0230: Effectiveness of switching Prasugrel's ‘low responders’ to ticagrelor after acute coronary syndrome

Abstract

This study aimed to assess the effectiveness and safety of switching from Prasugrel to Ticagrelor patients identified as Prasugrel low-responders one month after ACS. 540 patients admitted for ACS with coronary stent implantation and discharged on Prasugrel 10mg were screened. Prasugrel response was assessed one month after discharge using Platelet Reactivity Index Vasodilatator Stimulated Phosphoprotein (PRI VASP). High on-Treatment Platelet Reactivity (HTPR) was defined as VASP>50%. Patients with HTPR were enrolled and switched to Ticagrelor 90 mg twice a day. They were re-tested a month later. Primary endpoint was defined as: comparison of degree of platelet inhibition and incidence of HTPR one month after switching to Ticagrelor in patients with HTPR on Prasugrel therapy. The safety endpoint was the incidence of bleedings under Ticagrelor as compared with Prasugrel therapy, using the Bleeding Academic Research Consensus definition. Between March 2010 and November 2013, 19 patients were defined as HTPR on Prasugrel 10 mg one month after ACS, with a mean VASP of 59,3%. Among these patients, 14 were switched to Ticagrelor 180 mg daily and, at one month, we observed a significant decrease in PRI VASP, with a mean value at 19.6% (p<0.001). No patients remained HTPR and 4 patients (28.4%) were identified as Very Low on-Treatment Platelet Reactivity (VLTPR) (VASP<10%). No ischemic events were reported after switching, while 3 patients (21%) suffered from bleeding complications (2 BARC1 and 1 BARC2 bleedings) during Ticagrelor therapy. Switch to Ticagrelor in Prasugrel's “low responders” patients is an effective strategy, leading to an adequate platelet inhibition in a large majority of patients. This biological tailored approach could be useful in preventing ischemic complications, in this specific high risk population, potentially increasing bleeding risk. This hypothesis needs to be confirmed in large clinical studies. Abstract 0230 – Figure