Author + information
- Received February 21, 2014
- Revision received February 27, 2014
- Accepted February 27, 2014
- Published online October 1, 2014.
- Hiroyuki Hao, MD∗∗ (, )
- Kenichi Fujii, MD†,
- Takahiro Imanaka, MD†,
- Rika Kawakami, MD∗,
- Taro Kawano, MD‡,
- Tadateru Takayama, MD‡,
- Atsushi Hirayama, MD‡,
- Hatsue Ishibashi-Ueda, MD§,
- Tohru Masuyama, MD† and
- Seiichi Hirota, MD∗
- ∗Department of Surgical Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
- †Cardiovascular Division, Department of Internal Medicine, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
- ‡Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Itabashi-ku, Tokyo, Japan
- §Department of Pathology, National Cerebral and Cardiovascular Center, Suita, Osaka, Japan
- ↵∗Reprint requests and correspondence:
Dr. Hiroyuki Hao, Department of Surgical Pathology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo, 663-8501, Japan.
A 57-year-old man died of sepsis, and an autopsy was performed. He had undergone percutaneous coronary intervention of the right coronary artery with paclitaxel-eluting stent implantation 43 months before death. Postmortem ex vivo intravascular ultrasound (IVUS) (Terumo Corp, Tokyo, Japan), optical coherence tomography (OCT) (St. Jude Medical, St. Paul, Minnesota), and pathological examination were carried out at the stented segment. IVUS and OCT images illustrated neointimal hyperplasia, leading to moderate luminal narrowing. IVUS clearly showed the hypoechoic mass within the neointima on the stent struts (Figure 1A, asterisks). OCT indicated neointimal hyperplasia with rapid attenuation of the signals (Figure 1B, asterisks). Both intravascular images suggested the presence of neoatherosclerosis after drug-eluting stent implantation (1).
Pathological evaluation demonstrated massive hemorrhage within the neointimal hyperplasia (Figure 2A). This striking feature could not be identified by intravascular imaging, such as IVUS and OCT. High-magnification view of neointima showed the foam cell infiltration with red blood cells (Figure 2B). Although these foam cells existed directly under the vessel lumen, there was no histological evidence of plaque rupture and thrombus formation. Histological observation indicated the presence of tiny cholesterol clefts within the neointima (Figure 2C, arrows).
It is known that the plasma membrane of red blood cells is the important source of cholesterol esters in the vessel wall (2). In this case, massive hemorrhage within the neointima was observed, and red blood cells were adjacent to the tiny cholesterol clefts. Although large cholesterol clefts might penetrate from underlying plaque, the tiny cholesterol clefts, which are not commonly observed in the atherosclerosis of native coronary arteries, might be derived from the red blood cell membrane within the neointima.
These histological findings indicate the important role of hemorrhage for the lipid accumulation within the neointima. We might need to assume the distinct pathway for the development of neoatherosclerosis after drug-eluting stent implantation, which seems to progress more rapidly compared with that of atherosclerosis of native coronary arteries.
The authors gratefully acknowledge the technical assistance of Mrs. Mayumi Oka and Mr. Gen Satoh.
The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received February 21, 2014.
- Revision received February 27, 2014.
- Accepted February 27, 2014.
- American College of Cardiology Foundation