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Yonsei medical journal · Mar 2013
Early differential changes in coronary plaque composition according to plaque stability following statin initiation in acute coronary syndrome: classification and analysis by intravascular ultrasound-virtual histology.
- Dae Seong Hwang, Eun Seok Shin, Shin Jae Kim, LeeJun HoJH, Jong Min Kim, and Sang-Gon Lee.
- Department of Medicine, Ulsan University Hospital, University of Ulsan College of Medicine, 877 Bangeojinsunhwando-ro, Dong-gu, Ulsan 682-714, Korea.
- Yonsei Med. J. 2013 Mar 1; 54 (2): 336344336-44.
PurposeThe aim of this study was to demonstrate the early effects of statin treatment on plaque composition according to plaque stability on Intravascular Ultrasound- Virtual Histology at 6 months after a coronary event. Previous trials have demonstrated that lipid lowering therapy with statins decreases plaque volume and increases plaque echogenicity in patients with coronary artery disease.Materials And MethodsFifty-four patients (54 lesions) with acute coronary syndrome were prospectively enrolled. We classified and analyzed the target plaques into two types according to plaque stability: thin-cap fibroatheroma (TCFA, n=14) and non-TCFA (n=40). The primary end point was change in percent necrotic core in the 10-mm subsegment with the most disease.ResultsAfter 6 months of statin therapy, no change was demonstrated in the mean percentage of necrotic core (18.7±8.5% to 20.0±11.0%, p=0.38). There was a significant reduction in necrotic core percentage in patients with TCFA (21.3±7.2% to 14.4±8.9%, p=0.017), but not in patients with non-TCFA. Moreover, change in percent necrotic core was significantly correlated with change in high-sensitivity C-reactive protein levels (r=0.4, p=0.003). Changes in low-density lipoprotein cholesterol levels and lipid core percentage demonstrated no significant associations.ConclusionA clear reduction of lipid core was observed only for the TCFA plaque type, suggesting that changes in plaque composition following statin therapy might occur earlier in vulnerable plaque than in stable plaque; the effect may be related to the anti-inflammatory effects of statins.
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