Transmyocardial Laser Revascularization (TMLR) is a new experimental method for relief of angina pectoris in patients with severe coronary artery disease. TMLR aims at revascularizing chronic hibernating myocardium by creating transmural channels. One of the working mechanism hypotheses is that the endocardial side of the channels remains open, enabling perfusion of the hibernating myocardium directly from the left ventricle. Although the working mechanism of TMLR is still unknown (perfusion through patent channels, induction of angiogenesis, relief of angina through destruction of sympatic innervation, others?), first clinical studies are successful. Currently, the Heart LaserTM and other CO2 lasers, XeCl Excimer laser and Ho:YAG laser are under investigation for TMLR. The initial attempts of TMR with needles were soon replaced by laser induced channels. Efforts were focused on developing a CO2 laser that could penetrate a beating heart during its relaxation phase. Later, the position of the beam could be fixed in the myocardial wall using lasers with fiber delivery systems and perforation was achieved within multiple cycles. Various researchers reported on both patent and non-patent channels after TMLR. Our belief is that the extent of laser induced thermal damage is one of the factors that determine the clinical outcome and the extent of angiogenesis (and, possibly, the patency of the channel). The purpose of this study is to present a simple theoretical model to predict the extent of thermal damage around a transmyocardial channel. In vitro experiments were performed on myocardial bovine tissue and damage was assessed. The results were used to determine the final parameters of the approximating theoretical equation. To evaluate our results, we compared our results to in vitro data using the Heart LaserTM from the literature. Ablation velocities were also measured and the results were compared to ablation velocity calculations using a model described by Ostegar et al.