Background:Delay in the onset of antiplatelet action occurs in patients with ST-elevation myocardial infarction (STEMI) and is likely due to disturbed absorption. We hypothesized that patients presenting relatively late after the onset of symptoms would have faster antiplatelet action.Methods and Results:We analyzed patient-level data from 5 studies of 207 P2Y₁₂receptor antagonist-naïve patients with STEMI undergoing primary percutaneous coronary intervention (PCI). All patients had available platelet reactivity (PR) assessment with the VerifyNow assay (in P2Y₁₂reaction units; PRU) prior to and 2 h after loading. High PR (HPR) was defined as ≥208 PRU. Pain-to-antiplatelet loading time independently predicted PR at 2 h after loading: every 1-h increase in pain-to-antiplatelet loading time produced a 7% decrease in PR (P=0.001). Pretreatment PR, body mass index, morphine and novel P2Y₁₂receptor antagonist also affected PR 2 h after loading. Novel P2Y₁₂receptor antagonist use and per hour increase in pain-to-antiplatelet loading time were independently associated with lower probability for HPR with an OR (95% CI) of 0.145 (0.095–0.220) and 0.776 (0.689–0.873), P<0.001 for both (C-statistic, 0.752; 95% CI: 0.685–0.819).Conclusions:In STEMI patients undergoing primary PCI, pain-to-antiplatelet loading interval is a newly described factor affecting PR shortly after P2Y₁₂receptor antagonist loading, according to patient-level data pooled analysis. (Circ J 2016; 80: 442–449)