Defining Strategies of Modulation of Antiplatelet Therapy in Patients With Coronary Artery Disease: A Consensus Document from the Academic Research Consortium

Abstract

Antiplatelet therapy is the mainstay of pharmacologic treatment to prevent thrombotic or ischemic events in patients with coronary artery disease treated with percutaneous coronary intervention and those treated medically for an acute coronary syndrome. The use of antiplatelet therapy comes at the expense of an increased risk of bleeding complications. Defining the optimal intensity of platelet inhibition according to the clinical presentation of atherosclerotic cardiovascular disease and individual patient factors is a clinical challenge. Modulation of antiplatelet therapy is a medical action that is frequently performed to balance the risk of thrombotic or ischemic events and the risk of bleeding. This aim may be achieved by reducing (ie, de-escalation) or increasing (ie, escalation) the intensity of platelet inhibition by changing the type, dose, or number of antiplatelet drugs. Because de-escalation or escalation can be achieved in different ways, with a number of emerging approaches, confusion arises with terminologies that are often used interchangeably. To address this issue, this Academic Research Consortium collaboration provides an overview and definitions of different strategies of antiplatelet therapy modulation for patients with coronary artery disease, including but not limited to those undergoing percutaneous coronary intervention, and consensus statements on standardized definitions.

Safety and Efficacy of Ticagrelor Monotherapy in Patients With Acute Coronary Syndromes Undergoing Percutaneous Coronary Intervention: an Individual Patient Data Meta-analysis of TWILIGHT and TICO Randomized Trials

“…The experimental strategy examined herein represents one of several DAPT de-escalation approaches as articulated by the Academic Research Consortium. 30 Alternatives include switching from a more to less potent P2Y 12 inhibitor or reducing the dose of P2Y 12 inhibitor. With respect to the former, several studies have shown that switching from ticagrelor or prasugrel to clopidogrel after a minimum duration of DAPT, compared with not switching, reduces bleeding without compromising ischemic efficacy.…”

Stopping Aspirin Within 1 Month After Stenting for Ticagrelor Monotherapy in Acute Coronary Syndrome: The T-PASS Randomized Noninferiority Trial

“…1,2 Current guidelines recommend at least 12 months of dual antiplatelet therapy (DAPT), in the form of a combination of aspirin and a P2Y12 inhibitor, after implantation of a drug-eluting stent (DES) in patients with ACS, unless bleeding risks prevail. [3][4][5] However, maintaining long-term DAPT may be associated with excessive risk of bleeding. 5 Several randomized trials have evaluated de-escalation strategies for early stopping of aspirin to decrease bleeding events, [5][6][7][8][9][10][11][12] and recent meta-analyses from randomized trials have shown that eliminating aspirin after 1 to 3 months of treatment reduced the occurrence of bleeding events without increasing the number of ischemic events.…”

“…[3][4][5] However, maintaining long-term DAPT may be associated with excessive risk of bleeding. 5 Several randomized trials have evaluated de-escalation strategies for early stopping of aspirin to decrease bleeding events, [5][6][7][8][9][10][11][12] and recent meta-analyses from randomized trials have shown that eliminating aspirin after 1 to 3 months of treatment reduced the occurrence of bleeding events without increasing the number of ischemic events. [13][14][15] However, stopping aspirin within 1 month after implantation of a DES for ticagrelor monotherapy has not been exclusively evaluated for patients with ACS.…”

Antiplatelet Therapy After PCI: The Art and Science of De-Escalation

“…In this issue of Circulation , 3 papers contribute further to our knowledge in the context of contemporary clinical practice, 1–3 providing further insights into possible strategies for de-escalation of antiplatelet intensity. 4,5…”