Author + information
- Iñigo Lozano, MD, PhD∗ (, )
- Juan Rondan, MD, PhD,
- Jose M. Vegas, MD and
- Eduardo Segovia, MD
- ↵∗Cardiología, Hospital de Cabueñes, Avda. Los Prados 395, Gijón 33203, Spain
We read with great interest the paper by Montalescot et al. (1) and the editorial by McDaniel (2) on the effect of pre-hospital ticagrelor during the first 24 h after primary percutaneous coronary intervention (PCI). In the ATLANTIC trial, pre-hospital loading of ticagrelor compared with loading at presentation to the hospital reduced neither major adverse cardiac events (MACEs) at 30 days nor the primary endpoints of the proportion of patients achieving ≥70% ST-segment resolution and TIMI (Thrombolysis in Myocardial Infarction) flow grade 3 in the infarct artery before primary PCI (3). Similarly, in the present post hoc analysis, pre-hospital ticagrelor also failed to reduce MACEs at 24 h and the primary endpoints, and only after the inclusion of the bailout glycoprotein IIb/IIIa inhibitor use in the MACE composite were reductions in MACEs, stent thrombosis, and myocardial infarction achieved. However, as pointed out in the editorial (2), there were more anterior myocardial infarctions and numerically less pre-PCI glycoprotein IIb/IIIa use in patients receiving pre-hospital ticagrelor.
Although these results do not lend support to the advantage of loading in the ambulance, we believe that the hypothesis should not be completely abandoned. In our opinion, besides the limited difference of only 31 minutes between the 2 arms of the study and the possible influence of morphine administration, the fact that only patients in the first 6 h of symptoms were included may have played a role in the results. In the same way that fibrinolysis works effectively in the first 3 h but is clearly inferior to primary PCI after that interval and also the demonstrated advantage of prasugrel over clopidogrel in patients with more organized thrombus, that is, in secondary PCI (4), we believe that pre-hospital loading of ticagrelor may provide advantages not only in patients with longer transfers but also in those with more evolved infarctions.
Moreover, in PLATO (Platelet Inhibition and Patient Outcomes), in 7,544 patients with ST-segment elevation myocardial infarction, ticagrelor fulfilled the secondary endpoints of total mortality, myocardial infarction, and stent thrombosis, but the p value of the primary endpoint remained 0.07, because of a moderate increase in stroke with ticagrelor (5), and in patients with more evolved infarctions, the results would probably have been better for ticagrelor. In these patients with longer delays before reperfusion, the more potent effect of ticagrelor would favor reductions in total mortality, myocardial infarction, and stent thrombosis but with an expected same rate of stroke, because this latter complication would be a consequence of the proper characteristics of the patients, independent of delays in reperfusion.
In summary, the results of ATLANTIC may be due to the short difference in the moment of administration of the drug and the influence of morphine, but an advantage of pre-hospital administration of ticagrelor cannot be ruled out for more evolved infarctions.
Please note: Dr. Lozano has given lectures about ticagrelor. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- American College of Cardiology Foundation
- Montalescot G.,
- van ’t Hof A.W.,
- Bolognese L.,
- et al.
- McDaniel M.
- Steg P.G.,
- James S.,
- Harrington R.A.,
- et al.