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| The effects of perindopril on regression and compositional changes of plaque in patients with acute myocardial infarction: Virtual histology-intravascular ultrasound study |
| 전남대학교병원1, 건양대학교병원2, 중앙대학교병원3, 계명의대동산의료원4, 가천의대인천길병원5, 고려대학교구로병원6, 대구카톨릭대학교병원7, 분당서울대학교병원8, 부산수영한서병원9, 원광대학교병원10; Livalo (Pitavastatin) in Acute Myocardial Infarction Study (LAMIS) Group |
| 홍영준1, 정명호1, 안영근1, 배장호2, 김상욱3, 허승호4, 최윤하1, 마은혜1, 안태훈5, 라승운6, 김기식7, 채인호8, 김종현9, 윤경호10 |
Background: There are very limited data regarding the effect of pitavastatin (Livalo) on regression and compositional changes of plaque in acute myocardial infarction (AMI) patients.
Objectives: We used serial virtual histology-intravascular ultrasound (VH-IVUS) to assess the efficacy of pitavastatin (dosage: 2mg/day) on plaque regression and compositional changes in non-intervened non-significant lesions in AMI patients who were enrolled in Livalo in Acute Myocardial Infarction Study (LAMIS).
Methods: A total of 37 lesions in 37 patients were evaluated using serial [baseline and follow-up (mean 7.7 months)] VH-IVUS analysis retrospectively. Efficacy parameters included changes in atheroma volume and plaque composition.
Results: Low density lipoprotein-cholesterol (LDL-C) and high sensitivity C-reactive protein (hs-CRP) levels reduced from 123±34 mg/dL to 86±20 mg/dL (30% decrease, p<0.001) and from 0.89±1.45 mg/dL to 0.23±0.41 mg/dL (74% decrease, p<0.001). However, there were no significant changes in total atheroma volume (Δ=+0.43±8.30 mm3, p=0.8) and absolute and relative plaque volumes from baseline to follow-up (Δfibrotic; +1.50±8.19 mm3, p=0.4, Δfibro-fatty; +1.08±7.65 mm3, p=0.5, Δdense calcium; +0.38±2.78 mm3, p=0.5, Δnecrotic core; -0.66±5.58 mm3, p=0.6, and Δ%fibrotic; +2.3±8.5%, p=0.2, Δ%fibro-fatty; -0.5±7.2%, p=0.7, Δ%dense calcium; +0.4±4.9%, p=0.7, Δ%necrotic core; -2.2±7.5%, p=0.165). Follow-up LDL-C did not correlate with changes (Δ) of absolute and relative plaque components, however, follow-up hs-CRP correlated with changes (Δ) of absolute and relative necrotic core (r=0.475, p=0.026, and r=0.434, p=0.043, respectively) and dense calcium components (r=0.699, p<0.001, and r=0.635, p=0.002, respectively)
Conclusions: Although usual dose of pitavastatin decrease LDL-C and hs-CRP levels effectively, it could not contribute to the effective plaque regression and compositional change in non-significant lesions in AMI patients in LAMIS. Not follow-up LDL-C but follow-up hs-CRP is associated with changes of plaque components by statin treatment in AMI patients.
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