Detection of hypofibrinolysis in stable coronary artery disease using the overall haemostatic potential assay

Reddel, Caroline J.; Curnow, Jennifer; Voitl, Jasmin; Rosenov, Alexander; Pennings, Gabrielle J.; Morel-Kopp, Marie-Christine; Brieger, David

doi:10.1016/j.thromres.2013.03.015

Cited by 36 publications

(35 citation statements)

References 25 publications

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“…59 Despite the use of antiplatelet therapy, stable coronary disease patients demonstrate elevated PAI-1 levels and are also hypercoagulable as assessed by both overall hemostatic potential assay and calibrated-automated thrombogram. 60 Although activation of the plasminogen-activating system has been observed in CAD, any interaction with CD147 in relation to CAD requires further investigation. If CD147 does result in an upregulation of PAI-1, targeting of CD147 may help stabilize coronary lesions and reduce the thrombotic complications of CAD.…”

Section: Plasminogen-activating Systemmentioning

confidence: 99%

CD147 in Cardiovascular Disease and Thrombosis

Pennings

Kritharides

2014

Semin Thromb Hemost

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Thrombotic and inflammatory pathways play a key role in coronary artery disease (CAD) development. Extracellular matrix metalloproteinase (aka CD147) is a member of the immunoglobulin superfamily that is expressed on many cell types including hematopoietic, endothelial cells, leukocytes, keratinocytes, platelets, and others. The binding partners of CD147 are numerous and diverse, and give some indication to the various roles that CD147 can play; these include homophilic interactions, integrins, cyclophilins, glycoprotein VI (GPVI), caveolin 1, and monocarboxylate transporters. Recent evidence suggests a role for CD147 in both thrombosis and inflammation, as well as involvement in CAD and cancer. In this review, we summarize the role of CD147 and its binding partners in platelets, thrombosis, and arterial disease and assess mechanistic aspects of CD147 biology.

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Section: Plasminogen-activating Systemmentioning

confidence: 99%

CD147 in Cardiovascular Disease and Thrombosis

Pennings

Kritharides

2014

Semin Thromb Hemost

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“…[1][2][3][4] While CAD has been linked to an increased prothrombotic state, no marker has been identified that can accurately assess abnormalities of global haemostasis due to this process and to severity of disease. Identifying a global haemostatic marker of coagulability and fibrinolysis may be important in stratifying risk of atherothrombosis and providing the basis for individualised therapeutic management.…”

Section: Introductionmentioning

confidence: 99%

Characterisation of clot microstructure properties in stable coronary artery disease

et al. 2017

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BackgroundCoronary artery disease (CAD) is associated with an increased prothrombotic tendency and is also linked to unfavourably altered clot microstructure. We have previously described a biomarker of clot microstructure (df) that is unfavourably altered in acute myocardial infarction. The df biomarker assesses whether the blood will form denser or looser microstructures when it clots. In this study we assessed in patients with stable chest pain whether df can differentiate between obstructed and unobstructed CAD.MethodsA blood sample prior to angiography was obtained from 251 consecutive patients undergoing diagnostic coronary angiography. Patients were categorised based on angiographic findings as presence or absence of obstructive CAD (stenosis ≥50%). The blood sample was assessed using the df biomarker, standard laboratory markers and platelet aggregometry (Multiplate).ResultsA significant difference (p=0.028) in df was observed between obstructive CAD (1.748±0.057, n=83) and unobstructive CAD (1.732±0.052, n=168), where patients with significant CAD produce denser, more tightly packed clots. df was also raised in men with obstructive CAD compared with women (1.745±0.055 vs 1.723±0.052, p=0.007). Additionally df significantly correlated with the platelets response to arachidonic acid as measured by the ASPItest area under the curve readings from platelet aggregometry (correlation coefficient=0.166, p=0.008), a low value of the ASPItest indicating effective aspirin use was associated with looser, less dense clots.ConclusionsFor the first time, we characterise clot microstructure, as measured by df, in patients with stable CAD. df can potentially be used to risk-stratify patients with stable CAD and assess the efficacy of therapeutic interventions by measuring changes in clot microstructure.

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“…Indeed, in all the above‐mentioned conditions, hypercoagulation is a known indicator of the disease; e.g. sarcoidosis (Hasday et al , ; Nakstad et al , ), T2D (Tripodi et al , ; Pretorius et al , , ; Pretorius & Bester, ), coronary artery disease (Tantry et al , ; Reddel et al , ), chronic liver disease (Lisman et al , ) and periodontitis (Tonetti & Van Dyke, ). In addition, IL12 is thought to contribute to the development of atherosclerosis (Wegner et al , ).…”

mentioning

confidence: 99%

Interleukin‐12 and its procoagulant effect on erythrocytes, platelets and fibrin(ogen): the lesser known side of inflammation

2017

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SummaryInflammation, with its associated inflammatory molecules, is integral to most chronic diseases, including the various cardiovascular diseases. Interleukin 12 (IL12) is one of the inflammatory cytokines that is upregulated during inflammation; however, we know very little about its exact effect on red blood cells (RBCs), platelets and fibrin(ogen). IL12 is an important pleiotropic cytokine in early inflammatory responses and has potent immunomodulatory, antitumour and anti-infection activity. Here we investigate how low levels of circulating IL12, comparable to levels found during chronic inflammation, affect coagulation parameters, platelets and RBCs. We used thromboelastography, scanning electron microscopy, refractometery and wide-field microscopy. Our results show that IL12 caused hypercoagulation, platelet activation and spreading, as well as RBC agglutination. This phenomenon has far-reaching implications for treatment of the plethora of conditions where IL12 is upregulated, since it suggests aberrant haemorheology as agglutination affects blood flow. This information might be used in future to target the lowering of IL12 in inflammatory conditions, as well as address RBC agglutination.

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Detection of hypofibrinolysis in stable coronary artery disease using the overall haemostatic potential assay

Cited by 36 publications

References 25 publications

CD147 in Cardiovascular Disease and Thrombosis

CD147 in Cardiovascular Disease and Thrombosis

Characterisation of clot microstructure properties in stable coronary artery disease

Interleukin‐12 and its procoagulant effect on erythrocytes, platelets and fibrin(ogen): the lesser known side of inflammation

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