Abstract
Current evidence regarding the effect of intravenous morphine administration on reperfusion injury and/or cardioprotection in patients with myocardial infarction is conflicting. The aim of this study was to evaluate the impact of morphine administration, on infarct size and reperfusion injury assessed by cardiac magnetic resonance imaging (CMR) in a large multicenter ST-elevation myocardial infarction (STEMI) population. In total, 734 STEMI patients reperfused by primary percutaneous coronary intervention <12 h after symptom onset underwent CMR imaging at eight centers for assessment of myocardial damage. Intravenous morphine administration was recorded in all patients. CMR was completed within one week after infarction using a standardized protocol. The clinical endpoint of the study was the occurrence of major adverse cardiac events (MACE) within 12 months after infarction. Intravenous morphine was administered in 61.8% (n = 454) of all patients. There were no differences in infarct size (17%LV, interquartile range [IQR] 8–25%LV versus 16%LV, IQR 8–26%LV, p = 0.67) and microvascular obstruction (p = 0.92) in patients with versus without morphine administration. In the subgroup of patients with early reperfusion within 120 min and reduced flow of the infarcted vessel (TIMI-flow ≤2 before PCI) morphine administration resulted in significantly smaller infarcts (12%LV, IQR 12–19 versus 19%LV, IQR 10–29, p = 0.035) and reduced microvascular obstruction (p = 0.003). Morphine administration had no effect on hard clinical endpoints (log-rank test p = 0.74) and was not an independent predictor of clinical outcome in Cox regression analysis. In our large multicenter CMR study, morphine administration did not have a negative effect on myocardial damage or clinical prognosis in acute reperfused STEMI. In patients, presenting early ( ≤120 min) morphine may have a cardioprotective effect as reflected by smaller infarcts; but this finding has to be assessed in further well-designed clinical studies
Highlights
Platelet inhibition by dual antiplatelet therapy with aspirin and a P2Y12 receptor inhibitor is the cornerstone of treatment for prevention of thrombotic events in patients with acute coronary syndrome (ACS) undergoing primary percutaneous coronary intervention (PPCI) [1,2]
The use of morphine was associated with higher mortality in patients with non-ST-elevation myocardial infarction (NSTEMI) [10], and with suboptimal reperfusion success after PPCI in patients with ST-elevation myocardial infarction (STEMI) [11]
Morphine status was available in 791 patients (99.4%) (Figure 1)
Summary
Platelet inhibition by dual antiplatelet therapy with aspirin and a P2Y12 receptor inhibitor is the cornerstone of treatment for prevention of thrombotic events in patients with acute coronary syndrome (ACS) undergoing primary percutaneous coronary intervention (PPCI) [1,2]. Morphine inhibits gastric emptying, reduces intestinal motility, and induces nausea or vomiting [6]. These effects are associated with a slower uptake, delayed onset of action, and diminished effects of oral antiplatelet agents, which may lead to decreased peak plasma levels and subsequent early treatment failure [7]. In patients with ACS, morphine significantly decreased the plasma concentrations of ticagrelor and its active metabolite with subsequent impaired inhibition of platelets [7,8,9]. The use of morphine was associated with higher mortality in patients with non-ST-elevation myocardial infarction (NSTEMI) [10], and with suboptimal reperfusion success after PPCI in patients with ST-elevation myocardial infarction (STEMI) [11]
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