Morphine slows antiplatelet drug action during PCI

Last Updated: 2015-01-08

By Anne Harding

NEW YORK (Reuters Health) - Clinicians should reconsider the common practice of giving morphine for chest pain to patients who are undergoing primary percutaneous intervention (PCI), new findings suggest.

Researchers found a delayed onset of oral antiplatelet agent action in patients who received morphine, even after adjustment for the propensity to receive morphine and omission of patients with vomiting.

Such delayed action is linked to a higher risk of thrombotic complications, Dr. Guido Parodi of Careggi University Hospital in Florence, Italy, and colleagues noted online December 31 in Circulation: Cardiovascular Intervention.

"When using morphine to relieve chest pain in AMI patients, physicians must be aware that hypotension, respiratory depression, vomiting, and delayed onset of action of antiplatelet agents are potential unwanted side effects of the drug," Dr. Parodi told Reuters Health via email.

Morphine could be reserved for patients with pulmonary edema or persistent severe chest pain, he said.

"Myocardial ischemia relief (i.e., reperfusion) should be considered the definitive chest pain control strategy," he said.

Morphine is "strongly" recommended for patients with ST-segment elevation myocardial infarction (STEMI), Dr. Parodi and colleagues note, despite the lack of evidence for the recommendation. When patients must undergo PCI, they add, they may receive several different drugs, increasing the risk of drug-to-drug interaction.

A small study suggested that morphine could delay the effect of prasugrel and ticagrelor in STEMI patients, the researchers add. (The study is here: http://bit.ly/1BFjUUa.)

They point out, "There may be a biologically plausible cause-effect relation in this association, given that morphine inhibits gastric emptying, thereby delaying absorption and possibly resulting in decreased peak plasma levels of orally administered drugs."

The researchers assessed platelet reactivity in 300 patients undergoing primary PCI for STEMI, including 95 who received prasugrel and 205 who received ticagrelor.

Ninety-five (32%) had received morphine. These patients were more likely to vomit (15% vs 2%).

Two hours after the loading dose of antiplatelet medication, prasugrel and ticagrelor reactivity units were 187 for the patients who received morphine and 133 for those who did not (p<0.001). The difference remained after excluding the patients with vomiting.

At two hours, 53% of patients given morphine had high residual platelet activity versus 29% of those who did not receive morphine. Patients who received morphine were nearly three times as likely to have high residual platelet reactivity at two hours. The only other independent predictor of platelet reactivity was age.

"The morphine-antiplatelet agent interaction is likely a non-drug-specific phenomenon and related to the inhibition of the normal muscular activity of the stomach and the intestines, which may lead to vomit or delayed gastric emptying, which in turn delays absorption and decreases peak plasma levels of orally administered drugs," the authors write.

"Given the key importance of platelet inhibition in patients treated by coronary stenting for acute myocardial infarction (AMI) and the absence of data that may support a potential clinical benefit of morphine in patients with AMI, more caution should be used regarding morphine administration in AMI patients, and a selective rather than routine morphine use seems to be reasonably recommended," Dr. Parodi said. "Prospective, randomized, clinical trials are needed to determine whether and how morphine should be administered to patients with chest pain and AMI."

Five of the 11 authors, including Dr. Parodi, reported financial relationships with pharmaceutical companies that make antiplatelet medications.

The current study had no commercial funding.

SOURCE: http://bit.ly/14vKqSY

Circ Cardiovasc Intv 2014.