P6084Morphine use in STEMI associated with enhanced platelet reactivity and larger infarct size, and this is negated by GPI use peri-PPCI

Background: The emergency management of ST-elevation myocardial infarction (STEMI) involves dual antiplatelet therapy (DAPT) administration and primary percutaneous coronary intervention (PPCI). Pain is treated with opiates, which may delay gastric transit, and reduce DAPT absorption. We sought to assess the effect of morphine on reperfusion, infarct size and thrombotic status, with a secondary analysis performed according to glycoprotein IIb/IIIa inhibitor (GPI) use. Methods: 300 patients presenting for PPCI were assessed for ST-segment resolution, coronary flow, thrombotic status and peak troponin. Morphine was given as required by emergency teams en route to the heart attack centre. All patients received DAPT and PPCI was performed according to standard care, with optional GPI use. Results: Patients receiving morphine (n=218; 72.7%) had significantly less spontaneous ST-segment resolution pre-PPCI, lower rate of TIMI 2/3 flow in the infarct-related artery pre-PPCI, and higher troponin level post-PPCI (1906 [1002–4398] vs. 1268 [249–2920]; p=0.016) than those who did not. Patients receiving morphine exhibited significantly enhanced platelet reactivity and impaired endogenous fibrinolysis on arrival, compared to no-morphine patients. Morphine administration was an independent negative predictor of spontaneous ST-segment resolution after adjustment for other variables (OR 0.26; CI 0.08–0.84; p=0.025). Among patients receiving GPI, there was no difference in pre-PPCI flow or peak troponin according to morphine use.