Prospective Assessment of Biomarkers of Hypercoagulability for the Identification of Patients With Severe Coronary Artery Disease. The ROADMAP-CAD Study

Gerotziafas, Grigoris T.; Zografos, Theodoros; Pantos, Ioannis; Lefkou, Eleftheria; Carlo, Audrey; Fareed, Jawed; Dreden, Patrick Van; Katritsis, Demosthenes G.

doi:10.1177/1076029620964590

Cited by 3 publications

(4 citation statements)

References 40 publications

(41 reference statements)

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“…The results of a large meta-analysis also indicated a weak, but still positive, association of the PAI-1 gene with CAD [76]. Increased levels of PAI-1 are associated to accelerated atherosclerosis with increased lipid content compared to vascular smooth muscle cells, thus leading to complications such as plaque rupture and thrombotic complications.…”

Section: Discussionmentioning

confidence: 98%

“…For example, the ROADMAP-CAD study is a prospective study that seeks to evaluate the utility of measuring hypercoagulability biomarkers to better diagnose severe coronary artery disease. This research by Gerotziafas et al showed promising results indicating that hypercoagulability assessment could be proposed to screen patients with severe CAD [76][77][78]-Table 3. • the anticardiolipin and anti-beta-2 glycoprotein-1 antibodies (IgG and IgM isotypes) and lupus anticoagulant;…”

Section: Discussionmentioning

confidence: 99%

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The Etiology of the Thrombotic Phenomena Involved in the Process of Coronary Artery Disease—What Is the Role of Thrombophilic Genes in the Development of This Pathology?

Bararu Bojan,

Dobreanu,

Vladeanu

et al. 2024

IJMS

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Cardiovascular diseases, among which includes coronary artery disease, represent one of the most important causes of mortality and morbidity worldwide. Research aimed at determining the risk factors involved recognizes a group of “traditional” risk factors, but also more recent studies identified over 100 “novel” ones which may have a role in the disease. Among the latter is the thrombophilia profile of a patient, a pathology well-established for its involvement in venous thromboembolism, but with less studied implications in arterial thrombosis. This paper reviews the literature, explaining the pathophysiology of the thrombophilia causes associated most with coronary thrombosis events. Results of several studies on the subject, including a meta-analysis with over 60,000 subjects, determined the significant involvement of factor V Leiden, prothrombin G20210A mutation, plasminogen activator inhibitor–1 and antiphospholipid syndrome in the development of coronary artery disease. The mechanisms involved are currently at different stages of research, with some already established and used as therapeutic targets.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

The Etiology of the Thrombotic Phenomena Involved in the Process of Coronary Artery Disease—What Is the Role of Thrombophilic Genes in the Development of This Pathology?

Bararu Bojan,

Dobreanu,

Vladeanu

et al. 2024

IJMS

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“…We hypothesized that one or several coagulation assays performed after HIT diagnosis could help detect the patients the most prone to thrombosis thus supporting resorting to a therapeutic dose of a non-heparin anticoagulant. We investigated three laboratory assays: a marker of intense platelet activation with circulating procoagulant phospholipids, associated with extracellular vesicles [ 7 ]; a biomarker of thrombin formation in vivo, namely a fibrin monomer assay [ 8 ]; and thrombin generation, which measures thrombin potential in vitro [ 9 , 10 ] whereas the two former are candidate prethrombotic biomarkers. This is a pilot study since to the best of our knowledge no data are available about those markers in the HIT setting.…”

Section: Introductionmentioning

confidence: 99%

How to assess hypercoagulability in heparin-induced thrombocytopenia? Biomarkers of potential value to support therapeutic intensity of non-heparin anticoagulation

