Abstract 11906: Coronary Intraplaque Hemorrhage Evoked Anti-inflammatory Macrophage Accelerates Ventricular Functional Recovery in Patients with Myocardial Infarction

Background: Coronary intraplaque hemorrhage (IPH) accelerates atherosclerosis and contributes to lesion development and destabilization. Extracellular hemoglobin is cleared by CD163, a macrophage scavenger receptor. This process provokes the secretion of the anti-inflammatory atheroprotective cytokine interleukin (IL)-10 by macrophage. Therefore, coronary plaque and thrombus related to IPH may contain anti-inflammatory macrophage, and modify the functional recovery of reperfused myocardium after successful PCI. Methods: In 40 patients with first myocardial infarction, coronary atherothrombotic debris was retrieved during primary PCI using a filter based distal protection device (Filtrap, NIPRO, Japan). The debris was stained with antibodies to CD163, CD14 (a proinflammatory macrophage surface marker), and IL-10. Left ventricular (LV) function was determined by echocardiography before, 20day after, and 6months after PCI. Patients were divided into two groups: CD163>10% (IPH+, n=20) and CD163 Results: Average CD163 positive macrophage (+) was 26.3±13.7% in IPH+, and 3.2±2.9% in IPH-. Compared to IPH-, IPH+ had larger debris, more CD14+ (19.6±9.2% vs 4.4±6.4%, p Conclusions: Coronary intraplaque hemorrhage has relation with large thrombus and impaired distal flow after primary PCI. However, it enhances anti-inflammatory macrophage expression and accelerates ventricular functional recovery after successful reperfusion.