflammatory conditions, which perpetuate coagulopathies in a number of diseases. In view of the increased medicinal use of marijuana, effects of THC on human monocytes and monocyte-derived microvesicles activated by lipopolysaccharide (LPS) were investigated.FindingsPeak levels of TF procoagulant activity developed in monocytes or microvesicles 6 h following LPS treatment and were unaltered by THC. After 24 h of LPS stimulation, TF activity declined in control-treated or untreated cells and microvesicles, but persisted with THC treatment. Peak TF protein occurred within 6 h of LPS treatment independent of THC; by 24 h, TF protein declined to almost undetectable levels without THC, but was about 4-fold greater with THC. Steady-state TF mRNA levels were similar up to 2 h in the presence of LPS with or without THC, while 10-fold greater TF mRNA levels persisted over 3–24 h with THC treatment. Activation of MAPK or NF-κB pathways was unaltered by THC treatment and inflammatory cytokine IL-6 levels were unchanged. In contrast, TNF and IL-8 levels were enhanced by 20–50 %.ConclusionsTHC enhances TF expression in activated monocytes resulting in elevated procoagulant activity. Marijuana use could potentiate coagulopathies in individuals with chronic immune activation such as HIV-1 infection or inflammatory bowel disease.

Whole-Blood Tissue Factor Procoagulant Activity Is Elevated in Type 1 Diabetes

OBJECTIVETo determine tissue factor procoagulant activity (TF-PCA) in patients with type 1 diabetes and to examine effects of hyperglycemia and hyperglycemia plus hyperinsulinemia on TF-PCA.RESEARCH DESIGN AND METHODSWe have determined circulating TF-PCA and other coagulation factors under basal (hyperglycemic) conditions, after acute correction of hyperglycemia, in response to 24 h of selective hyperglycemia, and in response to 24 h of hyperglycemia plus hyperinsulinemia in nine type 1 diabetic patients and in seven nondiabetic control subjects.RESULTSAs shown previously in patients with type 2 diabetes, basal TF-PCA and plasma coagulation factor VIIa (FVIIa) were higher in patients with type 1 diabetes than in nondiabetic control subjects. However, in contrast with type 2 diabetes, normalizing glucose did not decrease the elevated TF-PCA levels, and raising glucose or glucose plus insulin levels did not increase TF-PCA.CONCLUSIONSPatients with type 1 diabetes have elevated circulating TF-PCA and FVIIa levels and are in a procoagulant state that may predispose them to acute cardiovascular events. The mechanisms regulating TF-PCA in patients with type 1 and type 2 diabetes are different and should be further explored.

Elevated Circulating Tissue Factor Procoagulant Activity, Factor VII, Plasminogen Activator Inhibitor-1 and VCAM-1 in Childhood Obesity: Evidence of a Procoagulant State and Endothelial Dysfunction?,

