open access

Vol 25, No 1 (2018)
Original articles — Interventional cardiology
Published online: 2017-10-18
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In-stent restenosis-prone coronary plaque composition: A retrospective virtual histology-intravascular ultrasound study

Duck-Jun Seo, Yong-Kyun Kim, Young-Hoon Seo, In-Geol Song, Ki-Hong Kim, Taek-Geun Kwon, Hyun-Woong Park, Jang-Ho Bae
DOI: 10.5603/CJ.a2017.0124
·
Pubmed: 29064537
·
Cardiol J 2018;25(1):7-13.

open access

Vol 25, No 1 (2018)
Original articles — Interventional cardiology
Published online: 2017-10-18

Abstract

Background: The mechanism of in-stent restenosis (ISR) is multifactorial, which includes biological, mechanical and technical factors. This study hypothesized that increased inflammatory reaction, which is known to be an important atherosclerotic process, at a culprit lesion may lead to higher restenosis rates.

Methods: The study population consisted of 241 patients who had undergone percutaneous coronary intervention with virtual histology-intravascular ultrasound (VH-IVUS) and a 9-month follow-up coronary angiography. Compared herein is the coronary plaque composition between patients with ISR and those without ISR.

Results: Patients with ISR (n = 27) were likely to be older (66.2 ± 9.5 years vs. 58.7 ± 11.7 years, p = 0.002) and have higher levels of high-sensitivity C-reactive protein (hs-CRP, 1.60 ± 3.59 mg/dL vs. 0.31 ± 0.76 mg/dL, p < 0.001) than those without ISR (n = 214). VH-IVUS examination showed that percent necrotic core volume (14.3 ± 8.7% vs. 19.5 ± 9.1%, p = 0.005) was higher in those without ISR than those with ISR. Multivariate analysis revealed that hs-CRP (odds ratio [OR] 3.334, 95% con­fidence interval [CI] 1.158–9.596, p = 0.026) and age (OR 3.557, 95% CI 1.242–10.192, p = 0.018) were associated with ISR.

Conclusions: This study suggests that ISR is not associated with baseline coronary plaque composition but is associated with old age and increased expression of the inflammatory marker of hs-CRP. (Cardiol J 2018; 25, 1: 7–13)

Abstract

Background: The mechanism of in-stent restenosis (ISR) is multifactorial, which includes biological, mechanical and technical factors. This study hypothesized that increased inflammatory reaction, which is known to be an important atherosclerotic process, at a culprit lesion may lead to higher restenosis rates.

Methods: The study population consisted of 241 patients who had undergone percutaneous coronary intervention with virtual histology-intravascular ultrasound (VH-IVUS) and a 9-month follow-up coronary angiography. Compared herein is the coronary plaque composition between patients with ISR and those without ISR.

Results: Patients with ISR (n = 27) were likely to be older (66.2 ± 9.5 years vs. 58.7 ± 11.7 years, p = 0.002) and have higher levels of high-sensitivity C-reactive protein (hs-CRP, 1.60 ± 3.59 mg/dL vs. 0.31 ± 0.76 mg/dL, p < 0.001) than those without ISR (n = 214). VH-IVUS examination showed that percent necrotic core volume (14.3 ± 8.7% vs. 19.5 ± 9.1%, p = 0.005) was higher in those without ISR than those with ISR. Multivariate analysis revealed that hs-CRP (odds ratio [OR] 3.334, 95% con­fidence interval [CI] 1.158–9.596, p = 0.026) and age (OR 3.557, 95% CI 1.242–10.192, p = 0.018) were associated with ISR.

Conclusions: This study suggests that ISR is not associated with baseline coronary plaque composition but is associated with old age and increased expression of the inflammatory marker of hs-CRP. (Cardiol J 2018; 25, 1: 7–13)

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Keywords

intravascular ultrasonography, coronary artery disease, myocardial ischemia, inflammation, coronary stenosis

About this article
Title

In-stent restenosis-prone coronary plaque composition: A retrospective virtual histology-intravascular ultrasound study

Journal

Cardiology Journal

Issue

Vol 25, No 1 (2018)

Pages

7-13

Published online

2017-10-18

DOI

10.5603/CJ.a2017.0124

Pubmed

29064537

Bibliographic record

Cardiol J 2018;25(1):7-13.

