Introduction It is not well established whether non-responder patients(NR) to clopidogrel show, as a risk factor, higher number of platelet microaggregates (PMAs) than responder patients (R). These MAPs can affect the microcirculation and is a risk factor to forming larger thrombi, therefore the present study is interesting from this point of view. Material and methods Seventy-eight acute coronary syndrome (ACS) patients (78% male, aged 62.8±12.23 years) were included in this study. These patients underwent coronary stent implantation and treated with routine medication (clopidogrel 75 mg/day and aspirin 100 mg/day), after a loading bolus of 300 mg clopidogrel. The control group was made up of 50 healthy volunteers matched for age and gender who had not been given any pharmacological treatment. Using whole blood flow cytometry, ADP-stimulated and circulating platelet CD62 expression and platelet microaggregates was determined in the entire study population. After a week of treatment the number of circulating platelet microaggregates was evaluated by flow cytometry (EPICS-XL, Beckman-Coulter, Izasa), and the number of MAPs formed ex vivo by ADP 2.5 μM activation was also evaluated . With this aim, using healthy individuals, the platelet population was selected by their forward and side scatter values and as CD61-positive events. The subpopulation that occupied the upper 5% in this region where MAPs are detected,was chosen. After the analytical conditions were established, samples were analyzed. Patients were responders, or not, depending on the CD62 expression after being activated with ADP 2.5 μM. Results Seventy-eight patients showed a higher number of circulating MAPs than controls (177±75/5000 platelets vs. 121±62/5000 platelets; P<0.001). The increase in the MAPs number by ADP activation is higher in the 50 controls than in the 51 responder patients (79±45% vs. 23±18%; P<0.001). The 27 NR patients reacted to ADP in a similar way than controls, with a increase in the number of MAPs of 62±43%, significantly higher than in R ( P<0.001). The findings of this study demonstrate the beneficial effects of clopidogrel in reducing platelet reactivity in 66% of the study patients. These results demonstrate the wide inter-individual variability in ADP response in patients treated with clopidogrel and imply that individualized monitoring of this type of patient is advisable. Conclusions The method described enables us to explore platelet microaggregates formation and may be of great help in monitoring clopidogrel efficacy in ACS patients with stent.