医学
血管造影
罪魁祸首
血管内超声
纤维帽
急性冠脉综合征
血栓
放射科
血管造影
不稳定型心绞痛
内科学
心脏病学
心肌梗塞
作者
Yukio Ozaki,Meinoshin Okumura,Tevfik F Ismail,Sadako Motoyama,Hiroyuki Naruse,Kousuke Hattori,Hideki Kawai,Masayoshi Sarai,Yasushi Takagi,Junichi Ishii,Hirofumi Anno,Renu Virmani,Patrick W. Serruys,Jagat Narula
标识
DOI:10.1093/eurheartj/ehr189
摘要
Pathological and clinical optical coherence tomography (OCT) studies have indicated that acute coronary syndrome (ACS) lesions have either ruptured fibrous caps (RFC-ACS) or intact fibrous caps (IFC-ACS). Although computed tomographic (CT) angiographic characteristics of RFC-ACS include low-attenuation plaques and positive plaque remodelling, features associated with IFC-ACS have not been previously described. The aim of this study was to assess the CT characteristics of IFC-ACS lesions. Seventy-four patients with ACS/stable angina consented to multimodality imaging, of which 66 underwent CT angiography. Of these, 57 culprit lesions in 57 patients were evaluated with sufficient image quality from all four of OCT, angioscopy, intravascular ultrasound, and CT angiography. Intraluminal thrombus was assessed by OCT/angioscopy, and culprit lesions further classified by OCT-based demonstration of fibrous cap integrity. Of 35 culprit lesions with ACS, OCT revealed IFC with thrombus in 10 (29%) and RFC in the remaining 25 (71%); all 22 lesions with stable angina had intact fibrous caps. Fibrous caps were significantly thinner in RFC-ACS than IFC-ACS and stable angina (45 ± 12, 131 ± 57, and 321 ± 146 μm, respectively; P = 0.001). CT angiography revealed that low-attenuation plaques were more frequently observed in RFC-ACS than IFC-ACS and stable angina (88, 40, and 18%; P = 0.001) lesions. Similarly, positive remodelling was more predominantly seen in RFC-ACS than IFC-ACS and stable angina (96, 20, and 14%; P = 0.001). However, none of the specific CT angiography features clearly distinguished IFC-ACS from stable lesions. In contrast to the situation with RFC-ACS, distinct culprit lesion characteristics associated with non-rupture-related mechanisms are not identified by CT angiography. It will therefore not be possible to differentiate plaques likely to develop IFC-ACS from stable plaques.
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