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Ann Thorac Surg 1998;66:2029-2036
© 1998 The Society of Thoracic Surgeons


Original Articles

Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia

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

a Department of Surgery, Duke University Medical Center, Durham, North Carolina, USA
b Divisions of Cardiology, Duke University Medical Center, Durham, North Carolina, USA
c Department of Radiology, Duke University Medical Center, Durham, North Carolina, USA

Accepted for publication June 9, 1998.

Address reprint requests to Dr Landolfo, Duke University Medical Center, Box 3857, Durham, NC 27710
e-mail: Land001{at}mc.duke.edu

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.




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