Display options
Share it on

Ann Vasc Dis. 2010;3(1):52-9. doi: 10.3400/avd.AVDoa09009. Epub 2010 Jul 21.

Plaque Tissue Components Obtained from De Novo Lesions may Predict Restenosis after Directional Coronary Atherectomy.

Annals of vascular diseases

Kentaro Arakawa, Hatsue Ishibashi-Ueda, Hiroyuki Hao, Yoshihiko Ikeda, Atsushi Kawamura

Affiliations

  1. Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Suita, Osaka, Japan.

PMID: 23555388 PMCID: PMC3595808 DOI: 10.3400/avd.AVDoa09009

Abstract

BACKGROUND: A part of coronary stenotic lesions treated with directional coronary atherectomy (DCA) occur restenosis several months later. Specimens obtained by first DCA, present the histology of culplit lesions and may predict restenosis after PCI.

METHODS: The study group comprised 76 patients (male/female 65/11, age 61 ± 11 years). Restenosis, defined as > 50% stenosis diameter by quantitative cineangiography, was present in 26 patients. The other 50 patients (< 50% stenosis) constitute the "no restenosis" group. Inflammatory cells and other atheroma components were planimetrically quantified as a percentage of total tissue area.

RESULTS: As regards lymphocytes, neutrophils and smooth muscle cells, the grade of amount of cells did not differ between restenosis group and no restenosis group. The amount of obtained arterial media was similar, too. However, the area occupied by macrophages or calcified fragments was significantly larger in restenosis group than no restenosis group. And there was a tendency toward larger area occupied by cholesterol gruel, thrombus and myxomatous extracellular matrix (ECM) in restenosis group.

CONCLUSION: Rich macrophages infiltration, calcified fragments, cholesterol rich gruel and myxomatous ECM from primary lesions can be predictors of restenosis after DCA, suggesting a possible role in restenotic process after PCI.

Keywords: atherosclerosis; directional coronary athelectomy; inflammation; percutaneous coronary intervention; restenosis

References

  1. Clin Invest Med. 1988 Feb;11(1):62-7 - PubMed
  2. J Am Coll Cardiol. 1991 Feb;17(2):442-8 - PubMed
  3. Circulation. 2004 Aug 24;110(8):940-7 - PubMed
  4. Circulation. 1992 Nov;86(5):1394-9 - PubMed
  5. Am Heart J. 1996 Aug;132(2 Pt 1):428-36 - PubMed
  6. Circulation. 1996 Jul 1;94(1):35-43 - PubMed
  7. J Am Coll Cardiol. 2001 Apr;37(5):1271-6 - PubMed
  8. Circ Res. 2004 May 14;94(9):1158-67 - PubMed
  9. Jpn Circ J. 1990 Jan;54(1):43-56 - PubMed
  10. Circulation. 1992 Dec;86(6 Suppl):III47-52 - PubMed
  11. Arterioscler Thromb Vasc Biol. 1996 Jan;16(1):28-33 - PubMed
  12. J Am Coll Cardiol. 1992 Nov 1;20(5):1284-93 - PubMed
  13. Circulation. 2000 Nov 14;102(20):2528-34 - PubMed
  14. Circulation. 1995 Aug 1;92(3):657-71 - PubMed
  15. Circ Res. 1995 Sep;77(3):445-65 - PubMed
  16. Circ Res. 1996 Jan;78(1):38-43 - PubMed
  17. Coron Artery Dis. 1996 Aug;7(8):573-7 - PubMed
  18. J Am Coll Cardiol. 1995 Feb;25(2):516-20 - PubMed
  19. J Am Coll Cardiol. 1992 Nov 1;20(5):1101-10 - PubMed
  20. Cardiology. 2003;100(2):80-5 - PubMed
  21. Am Heart J. 2002 Oct;144(4):702-9 - PubMed
  22. Circulation. 1995 Nov 15;92(10):2995-3005 - PubMed
  23. Am J Cardiol. 2003 Feb 1;91(3):287-92 - PubMed
  24. Circulation. 1996 Dec 15;94(12):3098-102 - PubMed
  25. Circulation. 1995 Mar 1;91(5):1397-402 - PubMed
  26. Arterioscler Thromb Vasc Biol. 2006 Feb;26(2):326-32 - PubMed
  27. Heart. 2003 Jul;89(7):773-9 - PubMed
  28. Circulation. 2004 Feb 10;109(5):634-40 - PubMed

Publication Types