A recent study by Dr. van der Hoeven, published in the Journal of American Heart Association, has shown the superiority of ticagrelor over prasugrel in patients presenting with ST-segment-elevation myocardial infarction (STEMI). According to the author, ticagrelor has a higher efficacy in platelet inhibition as well as in improving endothelial function when compared with prasugrel. The p2y12 inhibitors ticagrelor and prasugrel are both recommended antiplatelet agents in the acute setting and maintenance therapy of patients with STEMI. However, some studies reported that equilibrative nucleoside transporter-1 inhibition of ticagrelor may be of clinical use in improving endothelial function and preventing microvascular injury in STEMI. The previous report of REDUCE-MVI (Evaluation of Microvascular Injury in Revascularized Patients with ST-Segment–Elevation Myocardial Infarction Treated With Ticagrelor Versus Prasugrel) trial failed to demonstrate the superiority of short-term treatment with ticagrelor over prasugrel in the setting of STEMI.
In a randomized, multicenter clinical trial, a total of 110 patients with STEMI were randomized to receive either ticagrelor 90 mg twice daily or prasugrel 10 mg once daily for maintenance therapy. There were no relevant differences in patient demographics between the two groups. Peripheral endothelial function measurement was done using reactive hyperemic peripheral arterial tonometry (RH-PAT). Information on platelet inhibition index, major adverse clinical events (MACE), and bleeding were also collected in both groups. Patients were followed for a period of 1 month, which had led to the previous report of REDUCE-MVI. However, the study participants were followed up to 1.5 years.
The results of the intention-to-treat (ITT) analysis showed no significant differences between the ticagrelor versus prasugrel regarding platelet inhibition. However, in per-protocol (PP) analysis, patients receiving ticagrelor showed higher platelet reactivity at 1-year follow-up. The peripheral endothelial function did not differ significantly between the two groups after 1-year follow-up in PP analysis. However, ITT analysis indicated significant improvement of endothelial function index in those randomized to ticagrelor group compared to those in the prasugrel group (p = 0.04 versus p = 0.56). MACE and bleeding events were similar in the ITT analysis in the two groups.
This study is limited by some points. First, this study is not powered to detect a significant in between-group differences in the secondary outcomes. Second, PP analysis of the study may have led to a selection bias. Third, adherence to the treatment regimen was only assessed via questionnaires rather than checking the serum levels of the randomized medications.
Finally, ticagrelor maintenance therapy in patients with STEMI was associated with higher platelet inhibition at 1 year as well as improvement in peripheral endothelial function. The platelet inhibition at a 1-month follow-up was significantly lower than that of a 1-year follow-up. Possible explanations for this finding can be either a hampered platelet inhibition in the subacute phase of STEMI or amplified platelet inhibition after 1 year of antiplatelet therapy.