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.
OBJECTIVE
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).


BACKGROUND
Identification of coronary lesion with morphological characteristics of rupture-prone plaques is still difficult.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Takarada
Shigeho
S
Department of Cardiovascular Medicine, Wakayama Medical University, Wakayama, Japan.
Imanishi
Toshio
T
Ishibashi
Kohei
K
Tanimoto
Takashi
T
Komukai
Kenichi
K
Ino
Yasushi
Y
Kitabata
Hironori
H
Kubo
Takashi
T
Tanaka
Atsushi
A
Kimura
Keizo
K
Mizukoshi
Masato
M
Akasaka
Takashi
T
D054058:Acute Coronary Syndrome / Q000097:blood / Q000175:diagnosis / Q000209:etiology / Q000628:therapy*; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications / Q000175:diagnosis / Q000628:therapy*; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology; D003430:Cross-Sectional Studies; D005260:Female; D005355:Fibrosis; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators / Q000097:blood*; D007564:Japan; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D016017:Odds Ratio; D018570:Risk Assessment; D012307:Risk Factors; D013997:Time Factors; D041623:Tomography, Optical Coherence; D016896:Treatment Outcome; D018084:Ultrasonography, Interventional
D015415:Biomarkers; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D018836:Inflammation Mediators; D002097:C-Reactive Protein