Chronic effects of transmyocardial laser revascularization in the nonischemic myocardium: a word of caution.
BACKGROUND
Transmyocardial laser revascularization (TMLR) has been shown to induce angiogenesis and improve regional myocardial blood flow. However, the biological response to laser of different energy doses in nonischemic myocardium has not been well studied. We study the time course of histological appearance following high- and low-energy TMLR in a rodent model of normal myocardium.


METHODS
The animals were randomized to two groups (high-energy (1.4 J/pulse) TMLR group and low-energy (0.6 J/ pulse) TMLR group). TMLR was applied to the anterolateral wall of the left ventricle. Then the animals were sacrificed (one every 2 or 3 days up to 6 weeks, then one every week) to give a series of hearts from 1 week to 12 weeks following TMLR.


RESULTS
No patent laser channels were identified. All laser channel remnants were composed of granulation tissue, fibrosis, and various amounts of vascular structures. Changes in vascular density demonstrated a similar pattern in both groups over time. The initial increase in vascular density within the laser channel remnants and the surrounding areas was more marked in group I than in group II. Gradual decline of vascular density occurred during a later follow-up. More fibrosis and less vasculature were demonstrated 12 weeks after laser therapy in group I.


CONCLUSIONS
Angiogenic response to the Holmium:YAG laser in the nonischemic myocardium is nonspecific and unsustainable. TMLR might chronically impair the myocardium function by enhancing regional scar formation. Therefore, we should clearly identify the ischemic area for laser therapy. Reduction of laser energy might prevent this potential complication.
Hubacek
Jaro
J
Department of Surgery, National University of Singapore, and National Heart Center, Singapore.
Sim
Eugene K W
EK
Zhang
Li
L
Shim
Winston S N
WS
D000818:Animals; D004195:Disease Models, Animal; D005355:Fibrosis; D005500:Follow-Up Studies; D053685:Laser Therapy; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000503:physiopathology / Q000601:surgery*; D009204:Myocardial Revascularization; D009206:Myocardium / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014654:Vascular Patency / Q000502:physiology