Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia

G. Chad Hughes, James E. Lowe, Alan P. Kypson, James D. St Louis, Anne M. Pippen, Kevin G. Peters, R. Edward Coleman, Timothy R DeGrado, Carolyn L. Donovan, Brian H. Annex, Kevin P. Landolfo

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

Background. The mechanism of clinical improvement after transmyocardial laser revascularization (TMR) is unknown. One hypothesis holds that TMR causes increased myocardial perfusion through neovascularization. This study sought to determine whether angiogenesis occurs after TMR in a porcine model of chronic myocardial ischemia. Methods. Six miniature pigs underwent subtotal left circumflex coronary artery occlusion to reduce resting blood flow to 10% of baseline. After 2 weeks in the low-flow state, dobutamine stress echocardiography and positron emission tomography were performed to document ischemic, viable myocardium. The animals then underwent TMR and were sacrificed 6 months later for histologic and immunohistochemical analysis. Results. Histologic analysis of the lased left circumflex region demonstrated many hypocellular areas filled with connective tissue representing remnant TMR channels. Histochemical staining demonstrated a highly disorganized pattern of neovascularization consistent with angiogenesis located predominantly at the periphery of the channels. Immunohistochemical analysis confirmed the presence of endothelial cells within neovessels. Vascular density analysis revealed a mean of 29.2 ± 3.6 neovessels per high-power field in lased ischemic myocardium versus 4.0 ± 0.3 (p < 0.001) in nonlased ischemic myocardium. Conclusions. This study provides evidence that neovascularization is present long term in regions of ischemic, viable myocardium after TMR. Angiogenesis may represent the mechanism of clinical improvement after TMR.

Original languageEnglish (US)
Pages (from-to)2029-2036
Number of pages8
JournalAnnals of Thoracic Surgery
Volume66
Issue number6
DOIs
StatePublished - 1998
Externally publishedYes

Fingerprint

Transmyocardial Laser Revascularization
Ischemia
Myocardium
Swine
Stress Echocardiography
Coronary Occlusion
Positron-Emission Tomography
Connective Tissue
Myocardial Ischemia
Blood Vessels
Coronary Vessels
Endothelial Cells
Perfusion
Staining and Labeling

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Hughes, G. C., Lowe, J. E., Kypson, A. P., St Louis, J. D., Pippen, A. M., Peters, K. G., ... Landolfo, K. P. (1998). Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia. Annals of Thoracic Surgery, 66(6), 2029-2036. https://doi.org/10.1016/S0003-4975(98)01095-9

Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia. / Hughes, G. Chad; Lowe, James E.; Kypson, Alan P.; St Louis, James D.; Pippen, Anne M.; Peters, Kevin G.; Coleman, R. Edward; DeGrado, Timothy R; Donovan, Carolyn L.; Annex, Brian H.; Landolfo, Kevin P.

In: Annals of Thoracic Surgery, Vol. 66, No. 6, 1998, p. 2029-2036.

Research output: Contribution to journalArticle

Hughes, GC, Lowe, JE, Kypson, AP, St Louis, JD, Pippen, AM, Peters, KG, Coleman, RE, DeGrado, TR, Donovan, CL, Annex, BH & Landolfo, KP 1998, 'Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia', Annals of Thoracic Surgery, vol. 66, no. 6, pp. 2029-2036. https://doi.org/10.1016/S0003-4975(98)01095-9
Hughes, G. Chad ; Lowe, James E. ; Kypson, Alan P. ; St Louis, James D. ; Pippen, Anne M. ; Peters, Kevin G. ; Coleman, R. Edward ; DeGrado, Timothy R ; Donovan, Carolyn L. ; Annex, Brian H. ; Landolfo, Kevin P. / Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia. In: Annals of Thoracic Surgery. 1998 ; Vol. 66, No. 6. pp. 2029-2036.
@article{d4e9c5e8fd624653a765217865284821,
title = "Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia",
abstract = "Background. The mechanism of clinical improvement after transmyocardial laser revascularization (TMR) is unknown. One hypothesis holds that TMR causes increased myocardial perfusion through neovascularization. This study sought to determine whether angiogenesis occurs after TMR in a porcine model of chronic myocardial ischemia. Methods. Six miniature pigs underwent subtotal left circumflex coronary artery occlusion to reduce resting blood flow to 10{\%} of baseline. After 2 weeks in the low-flow state, dobutamine stress echocardiography and positron emission tomography were performed to document ischemic, viable myocardium. The animals then underwent TMR and were sacrificed 6 months later for histologic and immunohistochemical analysis. Results. Histologic analysis of the lased left circumflex region demonstrated many hypocellular areas filled with connective tissue representing remnant TMR channels. Histochemical staining demonstrated a highly disorganized pattern of neovascularization consistent with angiogenesis located predominantly at the periphery of the channels. Immunohistochemical analysis confirmed the presence of endothelial cells within neovessels. Vascular density analysis revealed a mean of 29.2 ± 3.6 neovessels per high-power field in lased ischemic myocardium versus 4.0 ± 0.3 (p < 0.001) in nonlased ischemic myocardium. Conclusions. This study provides evidence that neovascularization is present long term in regions of ischemic, viable myocardium after TMR. Angiogenesis may represent the mechanism of clinical improvement after TMR.",
author = "Hughes, {G. Chad} and Lowe, {James E.} and Kypson, {Alan P.} and {St Louis}, {James D.} and Pippen, {Anne M.} and Peters, {Kevin G.} and Coleman, {R. Edward} and DeGrado, {Timothy R} and Donovan, {Carolyn L.} and Annex, {Brian H.} and Landolfo, {Kevin P.}",
year = "1998",
doi = "10.1016/S0003-4975(98)01095-9",
language = "English (US)",
volume = "66",
pages = "2029--2036",
journal = "Annals of Thoracic Surgery",
issn = "0003-4975",
publisher = "Elsevier USA",
number = "6",

