Abstract 9739: Impact of Statin Use Before the Onset of Acute Myocardial Infarction on Coronary Plaque Morphology of the Culprit Lesion

Abstract

Statin favorably stabilizes coronary plaque. We evaluated the impact of statin use before the onset of acute ST-elevation myocardial infarction (AMI) on culprit lesion plaque morphology. Methods: Patients (n=127, age 63.3 ± 13.1 year old, mean ± SD) with first AMI (within 12 hours after the onset) were divided into either a statin group (n=31) or a nonstatin group (n=96) based on statin use before the onset of AMI. Coronary plaque morphology of the culprit lesion was evaluated using intravascular ultrasound virtual histology (IVUS-VH) with radiofrequency data analysis before coronary intervention. The IVUS-VH identified 4 types of plaque components: fibrous, fibrofatty, dense calcium, and necrotic core. Values of high-sensitivity CRP (hs-CRP) at admission were measured. Dual SPECT using BMIPP and 201 Tl was performed within 2 weeks after the AMI to measure perfusion-metabolism mismatch score, an indicator of viable myocardium, from each total defect score of Tl/BMIPP using 17-segment model and a semiquantitative visual score (0: normal, to 4: no uptake). Results: The IVUS-VH showed less percentage of necrotic core area (7.6 ± 6.8% vs 25.5 ± 6.8%, statin vs nonstatin, p<0.001), greater percentage of fibrous area (70.0 ± 14.2% vs 59.0 ± 8.2 %, p<0.001), and greater percentage of fibrofatty area (19.3 ± 12.7 % vs 11.6 ± 9.9 %, p<0.001) of the culprit lesion in the statin group than in the nonstatin group. The values of hs-CRP were lower in the statin group than in the nonstatin group (1.2 ± 0.8 mg/L vs 2.1 ± 2.4 mg/L, p<0.05) The values of mismatch score was higher in the statin group than in the nonstatin group (8.0 ± 2.5 vs 5.3 ± 2.7, p<0.001) Conclusions: Statin use before the onset of AMI may have effects on coronary plaque morphology of the AMI culprit lesion with less necrotic core and greater fibrous and fibrofatty component. Reducing necrotic core component of the culprit lesion with statin use before the onset of AMI may be related with lower inflammatory response and greater viable myocardium after AMI.