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Thrombosis, haemostasis, and platelet biology 

Thrombosis, haemostasis, and platelet biology
Thrombosis, haemostasis, and platelet biology

Dr Paul Gurbel

, Dr Dean Kereiakes

, and Dr Udaya Tantry

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date: 25 July 2021

Coronary heart disease (CHD) is the leading cause of morbidity and mortality worldwide. An enhanced understanding of platelet receptor physiology and the development of new platelet inhibitors has led to a resurgence in the pharmacologic treatment of CHD in the past four decades. Overwhelming evidence suggests that platelet activation and aggregation at the sites of endothelial cell erosion and plaque rupture are the primary processes responsible for the development of ischaemic events in patients with CHD. Two major agonists—thromboxane A2 (TXA2) and adenosine diphosphate (ADP), released from activated platelets are responsible for amplifying platelet activation and aggregation and generation of a stable thrombus at the site of vascular injury. Therefore, pharmacologic management of patients with CHD mainly consists of aspirin and clopidogrel to inhibit TXA2 generation and the ADP-P2Y12 interaction, respectively. In addition, inhibition of the GPIIb/IIIa receptor, the final common pathway of platelet aggregation, is also an important treatment strategy in high risk CHD patients during acute conditions.

Aspirin (acetylsalicylic acid—ASA) is the bedrock of all antithrombotic therapies for both primary and secondary prevention of CHD. All new antiplatelet agents are combined with aspirin in the treatment of high-risk CHD patients. However, the demonstration of various limitations of clopidogrel and aspirin therapy (i.e. dual antiplatelet therapy—DAPT) such as continued ischaemic event occurrence, clopidogrel response variability and resistance, as well as the relationship of high on-treatment platelet reactivity in response to ADP have stimulated two recent important developments: (1) the development of more potent P2Y12 receptor blockers such as prasugrel and ticagrelor and (2) the advent of a personalized antiplatelet therapy concept based on objective measurement of platelet function in the individual patient. However, current treatment guidelines of the American Heart Association and the American College of Cardiology still recommend a ‘one size fits all’ strategy for oral antiplatelet therapy. Based on the results from numerous observational studies, recent treatment guidelines have given a Class IIb recommendation to perform genotyping or phenotyping in high risk PCI patients if a change in antiplatelet therapy will ensue based on the test results.. The latter may be due to a lack of consensus on the optimal method(s) to quantify high platelet reactivity in addition to cutoff values associated with clinical risk, as well as the availability of limited data to show that alterations of therapy based on platelet function measurements actually improve clinical outcomes.

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