1. Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia 
G.Chad Hughes, MD, James E Lowe, MD, Alan P Kypson, MD, James D St. Louis, MD, Anne M Pippen, Kevin G Peters, MD, R.Edward Coleman, MD, Timothy R DeGrado, PhD, Carolyn L Donovan, MD, Brian H Annex, MD, Kevin P Landolfo, MD 
The Annals of Thoracic Surgery 
Volume 66, Issue 6, Pages (December 1998)
DOI: /S (98)

2. Fig 1
Representative positron emission tomographic nitrogen 13 (13NH3) ammonia perfusion scan on the left demonstrating a flow defect in the lateral and posteroinferior walls of the left ventricle as seen on the short-axis view. The image was generated from emission data acquired over the interval 5 to 15 minutes after injection. Corresponding fluorine 18 fluorodeoxyglucose (18F-FDG) uptake scan is seen on the right, showing a relative increase in glucose utilization in the region of the flow defect consistent with preserved myocardial viability. The image was generated from emission data acquired over the interval 40 to 60 minutes after injection.
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

3. Fig 2
(A) Hematoxylin and eosin stain (×100 before 54% reduction) of a transmyocardial laser revascularization (TMR) channel sectioned longitudinally shows a hypocellular region representing the channel remnant at 6 months after TMR. (B) Masson trichrome staining (×100 before 54% reduction) showing a hypocellular TMR channel remnant filled with blue-staining connective tissue.
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

4. Fig 3
(A) Longitudinal section of a transmyocardial laser revascularization channel stained using anti–human tie-2 (×100 before 54% reduction), an antibody specific for the soluble extracellular domain of the TEK protein, a receptor tyrosine kinase expressed exclusively in endothelial cells. Note the numerous red-staining blood vessels seen within the channel remnant. Boxed region is shown in B. (B) Higher magnification (×330 before 54% reduction) of the region outlined in A, again demonstrating the immunostaining (antigen appears red) of endothelial cells in the walls of the neovessels.
The Annals of Thoracic Surgery  , DOI: ( /S (98) )

5. Fig 4
Anti–smooth muscle actin (HHF-35) staining (×40 before 54% reduction) of (A) numerous red-staining neovessels within a transmyocardial laser revascularization (TMR) channel and (B) normal penetrating intramyocardial vessels (arrows). Note relatively increased HHF-35 staining of neovessels versus normal vessels. Anti–collagen IV staining (×200 before 54% reduction) of (C) neovessel (arrow) at periphery of TMR channel and (D) normal penetrating vessels (arrows). Note relatively decreased collagen IV staining of neovessel versus normal vessels.
The Annals of Thoracic Surgery  , DOI: ( /S (98) )