Point-of-care tests of platelet reactivity and clot strength in risk assessment post-PCI: more insight into what really matters

This editorial refers to ‘Platelet-fibrin clot strength and platelet reactivity predicting cardiovascular events after percutaneous coronary interventions’, by O. Kwon et al., https://doi.org/10.1093/eurheartj/ehae296.In the majority of cases, coronary thrombosis is caused by disruption or fissuring of an atherosclerotic plaque. Locally exposed subendothelial thrombogenic material becomes exposed to flowing blood, resulting in platelet activation and subsequent platelet aggregation, with simultaneous activation of coagulation leading to thrombin generation. Thrombin is a key mediator in arterial thrombosis, being both the most potent platelet agonist as well as the essential step in coagulation, contributing to the stabilization of an initially loose platelet clot by generating cross-bound fibrin within the thrombus.1 Unchecked, this process results in occlusive thrombus formation. However, under physiological conditions, simultaneous activation of the intrinsic thrombolytic processes can help ‘lyse’ such thrombi, restore flow and prevent lasting downstream infarction (Graphical abstract).1,2