Why the study?
Does pharmacologic inhibition of factor IXa provide optimal anticoagulation in patients with acute coronary syndrome?
Does pharmacologic inhibition of factor IXa provide optimal anticoagulation in patients with acute coronary syndrome?
Factor IXa emerges as a promising therapeutic target for developing safer and more effective anticoagulants for patients with acute coronary syndrome.
Factor IXa inhibition merits clinical evaluation in ACS; leaves open whether it improves outcomes versus current anticoagulants.
Anticoagulant therapy, combined with platelet-directed inhibitors, represents a standard-of-care in the management of patients with acute coronary syndrome, particularly those who require percutaneous coronary interventions. While a vast clinical experience, coupled with large clinical trials have collectively provided guidance, an optimal anticoagulant drug and applied strategy, defined as one that reduces thrombotic and hemorrhagic events consistently, with minimal off-target effects and active control of systemic anticoagulation according to patient and clinical-setting specific need, remains at large. An advancing knowledge of coagulation, hemostasis, and thrombosis suggests that factor IXa, a protease that governs thrombin generation in common thrombotic disorders may represent a prime target for pharmacologic inhibition.
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Roser-Jones et al. (2011) studied this question.
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