Kataoka Yu, Wolski Kathy, Balog Craig, Uno Kiyoko, Puri Rishi, Tuzcu E Murat, Nissen Steven E, Nicholls Stephen J
South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia
C5 Research, Cleveland Clinic, Cleveland, OH, USA.
Eur Heart J Cardiovasc Imaging. 2014 Sep;15(9):1035-41. doi: 10.1093/ehjci/jeu065. Epub 2014 Apr 29.
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.
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).
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.
大斑块负荷、血管扩张性重塑和散在钙化被认为是导致急性冠状动脉事件的高危斑块的重要形态。尽管在尸检研究中已提出高危斑块的非闭塞性破裂是疾病进展的一种机制，但高危斑块稳定患者的冠状动脉粥样硬化自然病程尚未完全阐明。我们试图评估经灰阶血管内超声（IVUS）检测出有高危斑块的稳定患者的冠状动脉粥样硬化进展情况。
我们在八项临床试验中分析了4477例接受系列灰阶IVUS成像的稳定型冠状动脉疾病患者。我们比较了有和没有高危斑块患者（高危斑块定义为粥样硬化体积百分比（PAV）>63%、阳性重塑和散在钙化的组合）非罪犯节段的血管内超声（IVUS）容积数据。201例（4.5%）患者观察到高危斑块。有高危斑块的患者在基线时表现出更大的PAV（47.1±8.4%对37.7±8.7%，P<0.001）。然而，在系列评估中，观察到PAV有消退（-0.26±0.39%对0.24±0.32%，P=0.03）。在有高危斑块的患者中，未使用他汀类药物与粥样硬化进展加速相关，而在他汀类药物治疗下观察到粥样硬化消退（PAV变化：1.87±0.68%对-0.83±0.53%，P=0.01）。
有高危斑块的患者表现出广泛的粥样硬化负担，这可通过抗动脉粥样硬化治疗加以改变。这些发现强调了在有高危斑块的患者中使用他汀类药物进行风险修正。
