Background and objectives: Administration of a loading dose of a statin (HMG-CoA reductase inhibitor) prior to percutaneous coronary intervention (PCI) contributes to protection from myocardial ischemic-reperfusion injury. This trial was designed to investigate the effect and mechanism of loading-dose rosuvastatin therapy before PCI in patients with acute coronary syndrome.
Methods: One hundred and forty-three patients with acute coronary syndrome were randomized to either the loading-dose (rosuvastatin 40 mg given 4 h before PCI) or conventional-dose (rosuvastatin 10 mg given 4 h before PCI) group. Blood samples were collected before and 0, 24, and 72 h post-PCI for measurement of serum cardiac troponin-I (cTn I), creatine kinase-MB (CK-MB), superoxide dismutase (SOD), reactive oxygen species (ROS), and malondialdehyde (MDA). Echocardiography and the major adverse cardiac/cerebrovascular events (MACCE) rate were followed up for 6 months post-PCI.
Results: Blood serum CK-MB and cTn I were significantly lower in the loading-dose group than in the conventional-dose group at 24 and 72 h post-PCI [CK-MB: 26.90 ± 3.22 vs. 32.96 ± 2.65 IU/L, P = 0.024; 10.79 ± 4.65 vs. 15.18 ± 5.39 IU/L, P = 0.021. cTn I: 0.046 ± 0.007 vs. 0.055 ± 0.002 ng/mL, P = 0.015; 0.027 ± 0.006 vs. 0.041 ± 0.006 ng/mL, P = 0.026]. Echocardiography at 6 months after PCI revealed significant improvement in cardiac function in the loading-dose group compared with the conventional-dose group (P < 0.05). The MACCE rate at 6 months after PCI in the loading-dose group was lower than in the conventional-dose group (P = 0.0428). The levels of MDA and ROS were decreased and the SOD level was significantly higher in the loading-dose group than in the conventional-dose group at 0, 24, and 72 h post-PCI (P < 0.05).
Conclusion: Administration of loading-dose rosuvastatin in patients with acute coronary syndrome prior to PCI exerts myocardial protection by inhibition of oxidative stress.