Factors Affecting Platelet Reactivity 2 Hours After P2Y&lt;sub&gt;12&lt;/sub&gt; Receptor Antagonist Loading in Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction　– Impact of Pain-to-Loading Time –

Xanthopoulou, Ioanna; Davlouros, Periklis; Tsigkas, Grigorios; Koutsogiannis, Nikolaos; Patsilinakos, Sotirios; Deftereos, Spyridon; Hahalis, George; Alexopoulos, Dimitrios

doi:10.1253/circj.cj-15-0495

Cited by 15 publications

(5 citation statements)

References 38 publications

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“…Whether an initial delay in response to antiplatelet therapy might be one of the reasons for the observed finding remains speculative. Of note, besides confirming morphine use as a factor influencing platelet reactivity in STEMI patients, recent data identified the impact of pain-to-antiplatelet loading time on the onset of platelet inhibition (30). Hence, faster antiplatelet action was observed in patients with every 1 h increase in pain-to-antiplatelet LD time.…”

Section: Discussionmentioning

confidence: 85%

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

Flierl¹,

Zauner²,

Sieweke³

et al. 2017

Thromb Haemost

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Prasugrel, a potent thienopyridine, achieves stronger inhibition of platelet activation than clopidogrel. However, onset of inhibition is significantly delayed in patients with acute ST-elevation myocardial infarction (STEMI), as haemodynamic instability and morphine application seem to exhibit significant influence. Since rapid onset of effect was demonstrated in non-STEMI patients when prasugrel was administered only after percutaneous coronary intervention (PCI) without increasing cardiovascular event rates we assessed the efficacy of prasugrel loading immediately after PCI for STEMI instead of pre-loading before revascularisation. We investigated 50 consecutive patients with acute STEMI (mean age 56 ± 10 years) admitted for primary PCI. Prasugrel efficacy was assessed by platelet reactivity index (PRI; VASP assay) before, 1, 2, 4, 6, 12, and 24 hours following an oral loading dose of 60 mg immediately after PCI. High on-treatment platelet reactivity (HTPR) was defined as PRI>50 %. Prasugrel significantly and rapidly reduced platelet reactivity in acute STEMI patients (p<0.0001 at each time point vs control). Morphine application resulted in a significantly higher HTPR rate among patients having received morphine less than 1 hour before prasugrel loading (p<0.001) while concomitant metoclopramide (MCP) treatment did not significantly affect prasugrel efficacy. In conclusion, in contrast to previous reports describing a significant delay in onset of prasugrel-mediated P2Y inhibition in acute STEMI, we observed a rapid onset with low HTPR rates comparable to those observed in stable non-STEMI patients. Prasugrel administered directly after primary PCI might therefore be a useful therapeutic strategy in patients with STEMI to provide strong and effective P2Y inhibition.

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Section: Discussionmentioning

confidence: 85%

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

Flierl¹,

Zauner²,

Sieweke³

et al. 2017

Thromb Haemost

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“…Of these, two studies were excluded since only infarct size, based on cardiac magnetic resonance imaging, was reported as an outcome; a further study was excluded since it included a mixed group of patients with both STEMI and non‐ST elevation ACS where STEMI data could not be extricated; and another study was excluded as it included only patients with non‐ST elevation ACS . A further 17 studies were excluded for not reporting the clinical outcome of interest …”

Section: Resultsmentioning

confidence: 99%

Impact of Preadmission Morphine on Reinfarction in Patients With ST‐Elevation Myocardial Infarction Treated With Percutaneous Coronary Intervention: A Meta‐Analysis

