1. Modification of Infarct Material Properties Limits Adverse Ventricular Remodeling 
Masato Morita, MD, Chad E. Eckert, PhD, Kanji Matsuzaki, MD, PhD, Mio Noma, MD, Liam P. Ryan, MD, Jason A. Burdick, PhD, Benjamin M. Jackson, MD, Joseph H. Gorman, MD, Michael S. Sacks, PhD, Robert C. Gorman, MD 
The Annals of Thoracic Surgery 
Volume 92, Issue 2, Pages (August 2011)
DOI: /j.athoracsur
Copyright © 2011 The Society of Thoracic Surgeons Terms and Conditions

2. Fig 1
A sheep heart as seen through a left thoracotomy (A) immediately after coronary ligation (note the discolored apical region in the area of the infarct) and (B) immediately after dermal filler injection.
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )
Copyright © 2011 The Society of Thoracic Surgeons Terms and Conditions

3. Fig 2
Representative 2-dimensional long-axis echocardiograms are shown in (A) diastole and (B) systole in representative (C) treatment and (D) control hearts 8 weeks after infarction. Note the preservation of the normal elliptical left ventricular (LV) shape in the treated heart and the nearly spherical shape of the control heart. The white arrows identify the radiopaque filler material in the apical region of the treated heart. (LA = left atrium.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )
Copyright © 2011 The Society of Thoracic Surgeons Terms and Conditions

4. Fig 3
Representative examples are shown of long-axis sections taken from sheep left ventricles to assess regional myocardial thickness. (A) A normal uninfarcted heart. (B) A treated heart 8 weeks after injection of the tissue filler materia. The black arrow indicates where thickness measurements were made. (C) Section from an untreated control heart 8 weeks after infarction. Note the preservation in thickness of the apical region in the treated heart and the profound thinning experienced in the untreated heart.
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )
Copyright © 2011 The Society of Thoracic Surgeons Terms and Conditions

5. Fig 4
Masson trichrome staining in representative (A and C) control animals and (B and D) treatment animals 8 weeks after infarction. Panels A and B are at original magnification ×1; panels B and D are at original magnification ×1.2. Notice the exuberant collagen production (blue) and lack of fat infiltration in the treated animal relative to control. The increase in collagen was responsible for most of the increased infarct thickness. At 8 weeks after infarction, the carrier gel of the tissue filler had been completely absorbed and a cellular (red) infiltrate was left surrounding the calcium hydroxyapatite microspheres.
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )
Copyright © 2011 The Society of Thoracic Surgeons Terms and Conditions

6. Fig 5
Results are shown of the mechanical testing of the infarct tissue. (A) Representative stress-strain plots are presented of specimens from both groups. (B) Peak strain and (C) peak strain energy are shown for all groups. Longitudinal peak strain (E11) and total strain energy were significantly less in the treatment group than in the controls. As with the mean peak strain data, the directional strain energies were isotropic in the treatment group and anisotropic in the control group. *p < 0.05 between group difference. (E22= circumferential strain; E12= longitudinal-circumferential shear strain.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )
Copyright © 2011 The Society of Thoracic Surgeons Terms and Conditions