Barocas,

Savard,

Carlo

et al. 2023

Thrombosis J

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Background In case of heparin-induced thrombocytopenia (HIT), the switch to a non-heparin anticoagulant is mandatory, at a therapeutic dose. Such a treatment has limitations though, especially for patients with renal and/or hepatic failure. Candidate laboratory tests could detect the more coagulable HIT patients, for whom therapeutic anticoagulation would be the more justified. Patients and methods This was a monocentre observational prospective study in which 111 patients with suspected HIT were included. Nineteen were diagnosed with HIT (ELISA and platelet activation assay), among whom 10 were classified as HITT + when a thrombotic event was present at diagnosis or during the first following week. Two plasma prethrombotic biomarkers of in vivo activation of the haemostasis system, procoagulant phospholipids (ProcoagPPL) associated with extracellular vesicles and fibrin monomers (FM test), as well as in vitro thrombin potential (ST Genesia; low picomolar tissue factor) after heparin neutralization (heparinase), were studied. The results were primarily compared between HITT + and HITT- patients. Results Those HIT + patients with thrombotic events in acute phase or shortly after (referred as HITT+) had a more coagulable phenotype than HIT + patients without thrombotic events since: (i) clotting times related to plasma procoagulant phospholipids tended to be shorter; (ii) fibrin monomers levels were statistically significantly higher (p = 0.0483); (iii) thrombin potential values were statistically significantly higher (p = 0.0404). Of note, among all patients suspected of suffering from HIT, we did not evidence a hypercoagulable phenotype in patients diagnosed with HIT compared to patients for whom the diagnosis of HIT was ruled out. Conclusion The three tests could help identify those HIT patients the most prone to thrombosis.

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“… 22 Another factor associated with ischaemic heart disease that can affect platelet responsiveness is the hypercoagulable state of these patients. 23 24 Apart from the established platelet-activating role of thrombin, other coagulation-generated factors might alter platelet activation processes. 25 26 It is still unclear how the priming substances in patients with ischaemic heart disease influence the activation profiles of platelets and the formation of distinct platelet populations.…”

Section: Introductionmentioning

confidence: 99%

Effects of Platelet Agonists and Priming on the Formation of Platelet Populations

et al. 2021

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Platelets from healthy donors display heterogeneity in responsiveness to agonists. The response thresholds of platelets are controlled by multiple bioactive molecules, acting as negatively or positively priming substances. Higher circulating levels of priming substances adenosine and succinate, as well as the occurrence of hypercoagulability, have been described for patients with ischaemic heart disease. Here, we present an improved methodology of flow cytometric analyses of platelet activation and the characterisation of platelet populations following activation and priming by automated clustering analysis.Platelets were treated with adenosine, succinate, or coagulated plasma before stimulation with CRP-XL, 2-MeSADP, or TRAP6 and labelled for activated integrin αIIbβ3 (PAC1), CD62P, TLT1, CD63, and GPIX. The Super-Enhanced Dmax subtraction algorithm and 2% marker (quadrant) setting were applied to identify populations, which were further defined by state-of-the-art clustering techniques (tSNE, FlowSOM).Following activation, five platelet populations were identified: resting, aggregating (PAC1 + ), secreting (α- and dense-granules; CD62P + , TLT1 + , CD63 + ), aggregating plus α-granule secreting (PAC1 + , CD62P + , TLT1 + ), and fully active platelet populations. The type of agonist determined the distribution of platelet populations. Adenosine in a dose-dependent way suppressed the fraction of fully activated platelets (TRAP6 > 2-MeSADP > CRP-XL), whereas succinate and coagulated plasma increased this fraction (CRP-XL > TRAP6 > 2-MeSADP). Interestingly, a subset of platelets showed a constant response (aggregating, secreting, or aggregating plus α-granule secreting), which was hardly affected by the stimulus strength or priming substances.

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Prospective Assessment of Biomarkers of Hypercoagulability for the Identification of Patients With Severe Coronary Artery Disease. The ROADMAP-CAD Study

Cited by 3 publications

References 40 publications

The Etiology of the Thrombotic Phenomena Involved in the Process of Coronary Artery Disease—What Is the Role of Thrombophilic Genes in the Development of This Pathology?

The Etiology of the Thrombotic Phenomena Involved in the Process of Coronary Artery Disease—What Is the Role of Thrombophilic Genes in the Development of This Pathology?

How to assess hypercoagulability in heparin-induced thrombocytopenia? Biomarkers of potential value to support therapeutic intensity of non-heparin anticoagulation

Effects of Platelet Agonists and Priming on the Formation of Platelet Populations

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