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Abstract
Dual antiplatelet therapy is critical to inhibit platelet reactivity in order to prevent ischemic reccurences in stented patients. However, studies have observed a variable blockade of the P2Y12 adenosine diphosphate receptor between patients following clopidogrel intake. This interindividual variability in the biological response is not uncommon with clopidogrel (about 50%) and even prasugrel (20%). High on-treatment platelet reactivity (HTPR) is correlated with thrombotic events following percutaneous coronary intervention. Several studies suggested that tailoring of antiplatelet therapy based on platelet reactivity (PR) monitoring could safely reduce the rate of major adverse cardiovascular events in HTPR patients. In addition, low on-treatment PR was recently associated with bleeding events both in patients treated with prasugrel and clopidogrel. Of importance, bleedings are associated with a poor prognosis in stented patients. Overall, the potential of PR monitoring to individualize antiplatelet therapy might benefit stented patients by reducing both ischemic and bleeding risks. However, such strategies remain to be evaluated in adequately designed large-scale randomized clinical trials.
Financial & competing interests disclosure
The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.
No writing assistance was utilized in the production of this manuscript.
Key issues
• Platelet reactivity inhibition is mandatory to prevent ischemic events in stented patients.
• Due to clinical, biological and genetic factors, clopidogrel responsiveness presents an important interindividual variability.
• High on-treatment platelet reactivity is related to thrombotic events (stent thrombosis, myocardial infarction and cardiovascular death) in stented patients treated with either clopidogrel or prasugrel.
• Low on-treatment platelet reactivity is related to bleedings in patients treated with either clopidogrel or prasugrel.
• Ticagrelor and prasugrel induce a high platelet reactivity inhibition which may be responsible for the increased risk of bleedings.
• Although small studies suggested a benefit, recent large-scale randomized trials failed to confirm the benefit of individualized antiplatelet therapy based on platelet reactivity measurement to reduce the rate of ischemic or bleeding events in stented patients.