Platelets Reactivity as a Predictor of Microvascular Damage in STEMI Patients Undergoing Primary PCI

Background: Despite the optimized management of STEMI patients including primary PCI (PPCI) and use of novel anti-platelet agents, a substantial proportion of patients still display microvascular damage, resulting in inadequate myocardial reperfusion despite successful reopening of the infarct related artery. Platelets reactivity has been implicated in number of mechanisms suggested to account for this phenomenon, including distal embolization, microvascular platelets plugging and inflammation.

Methods: We prospectively evaluated 105 consecutive STEMI patients, with no prior coronary disease, who underwent PPCI. All patients underwent 2D-echocardiography within 48 hours of admission and cardiac MRI (CMR) 5 ± 1day post admission. All Patients were treated with dual antiplatelet agents and Blood sample were analyzed for platelets reactivity (PA) at 72 hours post admission, using arachidonic acid (AA) and adenosine diphosphate (ADP) as agonists. Aspirin hypo-responsiveness was defined as AA-PA≥30%, and P2Y12 non-responsiveness as ADP-PA ≥ 50%. CMR was evaluated for delayed enhancement (DE) and microvascular obstruction (MVO), which reflects microvascular damage. Both parameters were expressed as percentage of LV mass.

Results: AA and ADP inhibition were 22±17, and 34±16 respectively. A significant positive correlation was demonstrated between AA-PA and MVO (p=0.032) and DE extent (p=0.006). Accordingly, patients with aspirin hypo-responsiveness had significantly higher extent of DE (p=0.03) and MVO (p=0.003). A multivariate logistic regression analysis revealed that AA-PA hypo-responsiveness is an independent predictor of higher extent of microvascular damage as reflected by MVO% of scar and MVO% of LV mass(OR 3.6; 95% CI 1.15-10.3, p=0.027). As opposed to AA related platelets reactivity, no significant correlation was demonstrated between ADP induced platelets reactivity and measures of MVO or DE.

Conclusions: In patients undergoing PPCI for STEMI, platelets reactivity in response to AA is an independent predictor of the extent of both myocardial and microvascular damage.