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Bimodal response to aspirin loading in acute ST-elevation myocardial infarction
Paul Fefer1, Roy Beigel, David Varon
1Leviev Heart Center, Sheba Medical Center, Tel Hashomer, and Tel Aviv University, Israel.
Insights
Platelet hypo-responsiveness to aspirin (ASA) in ST-elevation myocardial infarction (STEMI) patients is common. Good responders showed better early ST-segment resolution after primary percutaneous coronary intervention (PCI).
Area of Science:
- Cardiology
- Pharmacology
- Thrombosis
Background:
- Platelet hypo-responsiveness to aspirin (ASA) is linked to adverse outcomes in stable coronary disease.
- Limited data exist on ASA response in ST-elevation myocardial infarction (STEMI) patients.
- Understanding ASA's acute effects in STEMI is crucial for treatment optimization.
Purpose of the Study:
- To evaluate the acute platelet response to a 300 mg chewable aspirin loading dose in STEMI patients.
- To assess the relationship between platelet reactivity and reperfusion after primary percutaneous coronary intervention (PCI).
Main Methods:
- 102 consecutive STEMI patients received 300 mg chewable aspirin upon admission.
- Platelet reactivity was measured using arachidonic acid (AA) stimulation before primary PCI.
- Patients were categorized into 'good' and 'poor' responders based on AA-induced platelet aggregation.
Main Results:
- A bimodal platelet response to AA was observed, with distinct 'good' and 'poor' responder groups.
- Good responders exhibited significantly higher rates of early ST-segment resolution (80% vs. 48%, p=0.001).
- Despite similar baseline characteristics, poor responders showed less effective platelet inhibition post-aspirin loading.
Conclusions:
- Early inhibition of AA-induced platelet aggregation after aspirin loading in STEMI is associated with improved myocardial reperfusion.
- A significant proportion of STEMI patients exhibit poor platelet response to aspirin loading during primary PCI.
- Further research is needed to address aspirin hypo-responsiveness in STEMI patients undergoing primary PCI.
Abstract:
Patients with stable coronary disease who exhibit platelet hypo-responsiveness to aspirin (ASA) have worse outcomes. Little data exist regarding platelet response to ASA in ST-elevation myocardial infarction (STEMI) patients. Our objective was to assess acute platelet response to ASA loading in STEMI patients undergoing primary percutaneous coronary intervention (PCI). The study comprised 102 consecutive patients with STEMI. All patients received a loading dose of 300 mg chewable ASA upon admission. Platelet reactivity was assessed immediately prior to primary PCI, at a median of 95(63 139) minutes after ASA loading. A bimodal response to arachidonic acid (AA) stimulation was observed, such that two distinct populations could be discerned: "good responders" had a mean AA-induced platelet aggregation of 36 ± 11% vs. 79 ± 9% for "poor responders." Despite equivalent demographic, clinical, and angiographic characteristics, good responders were significantly more likely to demonstrate early ST-segment resolution ≥70% after primary PCI (80% vs. 48%, p = 0.001), suggestive of better myocardial reperfusion. Early inhibition of AA-induced platelet aggregation post-ASA loading in the setting of STEMI is associated with better tissue reperfusion; however, a sizeable proportion of patients do not achieve significant inhibition of AA-induced platelet aggregation in response to ASA loading at the time of primary PCI.
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