Abstract 3338Childhood obesity is increasing in prevalence and associated with risk of type 2 diabetes (T2DM) and coronary disease. Adult obesity and T2DM are associated with alterations in the coagulation and fibrinolytic systems. Tissue Factor (TF) is the principal initiator of blood coagulation and is both prothrombotic and proinflammatory. In mouse models of obesity, TF and plasminogen activator inhibitor (PAI)-1 genes are upregulated. We tested the hypothesis that childhood obesity is associated with elevated levels of circulating TF and markers of coagulation, fibrinolysis, and endothelial dysfunction. Forty-seven children were recruited and classified based on Body Mass Index (BMI) percentile (CDC growth curves) as underweight (≤5th percentile; n=1), healthy weight (>5–84.9th percentile; n=22), overweight (≥85%-94.9th percentile; n=3) and obese (≥95th percentile; n=21). We compared the findings in 21 obese children (10.1±1.5 years, mean age ± SD) and 22 healthy weight children (9.9±1.6 years). Circulating membrane bound TF procoagulant activity (TF-PCA), measured in whole blood lysates by a two-stage clotting assay (Key et al, Blood;1998:91), was elevated in obese compared to healthy weight children (60.6±32.5 vs 34.0±13.5 U/ml, mean ± SD, p=0.005). TF-PCA levels in obese children were comparable to levels observed by us in adults with T2DM (69.5±11.5; n=18). Plasma factor (F) VIIC (1.00±0.20 vs 0.90±0.20 U/ml; p=0.03) was elevated in obese group. Plasma FVIIa, FVIII, TF antigen, fibrinogen, and thrombin-antithrombin III, and microparticles (MP) were not different between groups. In fibrinolytic system, plasma PAI-1 was elevated in obese group (37.3±18.0 vs 25.6±15.0 ng/ml; p=0.03), and tissue plasminogen activator (tPA) antigen (6.7±3.4 vs 5.1±2.0 ng/ml, p=0.07) showed a similar trend. Endothelial markers, soluble vascular cell adhesion molecule-1 (sVCAM-1; 709.2±444.5 vs 526.5±184.8 ng/ml; p=0.05) and von-Willebrand Factor (VWF; 1057.4±139.8 vs 987.9±130.8 mU/ml; p=0.07) showed a trend towards higher levels in obesity, suggesting endothelial dysfunction. BMI correlated with circulating TF-PCA (r=0.36; p=0.01), FVIIC (r=0.36; p=0.01), and PAI-1 (r=0.38; p=0.009). TF-PCA correlated with sVCAM-1 (r=0.36; p=0.01), suggesting a potential endothelial contribution to the circulating TF-PCA. Plasma FVIIa (r=−0.29; p=0.053) appeared to be inversely related to TF-PCA possibly related to removal of FVIIa from plasma by binding to membrane TF. There was an inverse relationship between MP and FVIII (r= −0.42; p=0.004) and VWF (r=−0.37; p=0.01), which may reflect binding of FVIII and vWF to microparticles. Conclusions:Obesity, even in children, causes a potential procoagulant state characterized by increased circulating TF-PCA, FVIIC and PAI-1, and is associated with evidence suggesting endothelial dysfunction. Elevated levels of endothelial markers have been shown to predict development of T2DM, and elevated FVIIC has been associated with carotid intima-media thickness in young adults. Overall, these alterations may be basis for the increased risk of cardiovascular disease now documented in childhood obesity as well. Larger studies are needed to define the effect of childhood obesity on the hemostatic systems and the impact of intervention with weight reduction on the observed changes. Disclosures:No relevant conflicts of interest to declare.

Circulating Tissue Factor Procoagulant Activity (TF-PCA) Is Elevated in Type 1 Diabetes Mellitus: Differential Regulation of TF-PCA in Type 1 and Type 2 Diabetes

