Key result
Coronary microvascular obstruction in STEMI is linked to significantly higher platelet activation vs complete reperfusion.
Why the study?
The mechanisms of coronary microvascular obstruction (MVO) after STEMI are incompletely understood, particularly the role of platelet activation in its pathogenesis.
Is platelet activation enhanced in STEMI patients with coronary microvascular obstruction compared to those with complete reperfusion or stable CAD?
Observational (n=68)
Is platelet activation enhanced in STEMI patients with coronary microvascular obstruction compared to those with complete reperfusion or stable CAD?
p-value: p=<0.05
Persistent enhanced platelet activation is observed in STEMI patients with coronary microvascular obstruction despite dual antiplatelet therapy, suggesting a potential mechanism and therapeutic target for this phenomenon.
Hypothesis-generating for intensified antiplatelet strategies in STEMI with microvascular obstruction; prospective trials needed before clinical adoption.
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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Aurigemma et al. (2013) conducted an observational in Acute myocardial infarction and coronary microvascular obstruction (n=68). Coronary microvascular obstruction (MVO) vs. Complete myocardial reperfusion (MR) and stable CAD was evaluated on Platelet receptor expression, fibrinogen binding availability, and monocyte-platelet aggregate formation (p=<0.05). Coronary microvascular obstruction in STEMI patients was associated with significantly increased platelet activation compared to complete reperfusion and stable CAD (p<0.05).
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