We sought to determine the effect of acidic fibroblast growth factor (aFGF) on ischemic and normal myocardium, and to determine whether direct application of aFGF to the heart could promote angiogenesis. Dogs underwent placement of an ameroid constrictor on the left anterior descending coronary artery (LAD). Three weeks later, a left internal mammary artery pedicle (IMA) was positioned over the LAD territory. A gortex or collagen I sponge saturated with aFGF (N=12) or saline (N=4) was interposed between the pedicle and the heart. Weekly angiography of the IMA was performed in all dogs, but significant IMA to coronary collaterals were not demonstrable in any dog. Eight dogs had histologic evidence of non-transmural infarction in the LAD territory (5 aFGF, 3 control). Striking smooth muscle cell (SMC) hyperplasia was present in arterioles and small arteries exclusively in areas of subendocardial infarction in all of the aFGF-treated dogs but in none of the control dogs (p<0.05). Non-infarcted myocardium appeared normal in all dogs. Two additional dogs received a similar aFGF-sponge but no ameroid; no pathology was seen. Thus, aFGF appears to stimulate SMC hyperplasia in areas subjected to infarction. Both injury and exposure to aFGF may be required to cause vascular SMC proliferation in the heart.
