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28 Impact of Opiate Analgesia on Platelet Reactivity in Patients Presenting for Primary Percutaneous Coronary Intervention
  1. Mohamed Farag1,
  2. Manivannan Srinivasan1,
  3. Diana A Gorog2
  1. 1East and North Hertfordshire NHS Trust
  2. 2Imperial College


Background ST-elevation myocardial infarction (STEMI) is caused predominantly by occlusive coronary thrombosis and treated with antiplatelet medications and primary percutaneous coronary intervention (PPCI). Pain is conventionally treated with opiates. Opiates may delay gastric transit and thus may reduce absorption of oral antiplatelet medication, which may impact on the ability of these drugs to reduce platelet reactivity. We sought to assess thrombotic state of STEMI patients receiving antiplatelet medications undergoing PPCI, according to morphine use.

Methods Patients with STEMI (n = 125) scheduled to undergo emergency PPCI, were assessed upon presentation (pre-PPCI) and again on day 2 of the admission after stabilisation on dual antiplatelet therapy. All patients were pre-treated with oral loading doses of 300 mg aspirin and either ticagrelor 180 mg (n = 23) or clopidogrel 600 mg (n = 102) approximately 30–60 min before blood sampling. Thrombotic status was assessed by testing venous blood using the point-of-care Global Thrombosis Test (GTT), which measures the time to form an occlusive thrombus under high shear (occlusion time, OT), and time to restore flow due to endogenous thrombolysis (lysis time, LT).

Results Patients treated with morphine (n = 101; 81%) exhibited enhanced platelet reactivity, as evidenced by shorter OT (mean ± SD; 358 ± 143s vs. 670 ± 134s; p < 0.001), and reduced thrombolytic potential, as evidenced by longer LT (median 1392s [IQR 1104–1864] vs. 1084s [875–1331]; p = 0.006) compared to those who had not received opiates. By day 2, no difference was apparent (OT: 485 ± 142s vs. 552 ± 173s; p=NS and LT: 1322s [1187–1587] vs. 1184s [1051–1405]; p=NS) between the two groups.

Conclusions Patients receiving morphine analgesia before arrival to the catheterisation laboratory demonstrate enhanced platelet reactivity and impaired endogenous thrombolysis compared to those who did not, which may be attributable to reduced absorption of antiplatelet medications due to opiate-induced delayed gastric transit. This difference was no longer apparent by day 2. Whether this impacts on recurrent early thrombosis risk, and whether non-opiate analgesia may proffer advantages in this setting, requires further assessment.

  • Acute Myocardial Infarction
  • Primary Percutaneous Coronary Intervention
  • Morphine

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