Acute coronary syndrome managed effectively by de-escalation method in DAPT: JACC
De-escalation was the most effective strategy for ACS treatment when compared with other established uses of DAPT, resulting in fewer bleeding events without increasing ischemic events ,suggests a new study result .The findings have been elaborated in Journal of the American College of Cardiology.Dual antiplatelet therapy (DAPT), the combination of aspirin (ASA), and a P2Y12 inhibitor,...
De-escalation was the most effective strategy for ACS treatment when compared with other established uses of DAPT, resulting in fewer bleeding events without increasing ischemic events ,suggests a new study result .The findings have been elaborated in Journal of the American College of Cardiology.
Dual antiplatelet therapy (DAPT), the combination of aspirin (ASA), and a P2Y12 inhibitor, protects against stent thrombosis and new atherothrombotic events after a stent implantation or an acute coronary syndrome, but exposes patients to an increased risk of bleeding. In most current practices, the P2Y12 inhibitor is stopped at 6 to 12 months and ASA is continued indefinitely. The advent of safer stents, with less risk of stent thrombosis, has challenged this standard of care, however. A number of alternative strategies involving earlier de-escalation of the antiplatelet therapy have therefore been proposed. In these approaches, standard DAPT is switched to a less potent antithrombotic combination at an earlier time-point than recommended by guidelines. Three different de-escalation variations have been tested to date. The first one maintains DAPT but switches from the potent P2Y12 inhibitors ticagrelor or prasugrel to either a lower dose or to clopidogrel, while maintaining ASA. The 2 other approaches involve changing DAPT to a single antiplatelet at some earlier time-point after the percutaneous coronary intervention procedure, by stopping either the P2Y12 inhibitor or ASA. These strategies have all demonstrated some benefit in clinical trials so far, but especially the contribution of ASA in secondary prevention is clearly evolving as its role in increasing bleeding complications while not providing increased ischemic benefit is becoming more and more clear.
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