Relation of internal elastic lamellar layer disruption to neointimal cellular proliferation and type III collagen deposition in human peripheral artery restenosis

Prakash Krishnan, K. Raman Purushothaman, Meerarani Purushothaman, Usman Baber, Arthur Tarricone, Miguel Vasquez, Jose M. Wiley, Annapoorna Kini, Samin K. Sharma, William N. O'Connor, Pedro R. Moreno

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Smooth muscle cell proliferation and extracellular matrix formation are responsible for disease progression in de novo and restenotic atherosclerosis. Internal elastic lamella (IEL) layer maintains the structural integrity of intima, and disruption of IEL may be associated with alterations in neointima, type III collagen deposition, and lesion progression in restenosis. Nineteen restenotic plaques (12 patients) procured during peripheral interventions were compared with 13 control plaques (12 patients) without restenosis. Hematoxylin & Eosin and elastic trichrome stains were used to measure length and percentage of IEL disruption, cellularity, and inflammation score. Type I and III collagens, smooth muscle cell (smc), fibroblast density, and nuclear proliferation (Ki67) percentage were evaluated by immunohistochemistry. IEL disruption percentage (28 ± 3.6 vs 6.1 ± 2.4; p = 0.0006), type III collagen content (0.33 ± 0.06 vs 0.17 ± 0.07; p = 0.0001), smc density (2014 ± 120 vs 923 ± 150; p = 0.0001), fibroblast density (2,282 ± 297 vs 906 ± 138; p = 0.0001), and Ki67 percentage (21.6 ± 2 vs 8.2 ± 0.65; p = 0.0001) were significantly increased in restenotic plaques compared to de novo plaques. Logistic regression analysis identified significant correlation between IEL disruption and neointimal smc density (r = 0.45; p = 0.01) and with type III collagen deposition (r = 0.61; p = 0.02) in restenosis. Increased IEL disruption may trigger cellular proliferation, altering collagen production, and enhancing restenotic neointima. In conclusion, understanding the pathologic and molecular basis of restenosis and meticulous-guided interventions oriented to minimize IEL damage may aid to reduce neointimal proliferation and the occurrence of restenosis.

Original languageEnglish (US)
Pages (from-to)1173-1179
Number of pages7
JournalAmerican Journal of Cardiology
Volume117
Issue number7
DOIs
StatePublished - Apr 1 2016
Externally publishedYes

Fingerprint

Collagen Type III
Smooth Muscle Myocytes
Arteries
Cell Proliferation
Neointima
Cell Count
Fibroblasts
Hematoxylin
Eosine Yellowish-(YS)
Collagen Type I
Extracellular Matrix
Disease Progression
Atherosclerosis
Collagen
Logistic Models
Immunohistochemistry
Regression Analysis
Inflammation

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Medicine(all)

Cite this

Relation of internal elastic lamellar layer disruption to neointimal cellular proliferation and type III collagen deposition in human peripheral artery restenosis. / Krishnan, Prakash; Purushothaman, K. Raman; Purushothaman, Meerarani; Baber, Usman; Tarricone, Arthur; Vasquez, Miguel; Wiley, Jose M.; Kini, Annapoorna; Sharma, Samin K.; O'Connor, William N.; Moreno, Pedro R.

In: American Journal of Cardiology, Vol. 117, No. 7, 01.04.2016, p. 1173-1179.

