Author + information
- Received April 20, 2010
- Revision received June 2, 2010
- Accepted July 10, 2010
- Published online December 1, 2010.
- Daiji Yoshikawa, MD⁎ (, )
- Hideki Ishii, MD, PhD,
- Yutaka Aoyama, MD,
- Hitoshi Ichimiya, MD,
- Yuuki Shimizu, MD,
- Satoshi Isobe, MD, PhD,
- Satoshi Shintani, MD, PhD,
- Yasuko Kureishi-Bando, MD, PhD and
- Toyoaki Murohara, MD, PhD
- ↵⁎Reprint requests and correspondence
: Dr. Daiji Yoshikawa, Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Shouwa-ku, Nagoya, Aichi 466-8550, Japan
A 62-year-old man with hypertension and dyslipidemia underwent successful primary percutaneous coronary intervention with thrombus aspiration and bare-metal stent (3.5 × 13 mm) (Liberté, Boston Scientific, Natick, Massachusetts) implantation (12 atm) at proximal left anterior descending coronary artery, due to ST-segment elevation myocardial infarction (Fig. 1). Optical coherence tomography (OCT) (Image Wire, Light-lab Imaging, Goodman Co., Ltd., Nagoya, Japan) revealed that some stent struts were well-apposed, with others embedded in intramural thrombus (Online Video 1, corresponds with Fig. 2, “Emergent procedure”).
Six-month follow-up angiography showed a coronary artery aneurysm (CAA) at the stented site without significant restenosis. The OCT imaging demonstrated that maximal luminal diameter of the CAA was 4.0 × 1.4 mm and longitudinal dimension was 4.8 mm with luminal surface described as a homogeneous, signal-rich structure absent of intramural thrombus (Figs. 1C and 1D). The intima-like structure of the CAA was continuous with vessel intima, suggesting this late-occurring CAA had a 3-layer wall. This CAA was classified as small, fusiform, true, and type IV (1). Almost all stent struts were well-apposed and covered by neointimal thickening, with some stent struts malapposed with tissue coverage (Online Video 2, corresponds with Fig. 2 “After 6 months”). Written informed consent was obtained before the procedure. We speculate the mechanisms for appearance of the CAA are: an early fibroatheroma transformed into a vulnerable plaque with a large lipid-core at the segment where excessive expansive vessel remodeling occurred (2). Plaque rupture followed by thrombus formation caused ST-segment elevation myocardial infarction. Thrombus accumulation might have obscured the intra-plaque cavity with ruptured fibrous-cap. Antiplatelet therapy and blood flow might have dissolved the thrombus, increasing flow against the diseased cavity (vascular) wall and reducing the tolerance of the diseased cavity (vascular) wall to intraluminal pressures, causing CAA formation (3). These mechanisms might be associated with stent malapposition or thrombosis in some cases. Long-term follow-up studies with large populations would be required to confirm the clinical significance of these findings obtained from OCT examinations.
All authors have reported that they have no relationships to disclose.
- Received April 20, 2010.
- Revision received June 2, 2010.
- Accepted July 10, 2010.
- American College of Cardiology Foundation