Abstract 540 Background:Type 1 diabetes mellitus (T1DM) is a hypercoagulable state associated with increased acute cardiovascular events. Potential risk factors for this include alterations in coagulation and fibrinolytic systems. Tissue factor (TF) is the principal initiator of blood coagulation. Several studies show that there is a circulating pool of TF in blood, which is thrombogenic, and elevated in thrombotic states. We have shown (J Clin Endo Metab 2007, 92:4352-8) that circulating TF procoagulant activity (TF-PCA) is elevated in patients with Type 2 DM (T2DM) and increases further with acute combined hyperglycemia-hyperinsulinemia and selective hyperinsulinemia. There is currently no information on circulating TF-PCA levels and TF responses to hyperglycemia and/or hyperinsulinemia in patients with T1DM who are at comparable risk for cardiovascular events as T2DM patients. Objective:To investigate circulating TF-PCA and other coagulation factors under basal conditions and in response to acute selective hyperglycemia, selective hyperinsulinemia and combined hyperglycemia and hyperinsulinemia in T1DM. Methods:Three study protocols were used: 1) acute correction of hyperglycemia (with IV insulin) followed by 24 h of hyperglycemia, 2) 24 h of selective hyperinsulinemia and 3) 24 h of combined hyperinsulinemia and hyperglycemia. Studies were performed in 9 T1DM patients and 7 non-diabetic subjects. T1DM patients were on a basal/bolus insulin regimen (insulin glargine, 15–70 units at night) or Novolog 70/30 mix twice daily (45-50 units). Circulating membrane bound TF-PCA was measured in whole blood lysates by a two-stage clotting assay (Key et al, Blood; 1998:91). Results:Basal TF-PCA (64.7 ± 6.0 vs. 24.6 ± 1.2 U/ml, p < 0.001) and plasma factor VIIa (104 ± 24 vs. 38 ± 8 mU/ml, p < 0.03), the activated form of factor VII, were higher in T1DM (n=9) than in non-diabetic controls (n= 7) indicating a chronic procoagulant state. Plasma FVIIc, FVIII, thrombin-antithrombin complexes (TAT) and soluble vascular cell adhesion molecule-1 (sVCAM-1) were not significantly different between patients and controls. When control subjects and T1DM patients were combined, HbA1C correlated with TF-PCA (r=0.71, p=0.0001, n=23). Plasma adiponectin was elevated in T1DM patients compared to control subjects (12.4 ± 1.9 vs 6.7 ± 2.0 μg/ml, p < 0.05).Acutely normalizing hyperglycemia in T1DM patients over 3–15 h did not decrease TF-PCA. There were also no changes in plasma FVIIc and FVIII. To explore effects of acutely raising plasma glucose, glucose was raised from 103 ± 8 to ∼ 300 mg/dl by infusion of 20% dextrose and maintained for 24 hours. Insulin concentrations were kept at basal concentrations (6 and 13 μU/ml) by IV infusion. In our previous studies in non-diabetic subjects (Diabetes 2006, 55,202-8) and in T2DM patients (J Clin Endo Metab 2007, 92,4352-8), raising glucose and insulin together produced a marked increase in circulating TF-PCA. We therefore raised glucose to ∼ 250 mg/dl and insulin to ∼ 100 μU/ml together in 8 T1DM patients. Raising glucose levels alone or in combination with insulin decreased circulating TF-PCA by 26% (p < 0.02) and 37% (p < 0.01), respectively, which is in striking contrast to the elevations noted in non-diabetic controls and T2DM patients. To explore effects of selective hyperinsulinemia, plasma insulin levels were raised in 3 T1DM patients by IV infusion of regular insulin from 15 ± 0.2 to ∼ 75 μU/ml and maintained for 24 hours while plasma glucose was kept at ∼ 100 mg by infusion of 20% dextrose. Again, in contrast to our studies in T2DM patients and healthy subjects we found no increase in TF-PCA Conclusions:Circulating TF-PCA and FVIIa levels are elevated in T1DM patients indicating a potential prothrombotic state. The studies on acutely induced hyperinsulinemia and hyperglycemia indicate that the regulation of TF expression is different in T1DM and T2DM. This may be due to multiple mechanisms, including a differential effect of insulin on monocytes TF expression in T1DM and T2DM, and due to differences in plasma adiponectin, which has been shown to inhibit TF expression and is elevated in T1DM. Additional studies are needed to obtain insights into the mechanisms regulating the differential expression of TF in the two forms of diabetes. Disclosures:No relevant conflicts of interest to declare.

No evidence for the presence of tissue factor in high-purity preparations of immunologically isolated eosinophils.

To date, there is no unequivocal opinion on whether human eosinophils express tissue factor (TF). Therefore, we studied the expression of TF protein and activity in resting or stimulated immunologically purified human eosinophils. By use of immunologic isolation, we achieved over 96% purity of eosinophil preparations, and contamination by CD14-positive cells was below 0.3%. Flow cytometric [fluorescence-activated cell sorting (FACS)] analysis of eosinophils revealed no surface expression of TF antigen in resting or stimulated eosinophils. Immunoblotting of eosinophil lysates did not show any TF protein under resting or stimulated conditions. The lysates of resting or stimulated eosinophils contained no detectable levels of TF procoagulant activity. In contrast, monocytes, stimulated in plasma or medium, possessed readily detectable TF levels on the cell surface and in cell lysates as detected by FACS and immunoblotting. This was active TF antigen, as confirmed by TF activity assay (19.2 +/- 4.2 and 28.6 +/- 3.1 mU per 10(6) cells, stimulated in medium or plasma, respectively). We found no detectable TF mRNA levels in resting or stimulated eosinophils by real-time polymerase chain reaction (PCR), whereas in monocytes TF mRNA levels were significantly increased after stimulation. Our data indicate that there is no evidence for TF expression in high-purity preparations of immunologically isolated eosinophils.

