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Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
On-treatment platelet reactivity in peripheral and coronary blood in patients undergoing primary PCI for ST-segment
Luca Spiezia1, Ahmed Al Mamary2, Elena Campello1
1a Department of Medicine, Thrombotic and Haemorrhagic Diseases Unit , University of Padua , Padua , Italy.
Insights
Platelet reactivity in ST-segment elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (p-PCI) is similar in coronary and peripheral blood. This finding holds true regardless of the antiplatelet drug used, including aspirin and thienopyridines.
Area of Science:
- Cardiology
- Pharmacology
- Clinical Trials
Background:
- Dual antiplatelet therapy is standard for ST-segment elevation myocardial infarction (STEMI) patients after primary percutaneous coronary intervention (p-PCI).
- Pre-analytical factors can impact platelet function test results, necessitating careful sample collection and analysis.
- Understanding on-treatment platelet reactivity is crucial for optimizing antiplatelet therapy efficacy and safety.
Purpose of the Study:
- To compare on-treatment platelet reactivity in peripheral arterial blood versus coronary arterial blood in STEMI patients.
- To evaluate if platelet reactivity differs based on the specific thienopyridine (clopidogrel, prasugrel, or ticagrelor) used in combination with aspirin.
- To assess the consistency of platelet function measurements between peripheral and coronary circulation.
Main Methods:
- One hundred and nine STEMI patients undergoing p-PCI were enrolled.
- Patients received intravenous aspirin and one of three thienopyridines (clopidogrel, prasugrel, or ticagrelor) before the procedure.
- Platelet reactivity was assessed using ASPI-test and ADP-test with multiple electrode aggregometry (MEA) on blood samples from both peripheral and coronary arteries.
- Low responders were defined based on pre-established normal ranges for ASPI-test and ADP-test values.
Main Results:
- No significant differences in ASPI-test or ADP-test values were observed between peripheral and coronary blood samples.
- The prevalence of low aspirin responders was 14% and low thienopyridine responders was 38% in peripheral blood, with similar rates in coronary blood.
- The prevalence of low clopidogrel responders (45%) was higher than prasugrel (36%) and ticagrelor (33%), consistent across both blood sources.
Conclusions:
- Platelet function measured by MEA in coronary arteries is consistent with peripheral arterial blood in STEMI patients on dual antiplatelet therapy.
- The choice of thienopyridine (clopidogrel, prasugrel, ticagrelor) influences the prevalence of low responders, irrespective of the sampling site.
- Further research is needed to clarify the clinical significance of peripheral versus coronary platelet reactivity in this patient population.
Abstract:
Dual antiplatelet therapy is recommended in patients undergoing primary percutaneous coronary intervention (p-PCI) for ST-segment elevation myocardial infarction (STEMI). Pre-analytical variables may influence platelet function analysis results. Our aim was to evaluate the on-treatment platelet reactivity in peripheral artery vs coronary blood in patients with STEMI. We enrolled one hundred and nine patients who consecutively underwent p-PCI at Cardiology Unit of Padua University Hospital between June 2014 and June 2015. Before the procedure, all patients received intravenous aspirin 250 mg and either of the thienopyridines; clopidogrel 600 mg, prasugrel 60 mg or ticagrelor 180 mg. ASPI-test and ADP-test using multiple electrode aggregometry (MEA) were performed in samples collected from both a peripheral artery and the culprit coronary artery. 'Low responders' were patients with an ASPI-test or ADP-test value greater than or equal to a pre-established normal range. No significant differences were observed in ASPI-test values between peripheral (19 (median) [3-49 (10-90 percentiles)] U) vs coronary (12 [1-40] U, p = .06) blood and in ADP-test (40 [14-82] U vs 33 [7-79] U, p =.68) blood. In peripheral blood, fifteen (14%) patients were 'low aspirin' and forty-one (38%) 'low thienopyridines' responders. The prevalence of 'low clopidogrel' responders was higher (45%) than prasugrel (36%) and ticagrelor (33%). Similar results were observed in coronary blood. In patients undergoing p-PCI for STEMI, MEA platelet function observed in coronary arteries was consistent with peripheral artery blood's independently of the antiplatelet drug used. The clinical significance of peripheral and coronary on-aspirin/thienopyridines platelet reactivity needs further clarification.
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