Keywords

intravascular ultrasonography
coronary artery disease
myocardial ischemia
inflammation
coronary stenosis

Authors

Duck-Jun Seo
Yong-Kyun Kim
Young-Hoon Seo
In-Geol Song
Ki-Hong Kim
Taek-Geun Kwon
Hyun-Woong Park
Jang-Ho Bae

References (20)
  1. Moses JW, Leon MB, Popma JJ, et al. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med. 2003; 349(14): 1315–1323.
  2. Stettler C, Wandel S, Allemann S, et al. Outcomes associated with drug-eluting and bare-metal stents: a collaborative network meta-analysis. Lancet. 2007; 370(9591): 937–948.
  3. Sabaté M, Jiménez-Quevedo P, Angiolillo DJ, et al. DIABETES Investigators. Randomized comparison of sirolimus-eluting stent versus standard stent for percutaneous coronary revascularization in diabetic patients: the diabetes and sirolimus-eluting stent (DIABETES) trial. Circulation. 2005; 112(14): 2175–2183.
  4. Stone GW, Ellis SG, Cannon L, et al. Comparison of a polymer-based paclitaxel-eluting stent with a bare metal stent in patients with complex coronary artery disease: a randomized controlled trial. JAMA. 2005; 294(10): 1215–1223.
  5. Cosgrave J, Agostoni P, Ge L, et al. Clinical outcome following aleatory implantation of paclitaxel-eluting or sirolimus-eluting stents in complex coronary lesions. Am J Cardiol. 2005; 96(12): 1663–1668.
  6. Dangas GD, Claessen BE, Caixeta A, et al. In-stent restenosis in the drug-eluting stent era. J Am Coll Cardiol. 2010; 56(23): 1897–1907.
  7. Costa MA, Simon DI. Molecular basis of restenosis and drug-eluting stents. Circulation. 2005; 111(17): 2257–2273.
  8. Rogers C, Welt FG, Karnovsky MJ, et al. Monocyte recruitment and neointimal hyperplasia in rabbits. Coupled inhibitory effects of heparin. Arterioscler Thromb Vasc Biol. 1996; 16(10): 1312–1318.
  9. Teirstein PS, Massullo V, Jani S, et al. Catheter-based radiotherapy to inhibit restenosis after coronary stenting. N Engl J Med. 1997; 336(24): 1697–1703.
  10. Stone GW, Kandzari DE, Mehran R, et al. Percutaneous recanalization of chronically occluded coronary arteries: a consensus document: part I. Circulation. 2005; 112(15): 2364–2372.
  11. Mintz GS, Nissen SE, Anderson WD, et al. American College of Cardiology Clinical Expert Consensus Document on Standards for Acquisition, Measurement and Reporting of Intravascular Ultrasound Studies (IVUS). A report of the American College of Cardiology Task Force on Clinical Expert Consensus Documents. J Am Coll Cardiol. 2001; 37(5): 1478–1492.
  12. Lee CS, Seo YH, Yang DJu, et al. Positive Vascular Remodeling in Culprit Coronary Lesion is Associated With Plaque Composition: An Intravascular Ultrasound-Virtual Histology Study. Korean Circ J. 2012; 42(11): 747–752.
  13. Sakakura K, Nakano M, Otsuka F, et al. Comparison of pathology of chronic total occlusion with and without coronary artery bypass graft. Eur Heart J. 2014; 35(25): 1683–1693.
  14. Karas SP, Gravanis MB, Santoian EC, et al. Coronary intimal proliferation after balloon injury and stenting in swine: an animal model of restenosis. J Am Coll Cardiol. 1992; 20(2): 467–474.
  15. Toutouzas K, Colombo A, Stefanadis C. Inflammation and restenosis after percutaneous coronary interventions. Eur Heart J. 2004; 25(19): 1679–1687.
  16. Meuwissen M, Piek JJ, van der Wal AC, et al. Recurrent unstable angina after directional coronary atherectomy is related to the extent of initial coronary plaque inflammation. J Am Coll Cardiol. 2001; 37(5): 1271–1276.
  17. Libby P. Inflammation in Atherosclerosis. Arterioscler Thromb Vasc Biol. 2012; 32(9): 2045–2051.
  18. De Gregorio J, Kobayashi Y, Albiero R, et al. Coronary artery stenting in the elderly: short-term outcome and long-term angiographic and clinical follow-up. J Am Coll Cardiol. 1998; 32(3): 577–583.
  19. Liuzzo G, Buffon A, Biasucci LM, et al. Enhanced inflammatory response to coronary angioplasty in patients with severe unstable angina. Circulation. 1998; 98(22): 2370–2376.
  20. Lasave LI, Abizaid AAC, Paiva e Maia J, et al. [Relationship between plasma C-reactive protein level and neointimal hyperplasia volume in patients with zotarolimus-eluting stents. Volumetric analysis by three-dimensional intracoronary ultrasound]. Rev Esp Cardiol. 2007; 60(9): 923–931.

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