}

TY - JOUR

T1 - Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia

AU - Hughes, G. Chad

AU - Lowe, James E.

AU - Kypson, Alan P.

AU - St Louis, James D.

AU - Pippen, Anne M.

AU - Peters, Kevin G.

AU - Coleman, R. Edward

AU - DeGrado, Timothy R

AU - Donovan, Carolyn L.

AU - Annex, Brian H.

AU - Landolfo, Kevin P.

PY - 1998

Y1 - 1998

N2 - Background. The mechanism of clinical improvement after transmyocardial laser revascularization (TMR) is unknown. One hypothesis holds that TMR causes increased myocardial perfusion through neovascularization. This study sought to determine whether angiogenesis occurs after TMR in a porcine model of chronic myocardial ischemia. Methods. Six miniature pigs underwent subtotal left circumflex coronary artery occlusion to reduce resting blood flow to 10% of baseline. After 2 weeks in the low-flow state, dobutamine stress echocardiography and positron emission tomography were performed to document ischemic, viable myocardium. The animals then underwent TMR and were sacrificed 6 months later for histologic and immunohistochemical analysis. Results. Histologic analysis of the lased left circumflex region demonstrated many hypocellular areas filled with connective tissue representing remnant TMR channels. Histochemical staining demonstrated a highly disorganized pattern of neovascularization consistent with angiogenesis located predominantly at the periphery of the channels. Immunohistochemical analysis confirmed the presence of endothelial cells within neovessels. Vascular density analysis revealed a mean of 29.2 ± 3.6 neovessels per high-power field in lased ischemic myocardium versus 4.0 ± 0.3 (p < 0.001) in nonlased ischemic myocardium. Conclusions. This study provides evidence that neovascularization is present long term in regions of ischemic, viable myocardium after TMR. Angiogenesis may represent the mechanism of clinical improvement after TMR.

AB - Background. The mechanism of clinical improvement after transmyocardial laser revascularization (TMR) is unknown. One hypothesis holds that TMR causes increased myocardial perfusion through neovascularization. This study sought to determine whether angiogenesis occurs after TMR in a porcine model of chronic myocardial ischemia. Methods. Six miniature pigs underwent subtotal left circumflex coronary artery occlusion to reduce resting blood flow to 10% of baseline. After 2 weeks in the low-flow state, dobutamine stress echocardiography and positron emission tomography were performed to document ischemic, viable myocardium. The animals then underwent TMR and were sacrificed 6 months later for histologic and immunohistochemical analysis. Results. Histologic analysis of the lased left circumflex region demonstrated many hypocellular areas filled with connective tissue representing remnant TMR channels. Histochemical staining demonstrated a highly disorganized pattern of neovascularization consistent with angiogenesis located predominantly at the periphery of the channels. Immunohistochemical analysis confirmed the presence of endothelial cells within neovessels. Vascular density analysis revealed a mean of 29.2 ± 3.6 neovessels per high-power field in lased ischemic myocardium versus 4.0 ± 0.3 (p < 0.001) in nonlased ischemic myocardium. Conclusions. This study provides evidence that neovascularization is present long term in regions of ischemic, viable myocardium after TMR. Angiogenesis may represent the mechanism of clinical improvement after TMR.

UR - http://www.scopus.com/inward/record.url?scp=0032459865&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032459865&partnerID=8YFLogxK

U2 - 10.1016/S0003-4975(98)01095-9

DO - 10.1016/S0003-4975(98)01095-9

M3 - Article

C2 - 9930489

AN - SCOPUS:0032459865

VL - 66

SP - 2029

EP - 2036

JO - Annals of Thoracic Surgery

JF - Annals of Thoracic Surgery

SN - 0003-4975

IS - 6

ER -