Gue

Spinthakis

Farag

et al. 2020

Clin Pharma and Therapeutics

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Opiates are the traditional analgesics used in patients with ST‐elevation myocardial infarction (STEMI). Pharmacodynamic studies indicate that opiates delay the absorption of orally administered P2Y12 inhibitors and the onset of platelet inhibition. Whether these negative effects on platelet inhibition have an impact on clinical outcomes is unclear. A systematic review and meta‐analysis was performed searching PubMed, MEDLINE, and Cochrane Central Register of Controlled Trials to identify studies comparing morphine and no‐morphine treatment in STEMI patients undergoing primary percutaneous coronary intervention. The primary end point was the occurrence of in‐hospital myocardial infarction, and secondary end points were in‐hospital stroke and death. Four observational studies were identified, including 3,220 patients with STEMI. Morphine‐treated patients had a higher unadjusted rate of reinfarction compared with patients not receiving morphine (1.5% vs. 0.67%, odds ratio (OR) 2.41; 95% confidence interval (CI), 1.11–5.21; P = 0.03). Unadjusted mortality rate was lower in morphine‐treated patients (1.7% vs. 4.2%, OR 0.43, 95% CI, 0.23–0.81; P = 0.009). Exclusion of the study with baseline differences between groups showed more frequent reinfarction in the morphine group, but this was no longer statistically significant (1.3% vs. 0.5%, OR 2.02; 95% CI, 0.39–10.43; P = 0.40). There was no difference in stroke according to morphine treatment. Patients pretreated with morphine appear to have a higher rate of reinfarction than patients not receiving morphine. This may be attributable to opiate‐related delay in P2Y12 inhibitor absorption and resultant delay in onset of platelet inhibition. These concerning findings indicate the need for prospective, randomized trials to assess the impact of opiates on clinical outcomes in STEMI.

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“…In another patient-level analysis of 207 STEMI patients from 5 studies, 82% of whom took ticagrelor or prasugrel, morphine use was a multivariable predictor of higher residual platelet reactivity: morphine resulted in a 0.334 increase in the log of expected platelet reactivity, corresponding to ≈40% increased platelet reactivity, P<0.001. 20 Interestingly though, in a study of 24 healthy subjects, morphine was again associated with diminished total exposure to ticagrelor and delayed achievement of maximal plasma levels, but no significant effects were observed in terms of platelet reactivity. 21 From the same group of researchers, a small crossover study showed in a group of 12 healthy volunteers only minimal effects of morphine on prasugrel absorption, resulting in reduced maximal plasma concentration without any significant interference with platelet inhibition.…”

Section: Prasugrel and Ticagrelormentioning

confidence: 96%

P2Y ₁₂ Receptor Antagonists and Morphine

Γιαννόπουλος

Deftereos

Kolokathis

et al. 2016

Circ: Cardiovascular Interventions

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Abstract-P2Y 12 receptor antagonists, concurrently administered with aspirin in what has come to be commonly called dual antiplatelet therapy, are a mainstay of treatment for patients with acute coronary syndromes. Morphine, on the contrary, is a commonly used drug in the acute phase of acute coronary syndromes to relieve pain-with the added potential benefit of attenuating acutely raised sympathetic tone. In current guidelines, though, morphine is recommended with decreasing strength of recommendation. One reason is that it raises concern regarding the potentially significant interaction with antiplatelet agents, leading to impaired inhibition of platelet activation. In any case, it is still considered a mandatory part of the inventory of available medications in prehospital acute myocardial infarction management. The goal of the present review is to present published evidence on morphine and its potential interactions with P2Y 12 receptor antagonists, as well as on the central issue of whether such interactions may underlie clinically significant effects on patient outcomes.

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Factors Affecting Platelet Reactivity 2 Hours After P2Y<sub>12</sub> Receptor Antagonist Loading in Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction　– Impact of Pain-to-Loading Time –

Cited by 15 publications

References 38 publications

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

Impact of Preadmission Morphine on Reinfarction in Patients With ST‐Elevation Myocardial Infarction Treated With Percutaneous Coronary Intervention: A Meta‐Analysis

P2Y ₁₂ Receptor Antagonists and Morphine

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Factors Affecting Platelet Reactivity 2 Hours After P2Y<sub>12</sub> Receptor Antagonist Loading in Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction – Impact of Pain-to-Loading Time –

Cited by 15 publications

References 38 publications

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

Efficacy of prasugrel administration immediately after percutaneous coronary intervention in ST-elevation myocardial infarction

Impact of Preadmission Morphine on Reinfarction in Patients With ST‐Elevation Myocardial Infarction Treated With Percutaneous Coronary Intervention: A Meta‐Analysis

P2Y 12 Receptor Antagonists and Morphine

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Factors Affecting Platelet Reactivity 2 Hours After P2Y<sub>12</sub> Receptor Antagonist Loading in Primary Percutaneous Coronary Intervention for ST-Elevation Myocardial Infarction　– Impact of Pain-to-Loading Time –

P2Y ₁₂ Receptor Antagonists and Morphine