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Updated: May 7, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Persistent enhanced platelet activation in patients with acute myocardial infarction and coronary microvascular
Cristina Aurigemma, Giancarla Scalone, Fabrizio Tomai
1Gaetano A. Lanza, MD, Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma, Italy, Tel.: +39 06 30154187,
Insights
Platelet activation contributes to coronary microvascular obstruction (MVO) in ST-segment elevation myocardial infarction (STEMI) patients. Enhanced platelet activation persists even with anti-platelet therapy, suggesting new treatment strategies are needed for MVO.
Area of Science:
- Cardiology
- Hematology
- Vascular Biology
Background:
- Coronary microvascular obstruction (MVO) affects 30% of ST-segment elevation myocardial infarction (STEMI) patients post-recanalisation.
- The precise mechanisms driving MVO remain incompletely understood.
- Platelet activation is a potential contributor to MVO pathogenesis.
Purpose of the Study:
- To investigate the role of platelet activation in the development of coronary MVO in STEMI patients.
- To compare platelet activation levels between STEMI patients with and without MVO.
- To assess the persistence of platelet activation post-STEMI and percutaneous coronary intervention (PCI).
Main Methods:
- Study included 48 STEMI patients (treated with primary PCI and dual anti-platelet therapy) and 20 stable coronary artery disease (CAD) controls.
- STEMI patients were categorized into complete myocardial reperfusion (MR) and MVO groups.
- Platelet activation assessed via platelet receptor expression and monocyte-platelet aggregates (MPAs) on admission and at 1-month follow-up.
Main Results:
- STEMI patients with MVO exhibited significantly higher platelet receptor expression and MPA formation compared to STEMI patients with MR and stable CAD controls.
- These differences in platelet activation markers were observed both on admission and at the one-month follow-up.
- Enhanced platelet activation persisted in MVO patients despite dual anti-platelet therapy.
Conclusions:
- Elevated platelet activation is associated with coronary MVO in STEMI patients following successful PCI.
- Platelet activation plays a significant role in the pathogenesis of MVO.
- Current anti-platelet therapies may be insufficient for patients with MVO, necessitating exploration of novel therapeutic strategies.
Abstract:
About 30% of patients with acute ST-segment elevation myocardial infarction (STEMI) undergoing recanalisation of the infarct-related coronary artery do not achieve valid myocardial reperfusion (no-reflow phenomenon or coronary microvascular obstruction [MVO]). The mechanisms of MVO are incompletely understood. In this study we investigated the role platelet activation in the pathogenesis of coronary MVO in STEMI patients. We enrolled 48 STEMI patients (age 56.2 ± 11 years; 31 men), treated by primary percutaneous coronary intervention (PCI) followed by double anti-platelet treatment, and 20 control patients with stable coronary artery disease (CAD) on single anti-platelet treatment (age 57.5 ± 6 years, 12 men). STEMI patients were divided into two groups: 35 patients with complete myocardial reperfusion (MR) and 13 patients with coronary MVO despite successful PCI. Platelet activation was assessed on admission and at one-month follow-up by measuring platelet receptor expression and monocyte-platelet aggregates (MPAs). Platelet receptor expression, platelet receptor conformational change for fibrinogen binding availability and MPA formation were increased in STEMI patients with MVO compared to both STEMI patients with MR and stable CAD patients, both on admission and at one-month follow-up (p<0.05 for all).Among STEMI patients, platelet activation is greater in those who display coronary MVO, compared to those with MR, after successful PCI, both on admission and one month after STEMI, suggesting that enhanced platelet activation might be involved in the pathogenesis of MVO. The persistence of enhanced platelet activation despite double classical anti-platelet therapy suggests that new anti-platelet strategies should be considered in patients with coronary MVO.
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