Abstract 4413: Effect of Atorvastatin on the Stability of Thin-cap Fibroatheroma: A Three-Vessel Optical Coherence Tomography and Intravascular Ultrasound Study
Background: It is well known that administration of statins for patients with acute myocardial infarction is effective for secondary prevention of cardiovascular events. It is generally assumed that effects of statins would result from their effects on atherosclerotic lesions including stabilization of plaques, but effects of statins on plaque vulnerability have not been fully elucidated. Therefore, we evaluated the impact of atorvastatin on the fibrous cap thickness of thin-cap fibroatheroma (TCFA), which is recognized as precursor lesion of plaque rupture, using optical coherence tomography (OCT) and intravascular ultrasound (IVUS) in vivo.
Methods: OCT and IVUS examinations were performed in all 3-coronary arteries for 46 acute myocardial infarction patients to identify TCFA at non-culprit segments. After the baseline treatment, all patients were randomly assigned into receive either low-dose (5mg) or high-dose (20mg) atorvastatin. OCT and IVUS were repeated after 12 months to evaluate TCFA stability; thickness of fibrous cap, arc of lipid core, and plaque area. OCT criteria for TCFA was lipid-rich plaque with cap thickness <65microm.
Results: A total of 47 non-culprit TCFAs was identified in 26 patients (13 low and 13 high dose atorvastatin). LDL-cholesterol level in the high dose atorvastatin group was significantly lower than that in the low dose atorvastatin group at follow-up. Plaque area measured by IVUS did not change between baseline and follow-up in both groups. The average number of lipid core arc did not change from baseline to follow-up in both groups (142.4±31.9° to 137.3±33.8 and 127.2±28.5° to 125.9±34.5°, p=NS). The average number of fibrous cap thickness significantly decrease from baseline to follow-up (57.7±4.1 to 63.8±14.2μm, p<0.01). However, the extent of change in cap thickness was similar both in high dose atorvastatin and low dose atorvastatin groups (55.6±3.9 to 61.5±11.9μm and 59.6±3.2 to 65.9±16.0μm, P=NS).
Conclusions: The lipid-lowering therapy with atorvastatin for 12 months after the onset of acute myocardial infarction influences the fibrous-cap thickness of TCFA. However, a dose-related effect of atorvastatin in increasing the fibrous cap thickness was not observed.