Morphine at Acute MI May Blunt Short-Term Antiplatelet Response

Marlene Busko

April 03, 2016

CHICAGO, IL ( corrected ) — Among patients who presented with an acute ST-segment-elevation MI (STEMI) who were about to undergo PCI, those who had received morphine to ease severe chest pain had a weakened response to antiplatelet agents compared with other patients, in a new small study[1].

Blood tests showed that the patients who had received morphine in the ambulance en route to the hospital had worse measures of platelet activity within an hour of receiving a loading dose of aspirin plus ticagrelor (Brilinta, AstraZeneca) or clopidogrel—but this difference disappeared within 48 hours.

"Morphine has been widely used to alleviate chest pain and anxiety of patients suffering from an acute MI, but it is also known that this drug can delay gastric emptying and reduce the absorption of other oral medications," such as the ADP-receptor antagonists that patients are given to prevent stent thrombosis and reinfarction, Dr Nikolaos Spinthakis (East and North Hertfordshire NHS Trust, UK) explained to heartwire from Medscape at a poster session here at the American College of Cardiology (ACC) 2016 Scientific Sessions.

This study showed that "opioid treatments can reduce the antiplatelet effect of ADP-receptor antagonists," he said. Large clinical trials are needed to confirm this and see how this effect on platelets translates into patient outcomes, but "until then, caution should be exercised in the use of IV morphine and consideration given to other intravenous medication if morphine treatment is to be used," according to Spinthakis.

"There are other alternatives that we can explore, such as nonopioid medication such as IV paracetamol," he noted, adding that "once morphine is given, we may consider giving other IV agents that bypass the gastric emptying, such as GP IIb/IIIa inhibitors or bivalirudin."

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The researchers examined 125 consecutive patients with STEMI who were scheduled to undergo emergency primary PCI. Most patients (101 patients, 81%) had received morphine. They had a mean age of 66 and 93% were male. About half had hypertension, 42% were smokers, and 16% had type 2 diabetes.

The patients were all given a loading dose of 300-mg aspirin along with 600 mg of clopidogrel (102 patients) or 180-mg ticagrelor (23 patients).

Within 30 to 60 minutes, the patients had a point-of-care global thrombosis blood test done in the cardiac cath lab to determine the time to form an occlusive thrombus under high shear (occlusion time) and the time to restore flow due to endogenous thrombolysis (lysis time).

Compared with the patients who had not received opiates, those who had received morphine had had a shorter mean occlusion time (358 s vs 670 s; P<0.001), indicating enhanced platelet reactivity, and they had a longer median lysis time (1392 s vs 1184 s; P=0.006), indicating a reduced thrombolytic potential.

However, by day 2, the two groups had similar occlusion times (485 s vs 552 s) and lysis times (1322 s vs 1184 s).

The study was not powered to determine hard safety end points, but there was a nonsignificant trend to greater in-hospital adverse events in the 101 patients who had received morphine vs the other 24 patients (1 vs 0 deaths, 1 vs 0 MIs, and 2 vs 0 strokes).

"Whether this [effect of morphine] affects recurrent early thrombosis risk and whether nonopiate analgesia may proffer advantages in this setting require further assessment," the researchers conclude.

[Editor's note: An earlier version of this story incorrectly identified Spinthakis, the presenter, as a different coauthor. heartwire regrets the error.]

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