Objectives: To evaluate the effect of statins on the prognosis of acute myocardial infarction after percutaneous coronary intervention (PCI).
Methods: We reviewed 280 patients with acute myocardial infarction who underwent PCI within 12 hr after the onset of symptoms. Statin therapy was initiated in 72 patients within 8.6 +/- 7.6 days after the onset (statin group) but not in the remaining 208 (no statin group). The time sequential changes of low-density lipoprotein cholesterol (LDL-C) and C-reactive protein (CRP) levels, and the angiographic findings at 6 months after PCI were compared.
Results: At onset, LDL-C levels in the statin group were significantly higher than those in the no statin group (140 +/- 35 vs 118 +/- 28 mg/dl, p < 0.01). However, at restudy, the values were similar between the two groups (113 +/- 19 vs 118 +/- 21 mg/dl, p = 0.19). CRP levels at restudy tended to be lower in the statin group than in the no statin group (0.11 +/- 0.12 vs 0.14 +/- 0.13 mg/dl, p = 0.07). Although the binary restenosis rates of the culprit lesion were almost equivalent (statin group 29% vs no statin group 23%, p = 0.30), new lesions in the non-culprit vessels tended to be found more frequently in the no statin group than in the statin group (13% vs 4%, p = 0.07). CRP levels at restudy were significantly higher in the patients with new lesions (n = 27) than in those without (n = 253; 0.25 +/- 0.17 vs 0.11 +/- 0.19 mg/dl, p < 0.01), whereas LDL-C levels were similar between the two groups (117 +/- 20 vs 113 +/- 27 mg/dl, p = 0.75). LDL-C, CRP at restudy and the rates of new lesions were similar in the patients receiving water-soluble statins (n = 42) and liposoluble statins (n = 30).
Conclusions: Statin therapy initiated at the early phase of acute myocardial infarction might prevent the development of new lesions in non-culprit vessels without any influence on the restenosis rate of the culprit lesion.