Abstract 2843: Significant Association between Neutrophil Aggregation in Aspirated Thrombus and Myocardial Damage in Patients with ST-segment Elevation Acute Myocardial Infarction

Background : The previous flow cytometric study demonstrated that circulating neutrophil-platelet aggregate formation is useful in vivo marker for platelet activation (

; : –37 ). However, in patients with acute myocardial infarction (AMI), the relationships between myocardial damage, platelet activation and platelet-neutrophil aggregation remains unclear. Thrombotic samples aspirated in the culprit lesions may provide intraluminal pathological information.

Methods : We studied 107 patients with ST-segment elevation AMI (M/F:77/30, age:66±12 [mean±SD]years), in whom aspiration catheter was used during emergency percutaneous coronary intervention. Patients were divided into the following two groups according to the density of neutrophils in the aspirated samples: group L (n=53), ≤100 neutrophils/0.025mm ² thrombus; group H (n=54), >100 neutrophil/0.025mm ² thrombus). Left ventricular ejection fraction (LVEF) was reassessed six months after the onset of AMI.

Results : Neutrophil density in thrombus was not time-dependent. Impaired myocardial reperfusion, defined as myocardial blush grade of 0/1 and no ST-segment resolution (<50% of initial value) was more frequently found in group H than in group L. Peak creatinine phosphokinase (CPK) level was higher and LVEF at six months after the onset was lower in group H than group L. Multivariate analysis showed that high neutrophil density in aspirated thrombus was an independent predictor of myocardial blush grade 0/1, no ST-segment resolution and LVEF at six months after the onset with odds ratio of 13.3, 8.72 and 5.09, respectively (P<0.01).

Conclusions : Platelet-neutrophil aggregates retrieved from ruptured plaque may be associated with impairment of coronary microcirculation and resultant myocardial necrosis/dysfunction. These findings indicate the clinical importance of the interaction between thrombosis and inflammation in pathogenesis of AMI.