Chemotherapy-induced thrombin generation via procoagulant endothelial microparticles is independent of tissue factor activity.

Cisplatin-based chemotherapy predisposes cancer patients to thromboembolic events. To investigate whether endothelial damage, via formation of procoagulant endothelial microparticles (EMPs), contributes to cisplatin-related hypercoagulability. Cell viability and caspase-3/7 activities were assessed in two endothelial cell (EC) lines [human umbilical vein ECs (HUVECs) and human pulmonary microvascular ECs (HMVEC-Ls)] after exposure to cisplatin (1, 2.5, 5, 10 and 20 microm) for up to 120 h. Counts and procoagulant activity of EMPs were measured by flow cytometry and a thrombin generation assay, respectively. Tissue factor (TF) antigen and TF-dependent procoagulant activity of EMP were determined by enzyme-linked immunosorbent assay and a novel functional assay. By inducing apoptosis, cisplatin dose- and time-dependently decreased the viability of confluent HUVECs and HMVEC-Ls. Progression of EC death was accompanied by an increased release of EMPs (relative increase at 20 microm cisplatin for 48 h vs. control: HUVECs 6.5-fold, P < 0.001; HMVEC-Ls 18.4-fold, P < 0.001). EMPs were highly procoagulant (relative increase at 20 microm cisplatin for 48 h vs. control: HUVECs 2.5-fold, P < 0.001; HMVEC-Ls 5.9-fold, P < 0.001). EMP-driven thrombin generation, however, was not dependent on TF: TF expression and TF procoagulant activity levels on microparticles were only marginal and EMP-associated thrombin generation remained unchanged when the extrinsic pathway was blocked by omission of factor VIIa and/or incubation with an anti-human TF antibody. In contrast, blocking of phospholipids by annexin V markedly diminished EMP-associated procoagulant activity. In vitro, cisplatin induced the release of EMPs that showed TF-independent procoagulant activity.

Hyperglycemia and Hyperinsulinemia Increase Circulating Tissue Factor Activity in Human Subjects.

