Prognostic value of plasma tissue factor and tissue factor pathway inhibitor for cardiovascular death in patients with coronary artery disease: the AtheroGene study

Morange, Pierre‐Emmanuel; Blankenberg, Stefan; Alessi, Marie‐Christine; Bickel, Christoph; Rupprecht, H. J.; Schnabel, Renate B.; Lubos, Edith; Münzel, Thomas; Peetz, D.; Nicaud, Viviane; Juhan‐Vague, I.; Tiret, Laurence; Investigators, Atherogene

doi:10.1111/j.1538-7836.2007.02372.x

Cited by 70 publications

(56 citation statements)

References 32 publications

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“…15,20 Levels of free TFPI have been reported to be elevated in acute myocardial ischemia. 23 In our numerical simulations, the collective contributions of AT, fII, and fVIII were most prominent. 22 In this study, we have evaluated the potential for alteration of the systemic coagulation system in ACS by studying injury to the peripheral microcirculation in non-anticoagulated patients undergoing AMI and compared their response to a control cohort with stable coronary artery disease (CAD).…”

Section: Introductionmentioning

confidence: 95%

Systemic blood coagulation activation in acute coronary syndromes

Undas

Szułdrzyński

Brummel‐Ziedins

et al. 2009

Blood

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We evaluated systemic alterations to the blood coagulation system that occur during a coronary thrombotic event. Peripheral blood coagulation in patients with acute coronary thrombosis was compared with that in people with stable coronary artery disease (CAD). Blood coagulation and platelet activation at the microvascular injury site were assessed using immunochemistry in 28 nonanticoagulated patients with acute myocardial infarction (AMI) versus 28 stable CAD patients matched for age, sex, risk factors, and medications. AMI was associated with increased maximum rates of thrombin-antithrombin complex generation (by 93.8%; P < .001), thrombin Bchain formation (by 57.1%; P < .001), prothrombin consumption (by 27.9%; P ‫؍‬ .012), fibrinogen consumption (by 27.0%; P ‫؍‬ .02), factor (f) Va light chain generation (by 44.2%; P ‫؍‬ .003), and accelerated fVa inactivation (by 76.1%; P < .001), and with enhanced release of platelet-derived soluble CD40 ligand (by 44.4%; P < .001). FVa heavy chain availability was similar in both groups because of enhanced formation and IntroductionAfter vascular injury, blood clotting is initiated when plasma factor (f) VIIa gains access to tissue factor (Tf). The resulting complex activates the plasma zymogens fIX and fX. 1 Factor Xa activates small amounts of thrombin, which activates platelets, and the procofactors fV and fVIII to their respective active forms. 2 These reactions result in the formation of the intrinsic fXase (fVIIIa-fIXa) and prothrombinase (fVa-fXa) on the activated platelet surface. 3 The major bolus of thrombin formed by the prothrombinase complex is largely responsible for the ultimate hemostatic process. 4 A potent, synergistic inhibitory system principally composed of tissue factor pathway inhibitor (TFPI), antithrombin (AT), and the thrombin-thrombomodulin (Tm)-catalyzed dynamic protein C (PC) system opposes thrombin generation. 5,6 The formation of fVa and its regulation by activated protein C (APC) are key processes for maintaining blood homeostasis. The fV activation process involves sequential cleavages to first produce a heavy chain (1-709) and subsequently a light chain resulting in the active cofactor. 7 The PC system inactivates fVa in a kinetically controlled series of cleavage reactions in which APC cleaves the heavy chain of fVa at 2 locations (R506 and R306); the resulting fVai can no longer function in the coagulation system. 8,9 The balance between activation and inactivation of fV is critical to the synergistic control of the coagulation process. 10 The activation of the Tf coagulation pathway appears to be central in arterial and venous thrombosis. 11 A major clinical manifestation of arterial thrombosis is represented by the acute coronary syndromes (ACS), which result from platelet-rich thrombus formation on the surface of ruptured or eroded atheromatosus plaque in the coronary artery. 12 Typical procoagulant abnormalities in ACS are increased circulating thrombin marker levels, such as prothrombin fragment 1.2 (F1.2) or thrombin-antithrombi...

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Section: Introductionmentioning

confidence: 95%

Systemic blood coagulation activation in acute coronary syndromes

Undas

Szułdrzyński

Brummel‐Ziedins

et al. 2009

Blood

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“…The secreted TFPI from monocytes and most vascular wall cells may be associated within plaque through the binding with proteoglycans and other TFPI binding protein on the cells (30,31). It has been reported in literature to be elevated in AMI patients (5,(7)(8)(9). Our results indicate increase levels in younger AMI patients while insignificant changes in the levels of plasma TFPI in elder AMI patients as compared to controls.…”

Section: Discussionmentioning

confidence: 99%

Circulating thrombotic and haemostatic components in patients with coronary artery disease

Shalia

Shah

Mashru

et al. 2010

Indian J Clin Biochem

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“…Some studies have described the role of the polymorphism +5466 A/G of the TF gene, showing that it is associated with the risk of thrombosis (Reny et al, 2004;Mälarstig et al, 2005;Morange et al, 2007;Davis and Erlich, 2008;Boles and Mackman, 2010) and a threefold increase in the risk of thrombosis in individuals that possess this polymorphism (Opstad et al, 2010a). Thus, several studies have reported the relationship between this polymorphism and regulation of TF expression and high levels of TF in cardiovascular disease (Campo et al, 2006;Undas et al, 2009;Opstad et al, 2010b).…”

Section: Discussionmentioning

confidence: 99%

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

Evangelista¹,

Rios²,

Ribeiro³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. Recent studies have shown an association between thrombosis and factor VII (FVII), tissue factor (TF), and angiotensinconverting enzyme (ACE). This suggests that individuals with FVII-402 G/A, FVII-401 G/T, TF+5466 A/G, and ACE-287 insertion/ deletion (I/D) polymorphisms present an increased risk of venous thrombosis, heart disease, and ischemic stroke compared with controls. In this study, we investigated the frequencies of these polymorphisms and their association with arterial and venous thrombosis. For the FVII-402 G/A polymorphism, there were 57.3% heterozygote (HT) genotypes and 8.3% homozygote (HM) genotypes in the patients, and 45.2% HT genotypes and 15.4% HM genotypes in the controls. For the FVII-401 G/T polymorphism, there were 37.5% HT genotypes and 3.1% HM genotypes in the patients, and 32.7% HT genotypes and 4.8% HM genotypes in the controls. The polymorphism TF+5466 A/G was not found in any of the samples analyzed. For the ACE-287 I/D polymorphism, there were 43 (40.6%) HT genotypes and 63 (59.4%) HM genotypes in the controls and 28 (45.2%) HT genotypes and 34 (54.8%) HM genotypes in the patients. No significant difference was observed by comparing patients and controls. In this study, no association was found between the presence of the evaluated polymorphisms and the occurrence of thrombotic events.

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Prognostic value of plasma tissue factor and tissue factor pathway inhibitor for cardiovascular death in patients with coronary artery disease: the AtheroGene study

Cited by 70 publications

References 32 publications

Systemic blood coagulation activation in acute coronary syndromes

Systemic blood coagulation activation in acute coronary syndromes

Circulating thrombotic and haemostatic components in patients with coronary artery disease

Lack of association between potential prothrombotic genetic risk factors and arterial and venous thrombosis

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