Research output: Contribution to journalArticle

Krishnan, P, Purushothaman, KR, Purushothaman, M, Baber, U, Tarricone, A, Vasquez, M, Wiley, JM, Kini, A, Sharma, SK, O'Connor, WN & Moreno, PR 2016, 'Relation of internal elastic lamellar layer disruption to neointimal cellular proliferation and type III collagen deposition in human peripheral artery restenosis', American Journal of Cardiology, vol. 117, no. 7, pp. 1173-1179. https://doi.org/10.1016/j.amjcard.2016.01.006
Krishnan, Prakash ; Purushothaman, K. Raman ; Purushothaman, Meerarani ; Baber, Usman ; Tarricone, Arthur ; Vasquez, Miguel ; Wiley, Jose M. ; Kini, Annapoorna ; Sharma, Samin K. ; O'Connor, William N. ; Moreno, Pedro R. / Relation of internal elastic lamellar layer disruption to neointimal cellular proliferation and type III collagen deposition in human peripheral artery restenosis. In: American Journal of Cardiology. 2016 ; Vol. 117, No. 7. pp. 1173-1179.
@article{a1cd8bdf34dc40e789e74d5bcda62a55,
title = "Relation of internal elastic lamellar layer disruption to neointimal cellular proliferation and type III collagen deposition in human peripheral artery restenosis",
abstract = "Smooth muscle cell proliferation and extracellular matrix formation are responsible for disease progression in de novo and restenotic atherosclerosis. Internal elastic lamella (IEL) layer maintains the structural integrity of intima, and disruption of IEL may be associated with alterations in neointima, type III collagen deposition, and lesion progression in restenosis. Nineteen restenotic plaques (12 patients) procured during peripheral interventions were compared with 13 control plaques (12 patients) without restenosis. Hematoxylin & Eosin and elastic trichrome stains were used to measure length and percentage of IEL disruption, cellularity, and inflammation score. Type I and III collagens, smooth muscle cell (smc), fibroblast density, and nuclear proliferation (Ki67) percentage were evaluated by immunohistochemistry. IEL disruption percentage (28 ± 3.6 vs 6.1 ± 2.4; p = 0.0006), type III collagen content (0.33 ± 0.06 vs 0.17 ± 0.07; p = 0.0001), smc density (2014 ± 120 vs 923 ± 150; p = 0.0001), fibroblast density (2,282 ± 297 vs 906 ± 138; p = 0.0001), and Ki67 percentage (21.6 ± 2 vs 8.2 ± 0.65; p = 0.0001) were significantly increased in restenotic plaques compared to de novo plaques. Logistic regression analysis identified significant correlation between IEL disruption and neointimal smc density (r = 0.45; p = 0.01) and with type III collagen deposition (r = 0.61; p = 0.02) in restenosis. Increased IEL disruption may trigger cellular proliferation, altering collagen production, and enhancing restenotic neointima. In conclusion, understanding the pathologic and molecular basis of restenosis and meticulous-guided interventions oriented to minimize IEL damage may aid to reduce neointimal proliferation and the occurrence of restenosis.",
author = "Prakash Krishnan and Purushothaman, {K. Raman} and Meerarani Purushothaman and Usman Baber and Arthur Tarricone and Miguel Vasquez and Wiley, {Jose M.} and Annapoorna Kini and Sharma, {Samin K.} and O'Connor, {William N.} and Moreno, {Pedro R.}",
year = "2016",
month = "4",
day = "1",
doi = "10.1016/j.amjcard.2016.01.006",
language = "English (US)",
volume = "117",
pages = "1173--1179",
journal = "American Journal of Cardiology",
issn = "0002-9149",
publisher = "Elsevier Inc.",
number = "7",

}

TY - JOUR

T1 - Relation of internal elastic lamellar layer disruption to neointimal cellular proliferation and type III collagen deposition in human peripheral artery restenosis

AU - Krishnan, Prakash

AU - Purushothaman, K. Raman

AU - Purushothaman, Meerarani

AU - Baber, Usman

AU - Tarricone, Arthur

AU - Vasquez, Miguel

AU - Wiley, Jose M.

AU - Kini, Annapoorna

AU - Sharma, Samin K.

AU - O'Connor, William N.

AU - Moreno, Pedro R.