Patients with diabetes mellitus (DM) have increased atherosclerotic and acute vascular events, and both hyperglycemia and hyperinsulinemia are independent risk factors for increased mortality. To evaluate the effects of hyperglycemia and hyperinsulinemia on the tissue factor (TF) pathway, we studied 3 groups of healthy individuals. Group A(Euglycemia and Hyperinsulinemia): 7 subjects were infused for 24h with insulin to maintain serum insulin levels at ~ 1000 pmol/l and with glucose at variable rates to maintain at 5.6 mmol/l (~ 100 mg/dl). Group B (Hyperglycemia and Hyperinsulinemia): 7 subjects were infused with glucose to maintain levels at ~ 11 mmol/l (~ 200 mg/dl) for 24 h. Group C(Euglycemia and Euinsulinemia): 4 subjects received saline for 24 h. Glucose was maintained at ~ 5.6 mmol/l with variable, small glucose infusions. Blood samples collected every 6 h. We assessed TF procoagulant activity (TF-PCA) in whole blood by clotting assay (Key et al, Blood 1998; 91: 4216), and plasma levels of activated factor VII (FVIIa), FVII activity (FVIIC), FVIII coagulant activity (FVIIIC), and thrombin-antithrombin (TAT) complexes. TF-PCA levels increased significantly from basal levels of 14 ± 1 and 20 ± 3 U/ml (mean±SE) to 79 ± 4 and 172 ± 6 U/ml at 24 h in Groups A and B, respectively. There was no increase in Group C.GroupsTFPCA (U/ml)FVIIa (mU/ml)FVIIC (U/ml)FVIIIC (U/ml)0 hr/24 hr0 hr/24 hr0 hr/24 hr0 hr/ 24 hrA)Euglycemia - Hyperinsulinemia(n=7)14 ± 1 / 79 ± 4*83 ± 9 / 45 ± 8*0.88 ± 0.09 / 0.72 ± 0.08*0.93 ± 0.05 / 0.98 ± 0.06†B)Hyperglycemia -HyperInsulinemia(n=7)20 ± 1 / 172 ± 6*85 ± 10 / 52 ± 6*1.02 ± 0.1 / 0.84 ± 0.1*1.03± 0.04 / 1.28 ± 0.07*C)Euglycemia and Euinsulinemia (n=4)19 ± 2 / 19 ± 156 ± 13 / 55 ± 140.83 ± 0.05 / 0.81 ± 0.080.86± 0.08 / 0.85 ± 0.08Shown mean±SE;†p<0.05;*p<0.001:Analysis of variance; comparison 0 to 24 hrs.By flow cytometry, percentage of monocytes expressing TF (Groups A and B combined) increased from 19.5 ± 4.2% at 0 h to 25.2 ± 4.4 % at 24 h (p = 0.03). Plasma FVIIa and FVIIC were significantly decreased, and plasma FVIIIC increased at 24 h in Groups A and B. There was an inverse relationship between plasma FVIIa and TF-PCA (Group A r = −0.51; Group B r = −0.51, p =0.002). Plasma FVIII levels correlated with TF-PCA in Group B (r = 0.48, p = 0.003). At 18 h, TAT levels increased from 13.4 ± 8 and 6.8 ± 2.5 to 46.9 ± 6.2 (p = 0.04) and 39.4 ± 6.7 μg/l (p=0.015) in Group A and B, respectively. No changes were noted in any measurements in Group C.Conclusions: Both hyperinsulinemia (Group A) alone and hyperglycemia with hyperinsulinemia (Group B) induce an increase in circulating TF-PCA, which is greater with the combination. This is associated with a decline in FVIIa and FVIIC, and increase in FVIIIC. We postulate that the decrease in FVIIa and FVIIC reflects enhanced binding of FVII to cellular TF. These studies provide evidence for enhanced expression of circulating TF by hyperglycemia and hyperinsulinemia even in healthy individuals. This increase may contribute to acute vascular events in DM patients.

Elevated whole-blood tissue factor procoagulant activity as a marker of restenosis after percutaneous transluminal coronary angioplasty and stent implantation.

Experimental data suggest that tissue factor (TF) may induce neointimal hyperplasia after arterial injury. In this study, we investigated the hypothesis that elevated levels of TF in the circulation contribute to the development of restenosis after percutaneous transluminal coronary angioplasty (PTCA) or stent implantation. Whole-blood TF procoagulant activity (TF-PCA) was measured using a previously described assay before, at 3 hours after, and at 24 hours after the intervention in 61 patients with stable angina undergoing PTCA (n=20) or stent implantation (n=41). Coronary angiography was performed 4 to 6 months after the intervention, and luminal narrowing > or =50% was defined as restenosis. Whole-blood TF-PCA levels did not correlate with intracellular monocyte tumor necrosis factor-alpha expression, a marker of activation of these cells. Baseline levels and time course of whole-blood TF-PCA after the intervention were compared in patients who did or did not subsequently develop restenosis. Whole-blood TF-PCA levels did not change significantly in the 24 hours after either intervention. However, in both the PTCA and stent groups, initial TF-PCA was significantly higher in patients who subsequently developed restenosis (P=0.018 and 0.039 compared with those who did not develop restenosis for PTCA and stent groups, respectively). Higher baseline values of whole-blood TF-PCA may be a predictor of restenosis after PTCA and stent implantation.