The new mapping method is highly accurate and reproducible. The ability to combine electrophysiological and spatial information provides a unique tool for both research and clinical electrophysiology. Consequently, the main shortcomings of conventional mapping-namely, prolonged x-ray exposure, low spatial resolution, and the inability to accurately navigate to a predefined site-can all be overcome with this new method.

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Background-Low-energy laser irradiation (LELI) has been found to attenuate various biological processes in tissue culture and experimental animal models. The aim of the present study was to investigate the effect of LELI on the formation of scar tissue in experimentally induced chronic infarct in rats and dogs. Methods and Results-Myocardial infarction (MI) was induced in 50 dogs and 26 rats by ligation of the left anterior descending coronary artery. After induction of MI, the laser-irradiated (LI) group received laser irradiation (infrared laser, 803-nm wavelength) epicardially. Control MI-induced non-laser irradiated (NLI) dogs were sham-operated, and laser was not applied. All dogs were euthanized at 5 to 6 weeks after MI. Infarct size was determined by TTC staining and histology. The laser treatment (PϽ0.05) lowered mortality significantly, from 30% to 6.5%, after induction of MI. The infarct size in the LI dogs was reduced significantly (PϽ0.0001) (52%) compared with NLI dogs. Histological observation of the infarct revealed a typical scar tissue in NLI dogs and cellularity in most of the LI dogs. Only 14Ϯ3% of the mitochondria in the cardiomyocytes in the ischemic zone (4 hours after MI) of LI MI-induced rats were severely damaged, compared with 36Ϯ1% in NLI rats. Accordingly, ATP content in that zone was 7.6-fold (significantly) higher in LI than in NLI rats. Conclusions-Our observations indicate that epicardial LELI of rat and dog hearts after chronic MI caused a marked reduction in infarct size, probably due to a cardioprotective effect of the LELI. Key Words: ischemia Ⅲ myocardial infarction Ⅲ antioxidants Ⅲ lasers T he approach to acute myocardial infarction (MI) has moved in the past decade from simple monitoring of coronary events to aggressive interventions in the processes underlying coronary thrombosis. Cardiac repair after infarct is a complex process involving diverse inflammatory components, extracellular matrix remodeling, and responses of the cardiomyocytes to the ischemia. 1,2 The sequential events that take place in the myocardium after occlusion of the left anterior descending coronary artery (LAD) in experimental animals (including dogs) have been well documented. 1,2 After necrosis of the cardiomyocytes and a rather long inflammatory phase, the ischemic zone is subsequently replaced by fibrotic tissue.Many studies have been directed toward the use of drugs, growth factors, and various interventional technologies in reducing myocardial infarct size and improvement of heart function after MI in experimental animals and humans. For example, recombinant adenovirus-mediated transfer of genes encoding antioxidants to the myocardium has been demonstrated to attenuate after ischemic dysfunction in neonatal mice. 3 Novel approaches to enhancing angiogenesis in the ischemic myocardium by introducing growth factors (mainly of the vascular endothelial growth factor family) were adapted and found to have a beneficial effect on patients with severe angina. 4 Low-energy laser irradiation (LELI) has b...

The results of the present study indicate that delivery of low-energy laser irradiation to infarcted myocardium in rats and dogs has a profound effect on the infarct size after MI.