1. Promoting angiogenesis protects severely hypertrophied hearts from ischemic injury 
Ingeborg Friehs, MD, Adrian M Moran, MD, Christof Stamm, MD, Yeong-Hoon Choi, MD, Douglas B Cowan, PhD, Francis X McGowan, MD, Pedro J del Nido, MD 
The Annals of Thoracic Surgery 
Volume 77, Issue 6, Pages (June 2004)
DOI: /j.athoracsur

2. Fig 1
(A) Representative sections of control, untreated, and VEGF treated hypertrophied hearts perfused with FITC-labeled lectin. Myocytes stained in red with desmin and nuclei stained with DAPI in blue. (B) Cumulative data of all vessels identified by the computer image analyzer within a calibrated graticule of randomly selected fields are summarized (*p < 0.05; versus untreated hypertrophied hearts). (C) Number of microvessels detected after FITC-labeled lectin perfusion, expressed per number DAPI-stained nuclei (*p < 0.05; versus untreated hypertrophied hearts). □ = control; ■ = untreated hypertrophy; ▨ = VEGF treated hypertrophy. (DAPI = 4',6-diamidino-2-phenylindole; FITC = fluorescein-isothiocyanate-conjugated; VEGF = vascular endothelial growth factor.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )

3. Fig 2
Coronary flow rate adjusted to (A) gram of total heart weight and (B) gram of LV weight, respectively, is shown with solid bars for untreated hypertrophied hearts, striped bars for VEGF treated hypertrophied hearts, and open bars for controls (*p < 0.05; versus untreated hypertrophy). (LV = left ventricular; VEGF = vascular endothelial growth factor.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )

4. Fig 3
Glucose transport was improved reaching levels found in nonhypertrophied hearts following VEGF treatment (*p < 0.05 versus untreated hypertrophy). ♦ = untreated hypertrophy; ■ = VEGF treated hypertrophy. (VEGF = vascular endothelial growth factor.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )

5. Fig 4
Preischemic developed pressure, indicated by the open bars, and postischemic developed pressure, indicated by the solid bars, showed improved postischemic recovery of myocardial function in VEGF treated hypertrophied hearts compared to untreated hypertrophied hearts (*p < 0.001; versus preischemia; #p < 0.001; versus untreated hypertrophied hearts). (VEGF = vascular endothelial growth factor.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )

6. Fig 5
(A) This graph shows LV mass-to-cavity volume measurements as indicators of hypertrophic growth. The VEGF treated hearts maintained an increase in LV mass over an extended period of time beyond the time point when untreated hypertrophied hearts already showed severe signs of ventricular dilatation (*p < 0.01; for differences between both group and time influence). (B) Measurement of contractility, depicted as Z-scores (data calculated based on previous echocardiographic measurements of nonhypertrophied control hearts over time) indicates that VEGF treatment preserved contractile function within the normal range at week 6 (−0.08 ± 0.48), while contractility fell significantly at the same time period in untreated hypertrophied hearts (−1.39 ± 0.35; p = 0.004). ♦ = untreated hypertrophy; ■ = VEGF treated hypertrophy. (LV = left ventricular; VEGF = vascular endothelial growth factor.)
The Annals of Thoracic Surgery  , DOI: ( /j.athoracsur )