The pathogenesis of acute coronary syndrome (ACS) inevitably involves thrombosis on a background of plaque rupture and erosion. To reduce future thrombosis, patients receive antithrombotic, antiplatelet and anticoagulant medications, after the index event, which also increase the risk of bleeding. Yet despite such treatment, 10-15% patients go on to have recurrent major adverse cardiac events (MACE), due predominantly to thrombotic complications. Newer antithrombotic and antiplatelet agents, whilst reducing recurrent thrombosis, significantly increase the risk of bleeding. Identification of patients at increased risk of future thrombotic events would be highly desirable, since this group could be targeted with more potent antithrombotic medications, allowing use of less potent medications in low-risk groups, to reduce bleeding. Ideally, such therapy should be personalized to the individual, to achieve the greatest benefit at the lowest risk for the population. In order to offer personalized antithrombotic therapy, it is necessary to identify which patients remain prothrombotic despite dual antiplatelet therapy (DAPT). ACS can manifest in unstable angina and non-ST elevation myocardial infarction (NSTEMI) if thrombosis is transient, and cause lasting coronary artery occlusion, with ST-elevation MI (STEMI) if thrombosis is persistent.1 Whether a thrombus causes persistent arterial occlusion causing infarction, or transient occlusion, is determined by the balance between prothrombotic drivers on the one hand, and the capacity of the innate endogenous thrombolytic system to naturally dissolve any thrombus, on the other.2 Until recently, endogenous thrombolysis has been difficult to measure. Factorial assays (PAI-1, t-PA, fibrinogen, TAFI etc.) do not reflect the overall state of endogenous thrombolysis.2 There are currently 2 methods to assess endogenous lysis; the ROTEM/TEG (which assesses thrombus formation and lysis at low shear rates, more akin to venous thrombus) and the newer Global Thrombosis Test (GTT, which assesses thrombus formation and lysis under arterial flow conditions of high shear).
|Short title||VaLiDate R|
|Effective start/end date||1/01/19 → 1/02/21|
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