Does morphine remain a standard of care in acute myocardial infarction?

Abstract

Morphine is routinely used for pain relief in patients with acute myocardial infarction. However, it was documented that morphine decreases the bioavailability and antiplatelet effect of P2Y 12 receptor inhibitors. Multiple strategies to overcome this undesirable interaction are currently under investigation; they include the following: administration of crushed ticagrelor tablets, co-administration of metoclopramide, bridging with intravenous antiplatelet agents, or replacement of morphine with other analgesic. Adequately powered randomised trials examining the clinical consequences of concomitant use of morphine and P2Y 12 receptor inhibitors are still lacking.

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“…Nevertheless, morphine may cause adverse effects, including bradycardia, hypotension, and impairment of the intestinal propulsive function or even suppression of the respiratory function [17]. Additionally, morphine leads to impaired absorption of orally administered antiplatelet drugs, delay of anti-aggregatory effect and its reduction [18]. Noteworthy, this issue not only concerns clopidogrel, but also the newer P2Y12 receptor antagonists prasugrel and ticagrelor [19][20][21].…”

“…According to the 2020 ESC guidelines, potent P2Y12 receptor inhibitors (ticagrelor or prasugrel) exhibit a fast onset of antiplatelet action, thereby allowing loading dose administration after diagnostic coronary angiography and directly before PCI [5]. However, the fast onset of action has been shown only in a stable setting [66][67][68][69], while in patients with MI the antiplatelet effect of both drugs was delayed, achieving satisfactory platelet inhibition in the majority of patients 2 hours after loading dose administration [17,18,70,71]. Of note, even 4 hours after administration of the loading dose of ticagrelor high platelet reactivity (as assessed with VASP assay) was found in 7-37% of patients (depending on concomitant morphine administration) [17,18,70,71].…”

“…However, the fast onset of action has been shown only in a stable setting [66][67][68][69], while in patients with MI the antiplatelet effect of both drugs was delayed, achieving satisfactory platelet inhibition in the majority of patients 2 hours after loading dose administration [17,18,70,71]. Of note, even 4 hours after administration of the loading dose of ticagrelor high platelet reactivity (as assessed with VASP assay) was found in 7-37% of patients (depending on concomitant morphine administration) [17,18,70,71]. Therefore, sufficient platelet inhibition at the time of PCI cannot be expected in patients in whom loading dose of ticagrelor or prasugrel was given after diagnostic coronary angiography and directly before PCI.…”

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“…Based on available data, the latest European Society of Cardiology (ESC) guidelines on the management of acute ST-segment elevation myocardial infarction patients reduced the class of recommendation of titrated opioid use to IIa [7]. Despite this, morphine is still a standard analgesic treatment in ACS patients and it should not be routinely withdrawn [8][9][10]. Based on available research, morphine, acting via µ-opioid receptors, was found to inhibit gastrointestinal motility or induce adverse effects such as nausea or vomiting [11].…”

Are All Wines Made From Various Grape Varieties Beneficial in the Prevention of Myocardial Infarction and stroke?

“…Blood tests using nonanticoagulated (native) blood and inducing thrombus formation solely by shear forces were developed in 1970 [ 14–21 ]. Recently, a commercially available point-of-care thrombosis test was shown to have pathological relevance to human arterial thrombosis [ 22–40 ].…”