• Thromb Haemostasis · Jan 2014

    Multicenter Study

    Persistent enhanced platelet activation in patients with acute myocardial infarction and coronary microvascular obstruction: clinical implications.

    • Cristina Aurigemma, Giancarla Scalone, Fabrizio Tomai, Luca Altamura, Giovanni De Persio, Alessandra Stazi, Gaetano A Lanza, and Filippo Crea.
    • Gaetano A. Lanza, MD, Istituto di Cardiologia, Università Cattolica del Sacro Cuore, Roma, Italy, Tel.: +39 06 30154187, E-mail:g.a.lanza@rm.unicatt.it.
    • Thromb Haemostasis. 2014 Jan 1; 111 (1): 122-30.

    AbstractAbout 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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