Coronary artery disease, which may lead to myocardial infarction (MI), is the primary cause of mortality world-wide. In a series of studies in which the rat and canine models were used, the effect of LLLT on infarct size after chronic myocardial infarction in rats was investigated. LLLT caused a profound (50-70%) reduction in infarct size and ventricular dilatation in the rat heart after chronic MI. This phenomenon was achieved by the cardioprotective effect of LLLT on mitochondria, elevation of cytoprotective heat shock proteins and enhanced angiogenesis in the myocardium following laser irradiation. The effect of LLLT on the expression of vascular endothelial growth factor (VEGF) and inducible nitric oxide synthase (iNOS) in the infarcted heart was also investigated. It was found that VGEF and iNOS expression in the infarcted rat heart is markedly upregulated by LLLT and is associated with enhanced angiogenesis and cardioprotection. The possible beneficial effects on implantation of autologeous mesenchymal stem cells (MSCs) that had been laser irradiated prior to their implantation into the infarcted rat heart was also investigated. These findings provided the first evidence that LLLT can significantly increase survival and/or proliferation of MSCs post implanation into the ischemic/ infarcted heart, followed by a marked reduction of scarring, and enhanced angiogenesis. The results of the animal studies may also have clinical relevance. It can be postulated that the use of laser following MI is most probably safe and our observations indicate that delivery of laser energy to the heart may have an important beneficial effect on patients after acute MI or ischemic heart conditions.