Electron-microscopic findings after transmyocardial laser revascularization in an acute ischemic pig model.

OBJECTIVE The clinical benefit in terms of angina reduction after transmyocardial laser revascularization (TMLR) in patients with diffuse coronary artery disease who are not candidates for conventional procedures has been proved. The exact mechanisms of TMLR however, are still unknown. The aim of this study was to investigate the cellular changes in relation to intramyocardial partial oxygen pressure (ptiO2) after TMLR in a model of acute ischemia in pigs by electron microscopical methods (TEM). METHODS Seven pigs were included in this study (five animals with acute myocardial ischemia and additional TMLR and two animals with acute myocardial ischemia and without TMLR for control). Acute ischemia was induced by ligation of diagonal branches of the left anterior descending artery (LAD). Intramyocardial partial oxygen pressure was measured before induction of ischemia and thereafter continuously for up to 6 h in all animals. Biopsies of all animals were taken before induction of ischemia and thereafter at 30 min, 3 and 6 h. Analysis of the myocardial ultrastructure was focused on mitochondria, cell nucleus, T-tubules and myofibrils. RESULTS Ultrastructural changes were seen in all animals. At 6 h after induction of ischemia, mitochondria showed a destruction of the internal as well as the external membrane and of the cristae. The nuclei showed margination of the chromatin. Myofibrils were characterized by ruptures in the Z-stripes. Lipid droplets as an indicator of ischemia could be identified. PtiO2 between 40 and 80 mmHg before intervention decreased down to 0-2 mmHg within the first 9 min after diagonal branch ligation and did not increase even after TMLR. CONCLUSIONS In this acute ischemic model using pigs, TEM evaluation following TMLR proves irreversible changes of the myocardial ultrastructure. Furthermore, TMLR was not able to increase ischemically induced decrease of ptiO2. These data provide some evidence that TMLR thus, may not be able to ameliorate acute ischemia at least in the pig model. Further investigations are needed to investigate the effect of TMLR in chronic myocardial ischemia.