The Effect of Lipid and Inflammatory Profiles on the Morphological Changes of Lipid-Rich Plaques in Patients With Non–ST-Segment Elevated Acute Coronary Syndrome: Follow-Up Study by Optical Coherence Tomography and Intravascular Ultrasound

Abstract

The aim of this study was to determine the relationship between the morphological changes of nonculprit lipid-rich plaques and several clinical profiles in patients with non-ST-segment elevated acute coronary syndrome (NSTEACS). Identification of coronary lesion with morphological characteristics of rupture-prone plaques is still difficult. Eighty-two consecutive patients with NSTEACS who underwent percutaneous coronary intervention were enrolled. The changes in total atheroma volume (TAV) of residual nonculprit lipid-rich plaques and the changes in the corresponding fibrous cap thickness (FCT) were assessed by intravascular ultrasound and optical coherence tomography, respectively, at baseline and after 9 months. The percentage changes in TAV (mm(3)) of lipid-rich plaques and in the corresponding FCT (microm) over the 9-month follow-up period were 3.1 +/- 11% and 15 +/- 17%, respectively. There was no significant correlation between the changes in TAV and those in FCT. The change in TAV showed a significant correlation with reduction of the low-density lipoprotein/high-density lipoprotein (LDL/HDL) ratio (r = 0.42, p < 0.01). In contrast, the change in FCT showed no correlation with LDL/HDL ratio but had a significant positive correlation with changes in high-sensitivity C-reactive protein (r = 0.44, p < 0.01). Furthermore, in multivariate logistic analysis, statin use was an independent predictor of changes in well-stabilized plaques that showed both TAV reduction and FCT increase. The changes in TAV and FCT of coronary plaques over a 9-month observation period were related to 2 different independent factors (i.e., reduction of LDL-cholesterol and high-sensitivity C-reactive protein, respectively). Furthermore, lipid-lowering therapy with statin has the potential to stabilize these parameters by both plaque reduction and FCT.