Abstract 5579: Possible Role of Platelet Reactivity in No-reflow Phenomenon in Patients With Acute Myocardial Infarction
Background The no-reflow phenomenon has been documented in about 30% of patients with acute myocardial infarction (AMI) undergoing successful recanalization of the infarct-related coronary artery. Several mechanisms have been suggested for no-reflow, including leukocyte and platelet plugging. In this study we investigated whether platelet reactivity and platelet-leukocyte interaction are increased in AMI patients with evidence of no-reflow phenomenon.
Methods We studied 14 patients 1 month after AMI (M/F 9/5; age 55±12), and 18 patients with stable coronary artery disease (CAD) (M/F 11/7; age 55±7). AMI patients were divided into two groups: 9 patients with normal coronary flow (group REFLOW) and 5 patients with no-reflow (TIMI flow ≤2 and myocardial blush grade ≤2: group NO-REFLOW). Flow cytometry was used to measure platelet expression of CD41 and glycoprotein IIb/IIIa epitope PAC-1, and monocyte-platelet aggregates (MPA, expressed as percentage of monocytes binding platelets).
Results Platelet CD41 were no different between three groups (p=0.84). Instead PAC-1 platelet expression, however, was increased in group NO-REFLOW compared to both group REFLOW (9.7±1.2 mfi vs 6.8±1.6 mfi; p=0.004) and stable CAD patients (6.2±1.4 mfi; p=0.001). Similarly, MPA were increased in group NO-REFLOW compared to both the group REFLOW (20.9±2.4% vs 14.6±3.8%; p=0.012) and stable CAD patients (10.1±1.2%; p<0.0001).
Conclusions Platelet reactivity is increased at 1-month follow-up in AMI patients with evidence of no-reflow after successful coronary revascularization. This findings suggest that increased platelet reactivity might be involved in the mechanisms responsible for the no-reflow phenomenon.