Tackling the gap in platelet inhibition with oral antiplatelet agents in high-risk patients undergoing percutaneous coronary intervention.

Introduction

Oral P2Y12 inhibitors represent the mainstay therapy for the prevention of thrombotic complications in patients presenting with an acute coronary syndrome and/or undergoing percutaneous coronary intervention (PCI). However, the onset of antiplatelet action of the oral P2Y12 inhibitors is affected by their need to be absorbed in the gastrointestinal (GI) tract before becoming systemically available.Areas covered: Following oral intake of P2Y12 inhibitors, the timeframe required for GI absorption leads to a window of inadequate antiplatelet protection during which patients are at increased thrombotic risk. The onset of action of the oral P2Y12 inhibitors is even further delayed in high-risk patients, underscoring the need to define strategies to bridge the gap in platelet inhibitory effects following their intake.Expert opinion: Multiple mechanisms may impair GI absorption leading to a delay in the onset of action of oral P2Y12 inhibitors. Several strategies have been tested to overcome the gap in platelet inhibition in high-risk patients undergoing PCI. These include administration of crushed or chewed tablets to improve the dissolution rate and use of opioid receptor antagonists or metoclopramide to counteract impairment of gastric motility induced by opioids. However, intravenous antiplatelet therapies represent the most effective strategy to bridge such gap in platelet inhibition.