Peri-Procedural Platelet Reactivity in Percutaneous Coronary Intervention

Abstract

Platelet activation and aggregation play a pivotal role in thrombotic complications occurring during percutaneous coronary intervention (PCI), and peri-PCI anti-platelet therapy represents a standard of care. High platelet reactivity prior to PCI has been correlated with an increased incidence of peri-procedural myonecrosis. Pre-PCI platelet reactivity predicts post-PCI platelet reactivity and has a prognostic impact on subsequent ischaemic and bleeding events, so as the platelet inhibition measured post-PCI. Many anti-platelet treatment strategies, including aspirin, glycoprotein IIb/IIIa inhibitors, P2Y receptor blockers and vorapaxar, are being used in the routine clinical practice to modify platelet reactivity at each stage, e.g. pre-, during and post-PCI. Anti-platelet strategies with a 'stronger and faster' pharmacodynamic effect than clopidogrel have been mostly adopted in patients with acute coronary syndromes. However, several issues regarding the anti-platelet treatment such as benefits/risks of anti-platelet therapy pre-treatment and duration, and definite association between speed and potency of various anti-platelet agents and clinical outcomes remain controversial. We believe that a better understanding of peri-PCI platelet reactivity and its relations to outcomes may lead to the development of more effective and safe treatment strategies.

Platelet Inhibition in Acute Coronary Syndrome and Percutaneous Coronary Intervention: Insights from the Past and Present

“…26,27 In ACS patients treated with PCI and DAPT including clopidogrel, persistent high on-treatment platelet reactivity (HTPR) to adenosine diphosphate was shown to be associated with a significant increase in nonfatal myocardial infarction, stent thrombosis, and cardiovascular mortality. [28][29][30][31][32][33][34] Furthermore, 20 to 30% of patients with ACS show an inadequate response to clopidogrel, depending on the platelet function test used. 35 Some 5 to 12% of the variation of adenosine diphosphate-induced platelet aggregation is related to genetic polymorphisms encoding CYP2C19, the hepatic enzyme responsible for biotransformation of clopidogrel to its active metabolite.…”

“…The speed of onset and intensity of platelet inhibition during PCI is an important determinant of PCI-related ischemic complications, and this is particularly relevant in ACS, especially STEMI. 33,51 However, the onset of action of oral P2Y 12 receptor inhibitors is attenuated in STEMI patients due to delayed absorption. 51 Crushing P2Y 12 inhibitor tablets has been shown to provide more rapid platelet inhibition than standard oral dosing.…”

Periprocedural Antithrombotic Treatment in Complex Percutaneous Coronary Intervention

“…The underlying thrombotic risk of those patients is exacerbated during PCI because of vascular injury, and this makes the periprocedural antithrombotic treatment mandatory to prevent vascular access, target lesion, and stent-related thrombotic complications. 1 Physicians have to find a subtle balance between thrombotic and hemorrhagic risk based mainly on the severity of the disease, patients' comorbidities, and the clinical setting of intervention (acute, primary or elective PCI). 2 A challenging clinical scenario that invasive cardiologists are dealing with is the optimal management of patients undergoing complex PCI (C-PCI).…”

Loading with Oral P2Y12 Receptor Inhibitors: To Crush or Not to Crush?

“…Platelets play a key role in the pathogenesis of acute coronary syndromes (ACSs) and become highly activated particularly in ST-segment elevation myocardial infarction (STEMI) patients, as well as during percutaneous coronary intervention (PCI). 1,2 During the last two decades, dual anti-platelet therapy consisting of a combination of aspirin and a P2Y 12 receptor inhibitor has been established as an essential therapy component for the treatment of ACS and/or PCI patients. Clopidogrel is the most broadly used oral P2Y 12 receptor inhibitor worldwide; however, both prasugrel and ticagrelor exhibit a faster and more consistent platelet inhibition than clopidogrel, especially in STEMI patients.…”