Cardioprotection of Rosuvastatin Against Cardiac Dysfunction After Coronary Microembolization via Alleviating Inflammatory Induced Microinfarctions

Backgrounds: It has been demonstrated that statins plays a critical role on prevention the risk of myocardial infarction. However, it is unclear about the effect of statins on coronary microembolization (CME), which is one of common complication after coronary intervention.Objectives: This experimental study was designed to evaluate the protective role of rosuvastatin on cardiac dysfunction caused by CME.Methods: Mice CME models were developed by injecting a total of 500,000 polyethylene micro-particles (average 9-12 diameters) into the left ventricle when transiently obstructed the ascending aorta for 15 seconds. There were three groups: sham-operation group (n=6), CME group (n=8) and rosuvastatin therapy group (n=7, oral received 20mg/kg per day one week before CME). Cardiac function was evaluated by echocardiography at baseline, 3 days and 10 days after procedure. HE staining was performed to detect the area of microinfarctions, while serum and myocardial expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were detected by ELISA and immunohistochemistry.Results: Compared with sham-operation group, left ventricular ejection fraction (LVEF) was significantly decreased in CME group (3 days later: 53.2±6.0% vs. 62.8±6.8%, P=0.002; 10 days later: 54.4±8.1% vs. 64.3±5.7%, P=0.014). Pre-treatment with oral rosuvastatin one week before CME improved cardiac dysfunction (3 days later: 59.8±5.4% vs. 53.2±6.0%, P=0.013; 10 days later: 61.2±5.2% vs. 54.4±8.1%, P=0.037). We also found that rosuvastatin therapy not only decreased the average area of microinfarctions (7.4±3.7% vs. 3.2±3.2%, P=0.012), but also inhibited myocardial expression of inflammatory factors, including TNF-α and IL-6.Conclusions: Inflammation mediated microinfarctions could be involved in cardiac dysfunction after coronary microembolization. Rosuvastatin could improve heart function by alleviating local myocardial inflammatory responses.