PY - 2016/4/1

Y1 - 2016/4/1

N2 - Smooth muscle cell proliferation and extracellular matrix formation are responsible for disease progression in de novo and restenotic atherosclerosis. Internal elastic lamella (IEL) layer maintains the structural integrity of intima, and disruption of IEL may be associated with alterations in neointima, type III collagen deposition, and lesion progression in restenosis. Nineteen restenotic plaques (12 patients) procured during peripheral interventions were compared with 13 control plaques (12 patients) without restenosis. Hematoxylin & Eosin and elastic trichrome stains were used to measure length and percentage of IEL disruption, cellularity, and inflammation score. Type I and III collagens, smooth muscle cell (smc), fibroblast density, and nuclear proliferation (Ki67) percentage were evaluated by immunohistochemistry. IEL disruption percentage (28 ± 3.6 vs 6.1 ± 2.4; p = 0.0006), type III collagen content (0.33 ± 0.06 vs 0.17 ± 0.07; p = 0.0001), smc density (2014 ± 120 vs 923 ± 150; p = 0.0001), fibroblast density (2,282 ± 297 vs 906 ± 138; p = 0.0001), and Ki67 percentage (21.6 ± 2 vs 8.2 ± 0.65; p = 0.0001) were significantly increased in restenotic plaques compared to de novo plaques. Logistic regression analysis identified significant correlation between IEL disruption and neointimal smc density (r = 0.45; p = 0.01) and with type III collagen deposition (r = 0.61; p = 0.02) in restenosis. Increased IEL disruption may trigger cellular proliferation, altering collagen production, and enhancing restenotic neointima. In conclusion, understanding the pathologic and molecular basis of restenosis and meticulous-guided interventions oriented to minimize IEL damage may aid to reduce neointimal proliferation and the occurrence of restenosis.

AB - Smooth muscle cell proliferation and extracellular matrix formation are responsible for disease progression in de novo and restenotic atherosclerosis. Internal elastic lamella (IEL) layer maintains the structural integrity of intima, and disruption of IEL may be associated with alterations in neointima, type III collagen deposition, and lesion progression in restenosis. Nineteen restenotic plaques (12 patients) procured during peripheral interventions were compared with 13 control plaques (12 patients) without restenosis. Hematoxylin & Eosin and elastic trichrome stains were used to measure length and percentage of IEL disruption, cellularity, and inflammation score. Type I and III collagens, smooth muscle cell (smc), fibroblast density, and nuclear proliferation (Ki67) percentage were evaluated by immunohistochemistry. IEL disruption percentage (28 ± 3.6 vs 6.1 ± 2.4; p = 0.0006), type III collagen content (0.33 ± 0.06 vs 0.17 ± 0.07; p = 0.0001), smc density (2014 ± 120 vs 923 ± 150; p = 0.0001), fibroblast density (2,282 ± 297 vs 906 ± 138; p = 0.0001), and Ki67 percentage (21.6 ± 2 vs 8.2 ± 0.65; p = 0.0001) were significantly increased in restenotic plaques compared to de novo plaques. Logistic regression analysis identified significant correlation between IEL disruption and neointimal smc density (r = 0.45; p = 0.01) and with type III collagen deposition (r = 0.61; p = 0.02) in restenosis. Increased IEL disruption may trigger cellular proliferation, altering collagen production, and enhancing restenotic neointima. In conclusion, understanding the pathologic and molecular basis of restenosis and meticulous-guided interventions oriented to minimize IEL damage may aid to reduce neointimal proliferation and the occurrence of restenosis.

UR - http://www.scopus.com/inward/record.url?scp=84961869691&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84961869691&partnerID=8YFLogxK

U2 - 10.1016/j.amjcard.2016.01.006

DO - 10.1016/j.amjcard.2016.01.006

M3 - Article

C2 - 26857165

AN - SCOPUS:84961869691

VL - 117

SP - 1173

EP - 1179

JO - American Journal of Cardiology

JF - American Journal of Cardiology

SN - 0002-9149

IS - 7

ER -