Morphine use and pharmacokinetics in patients with chest pain due to suspected or definite acute myocardial infarction

Everts, Bart; Karlson, BW; Herlitz, Johan; Hedner, Thomas

doi:10.1016/s1090-3801(98)90004-0

Cited by 10 publications

(5 citation statements)

References 25 publications

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“…The geometric mean morphine‐3‐glucuonide AUC 0‐∞ was ∼10‐fold higher than morphine‐6‐glucuronide AUC 0‐∞ in healthy subjects ( Figure ), consistent with literature reports . The percent difference in C max , time to reach C max (T max ), AUC 0‐last , AUC 0‐∞ , and t 1/2 for morphine‐3‐glucuronide in both subject groups ( Figure ) exhibited similar trends as morphine‐6‐glucuronide when evaluated separately.…”

Section: Resultssupporting

confidence: 88%

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Altered morphine glucuronide and bile acid disposition in patients with nonalcoholic steatohepatitis

Ferslew

Johnston

Tsakalozou

et al. 2015

Clin Pharma and Therapeutics

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The functional impact of altered drug transport protein expression on the systemic pharmacokinetics of morphine, hepatically-derived morphine glucuronide (morphine-3- and morphine-6-glucuronide), and fasting bile acids was evaluated in patients with biopsy-confirmed non-alcoholic steatohepatitis (NASH) compared to healthy subjects. The maximum concentration (Cmax) and area under the concentration-time curve (AUC0-last) of morphine glucuronide in serum were increased in NASH patients (343 vs. 225nM and 58.8 vs. 37.2μM*min, respectively; P≤0.005); morphine pharmacokinetics did not differ between groups. Linear regression analyses detected an association of NASH severity with increased morphine glucuronide Cmax and AUC0-last (P<0.001). Fasting serum glycocholate, taurocholate and total bile acid concentrations were associated with NASH severity (P<0.006). Increased hepatic basolateral efflux of morphine glucuronide and bile acids is consistent with altered hepatic transport protein expression in patients with NASH and may partially explain differences in efficacy and/or toxicity of some highly transported anionic drugs/metabolites in this patient population.

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Section: Resultssupporting

confidence: 88%

“…Morphine glucuronide was assumed to be eliminated by the kidney via glomerular filtration. Model optimization was guided by assessing the model output compared to data extracted from published clinical studies . The model was used to simulate altered disposition of morphine and metabolites in virtual patients.…”

Section: Methodsmentioning

confidence: 99%

Altered morphine glucuronide and bile acid disposition in patients with nonalcoholic steatohepatitis

Ferslew

Johnston

Tsakalozou

et al. 2015

Clin Pharma and Therapeutics

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“…Controlling pain at the acute phase of STEMI is challenging. Morphine has been used for years and the issues of its efficacy and its safety have been regularly raised [22,23]. It has also been linked to a delayed onset of action of oral antiplatelet drugs [4,5] Few alternatives to morphine have been studied in STEMI, and analgesics that are appropriate for the emergency setting (e.g.…”

Section: Discussionmentioning

confidence: 99%

Nitrous oxide/oxygen plus acetaminophen versus morphine in ST elevation myocardial infarction: open-label, cluster-randomized, non-inferiority study

Charpentier

Galinski

Bounes

et al. 2020

Scand J Trauma Resusc Emerg Med

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Background: Studies have shown disparate results on the consequences of morphine use in ST-segment elevation myocardial infarction (STEMI). No study has evaluated alternative treatments that could be at least non-inferior to morphine without its potentially damaging consequences for myocardial function and platelet reactivity. The aim of this study was to evaluate whether nitrous oxide/oxygen plus intravenous acetaminophen (NOO-A) is non-inferior to morphine to control chest pain in STEMI patients. Methods: This multicenter, open-label, cluster-randomized, controlled, non-inferiority study compared NOO-A with morphine in 684 prehospital patients with ongoing suspected STEMI of < 12 h duration and a pain rating score ≥ 4. The primary endpoint was the proportion of patients achieving pain relief (numeric rating score ≤ 3) after 30 min. Secondary safety endpoints included serious adverse events and death at 30 days. Results: The median baseline pain score was 7.0 in both groups. The primary endpoint occurred in 51.7% of the NOO-A group and 73.6% of the morphine group (absolute risk difference − 21.7%; 95% confidence interval − 29.6 to − 13.8). At 30 days, the rate of serious adverse events was 16.0 and 18.8% in the NOO-A and morphine groups respectively (p = NS). The rate of death was 1.8% (NOO-A group) and 3.8% (morphine group) (p = NS). Conclusion: Analgesia provided by NOO-A was inferior to morphine at 30 min in patients with acute STEMI in the prehospital setting. Rates of serious adverse events did not differ between groups. Trial registration: ClinicalTrials.gov: NCT02198378.

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“…There is also a lack of controlled studies with placebo or an active comparator. In an observational study on a large patient cohort, a mean morphine dose of 6.7 mg was given to patients with chest pain due to suspected AMI [ 27]. A substantial proportion of patients (44.5%) had only one pain attack, whilst 21.1% had two to three, and 34.4% had four or more pain attacks.…”

Section: Discussionmentioning

confidence: 99%

A comparison of metoprolol and morphine in the treatment of chest pain in patients with suspected acute myocardial infarction – the MEMO study

Everts

Karlson

Abdon

et al. 1999

Journal of Internal Medicine

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Objectives. To compare the analgesic effect of metoprolol and morphine in patients with chest pain due to suspected or definite acute myocardial infarction after initial treatment with intravenous metoprolol.Design. All patients, regardless of age, admitted to the coronary care unit at Uddevalla Central Hospital due to suspected acute myocardial infarction were evaluated for inclusion in the MEMO study (metoprolol-morphine). The effects on chest pain and sideeffects of the two treatments were followed during 24 h. Pain was assessed by a numerical rating scale. Results.A total of 265 patients were randomized in this prospective double-blind study and 59% developed a confirmed acute myocardial infarction. In both treatment groups, there were rapid reductions of pain intensity. However, in the patient group treated with morphine, there was a more pronounced pain relief during the first 80 min after start of double-blind treatment. The side-effects were few and were those expected from each therapeutic regimen. During the first 24 h, nausea requiring anti-emetics was more common in the morphine-treated patients. Conclusion.In suspected acute myocardial infarction, if chest pain persists after intravenous betaadrenergic blockade treatment, standard doses of an opioid analgesic such as morphine will offer better pain relief than increased dosages of metoprolol.

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Morphine use and pharmacokinetics in patients with chest pain due to suspected or definite acute myocardial infarction

Cited by 10 publications

References 25 publications

Altered morphine glucuronide and bile acid disposition in patients with nonalcoholic steatohepatitis

Altered morphine glucuronide and bile acid disposition in patients with nonalcoholic steatohepatitis

Nitrous oxide/oxygen plus acetaminophen versus morphine in ST elevation myocardial infarction: open-label, cluster-randomized, non-inferiority study

A comparison of metoprolol and morphine in the treatment of chest pain in patients with suspected acute myocardial infarction – the MEMO study

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