Progression of coronary atherosclerosis in stable patients with ultrasonic features of high-risk plaques.
OBJECTIVE
Large plaque burden, expansive vascular remodelling, and spotty calcification have been considered as important morphologies of high-risk plaques causing acute coronary events. Although non-occlusive rupture of high-risk plaques has been proposed as a mechanism for disease progression in post-mortem studies, the natural history of coronary atherosclerosis in stable patients with high-risk plaques has not been fully elucidated. We sought to evaluate coronary atheroma progression in stable patients with greyscale intravascular ultrasound (IVUS)-derived high-risk plaques.


RESULTS
We analysed 4477 patients with stable coronary artery disease underwent serial greyscale IVUS imaging in eight clinical trials. We compared volumetric intravascular ultrasound (IVUS) data in the non-culprit segments between patients with and without high-risk plaques, defined as the combination of per cent atheroma volume (PAV) >63%, positive remodelling and spotty calcification. High-risk plaques were observed in 201 (4.5%) of patients. Patients with high-risk plaques exhibited a greater PAV (47.1 ± 8.4 vs. 37.7 ± 8.7%, P < 0.001) at baseline. On serial evaluation, however, regression of PAV (-0.26 ± 0.39 vs. 0.24 ± 0.32%, P = 0.03) was observed. In patients with high-risk plaques, the non-statin use was associated with the accelerated atheroma progression, whereas atheroma regression was observed under statin therapy (change in PAV: 1.87 ± 0.68% vs. -0.83 ± 0.53%, P = 0.01).


CONCLUSIONS
Patients with high-risk plaques exhibit extensive atheroma burden, which is modifiable with anti-atherosclerotic therapies. These findings underscore risk modification using a statin in patients with high-risk plaques.
South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia jimmyk67@yahoo.co.jp.
Yu
Y
Kataoka
C5 Research, Cleveland Clinic, Cleveland, OH, USA.
Kathy
K
Wolski
C5 Research, Cleveland Clinic, Cleveland, OH, USA.
Craig
C
Balog
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH, USA.
Kiyoko
K
Uno
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH, USA.
Rishi
R
Puri
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH, USA.
E Murat
EM
Tuzcu
Department of Cardiovascular Medicine, Heart and Vascular Institute, Cleveland Clinic, Cleveland, OH, USA.
Steven E
SE
Nissen
South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.
Stephen J
SJ
Nicholls
D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000473:pathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D058226:Plaque, Atherosclerotic / Q000000981:diagnostic imaging* / Q000188:drug therapy / Q000473:pathology; D012307:Risk Factors; D018084:Ultrasonography, Interventional / Q000379:methods*
Atherosclerosis; Coronary; Intravascular ultrasound; Plaque progression; Statin