Author + information
- Received January 6, 2012
- Revision received February 8, 2012
- Accepted February 9, 2012
- Published online November 1, 2012.
- Jin-Ho Choi, MD, PhD⁎,†,
- Juan F. Granada, MD‡,
- Jung-Sun Kim, MD, PhD§,
- Young Bin Song, MD, PhD⁎,
- Joo-Yong Hahn, MD, PhD⁎,
- Seung Hyuk Choi, MD, PhD⁎,
- Armando Tellez, MD‡,
- Krzysztof Milewski, MD‡,
- Myeong-Ki Hong, MD, PhD§,
- Yangsoo Jang, MD, PhD§,
- Sang Hoon Lee, MD, PhD⁎ and
- Hyeon-Cheol Gwon, MD, PhD⁎,⁎ ()
- ↵⁎Reprint requests and correspondence:
Dr. Hyeon-Cheol Gwon, Department of Medicine, Cardiac and Vascular Center, Samsung Medical Center, Sungkyunkwan University School of Medicine,
50 Irwon-dong, Gangnam-gu, Seoul 135-710, Korea
Drug eluting stents (DES) have decreased substantially the neointimal formation after percutaneous coronary intervention (PCI). However, DES are not free from neointimal hyperplasia (NIH) and stent thrombosis, which are related to the delayed arterial healing following DES implantation. The recently introduced optical coherence tomography (OCT) enables a detailed investigation of vessel healing. The presence of peri-strut low intensity (PLI) has been described as a potential marker of abnormal neointimal healing (1,2). We investigated the late healing characteristics of stents implanted over 3 years, specifically the potential impact of PLI on NIH and restenosis.
OCT imaging (M2, Lightlab Imaging, Westford, Massachusetts) was performed in 99 patients who were treated with bare-metal stents (BMS), sirolimus-eluting stents (SES) (Cypher, Cordis, Bridgewater, New Jersey), or paclitaxel-eluting stents (PES) (Taxus, Boston Scientific, Natick, Massachusetts) from September 2007 to August 2009. The inclusion criteria were stent implanted in de novo lesion and time from index PCI >3 years. The exclusion criteria were left main, stent thrombosis, or target lesion revascularization.
Cross-sectional images of the stented segments were analyzed at 1-mm intervals. PLI was defined as homogenous low-intensity area around a stent strut without significant signal attenuation behind the area on a strut basis. The severity of PLI on a cross-sectional basis was evaluated semiquantitatively by PLI score by the extent of PLI occupying the number of quadrants. Neointimal thickness and malapposition of each strut, neointimal lipid pool, calcification, microvessel, and OCT-derived thin cap neoatheroma (OCT-TCNA) were also defined (Fig. 1A) (3). A total of 3,365 OCT cross sections from 125 stents were assessed. After exclusion of overlapping stents (2,197 struts [6.7%]) and side branches ≥1.5 mm (277 struts [0.8%]), a total of 30,302 struts (92.5%) and 3,053 cross sections were included in the analysis.
By the OCT strut-level analysis, PLI was most common in BMS (19.4%), followed by PES (12.6%) and SES (6.0%; p < 0.001) (Table 1). NIH was higher in struts displaying PLI than struts without PLI in all stents (p < 0.001 for all). Interestingly, the NIH thickness was <0.3 mm even in the BMS strut without PLI, and it was >0.5 mm in SES struts with PLI (Fig. 1B). Significant correlation between the severity of PLI and the degree of NIH was found in both the cross-sectional and stent-level analyses (r = 0.537 to 0.846; p < 0.05) (Fig. 1B, Table 1). The frequency of OCT-TCNA per stent was 7.9% to 15.6% and not different between stent types (p = nonsignificant) (Table 1). The severity of PLI correlated with angiographic late loss in all groups (r = 0.407 to 0.583; p < 0.05) (Fig. 1B, Table 1). The presence of PLI in one quadrant of OCT image was related to a 6.6- to 130.0-fold increase of binary restenosis after adjustment for stent area (p < 0.05) (Table 1).
The vascular healing response of BMS implantation is known to be initial regression of neointima followed by a plateau at least up to 3 years, whereas that of DES is a mild but continuous growth. Little is known about the characteristics of late neointima. Our study showed that PLI is a common finding long after stent implantation and appears to be involved in neointimal proliferation.
The histopathology of PLI is still not known well. PLI was correlated with the quality of the neointima with different stent types (2,4,5). In our study, the presence of PLI was the strongest factor related to neointimal proliferation. Considering contribution of continuous inflammation, fibrin deposition, extracellular matrix accumulation, or formation of neoatherosclerosis to the late neointimal growth, PLI may be the trace of burnt-out neointimal growth or sustained residual biological process occurring adjacent to the stent.
The limitations of this study are its cross-sectional nature and lack of neointimal histology. The histological validation and serial examination of our findings deserve further investigation because they may have clinical implications among patients undergoing stent implantation.
Support was provided by Clinical Research Development (CRS108-08-1) of Samsung Medical Center. All authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- Received January 6, 2012.
- Revision received February 8, 2012.
- Accepted February 9, 2012.
- American College of Cardiology Foundation
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