Neovascularization after transmyocardial laser revascularization in a model of chronic ischemia

Background. The mechanism of clinical improvement after transmyocardial las er revascularization (TMR) is unknown. One hypothesis holds that TMR causes increased myocardial perfusion through neovascularization. This study soug ht to determine whether angiogenesis occurs after TMR in a porcine model of chronic myocardial ischemia. Methods. Six miniature pigs underwent subtotal left circumflex coronary art ery occlusion to reduce resting blood flow to 10% of baseline. After 2 week s in the low-flow state, dobutamine stress echocardiography and positron em ission tomography were performed to document ischemic, viable myocardium. T he animals then underwent TMR and were sacrificed 6 months later for histol ogic and immunohistochemical analysis. Results. Histologic analysis of the lased left circumflex region demonstrat ed many hypocellular areas filled with connective tissue representing remna nt TMR channels. Histochemical staining demonstrated a highly disorganized pattern of neovascularization consistent with angiogenesis located predomin antly at the periphery of the channels. Immunohistochemical analysis confir med the presence of endothelial cells within neovessels. Vascular density a nalysis 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 ischem ic myocardium. Conclusions. This study provides evidence that neovascularization is presen t long term in regions of ischemic, viable myocardium after TMR. Angiogenes is may represent the mechanism of clinical improvement after TMR. (C) 1998 by The Society of Thoracic Surgeons.