[Mechanism of percutaneous myocardial laser revascularization in the treatment of experimental cardiac ischemia].

OBJECTIVE

To evaluate the cardiac angiogenesis after percutaneous myocardial laser revascularization (PMR).

METHODS

The left anterior descending coronary arteries of 10 healthy mongrel dogs weighing 14 - 18 kg were ligated partially so as to construct a model of chronic cardiac ischemia. Then the dogs were randomly divided into 2 groups of 5 dogs: PMR and control groups. Cardiogenesis Holmium: YAG laser system was used to make endomyocardial channels (15 +/- 3 channels/dog) in the ischemic ventricular walls in PMR group 2 weeks after the ligation. Sham procedure was conducted on the control group. Myocardial perfusion was examined by single photon emission computed tomography (SPECT) and left ventricle ejection fraction (LVEF) was examined by cardiac ultrasound before the ligation and 1, 4, and 12 weeks after PRM in the PMR group and before and 3, 6, and 14 weeks after the ligation in the control group. In the PRM group one dog was killed after the SPECT and LVEF examination 1 and 4 weeks after the PRM respectively and the remaining 3 dogs were killed after the SPECT and LVEF examination 12 weeks after the PRM. The dogs in the control group were killed after the SPECT and LVEF examination 14 weeks after the ligation. Myocardial pathology and cardiac angiogenesis analysis were conducted in both groups.

RESULTS

Three months after PMR or coronary artery ligation, the SPECT scores of the PMR and control groups decreased from 3.2 +/- 0.6 and 3.1 +/- 0.5 to 0.3 +/- 0.2 and 1.2 +/- 0.3 respectively (both P < 0.05), the LVEF of the 2 groups increased from 42.6 +/- 6.5 and 43.2 +/- 8.7 to 55.8 +/- 7.6 and 42.6 +/- 6.5 respectively (both P < 0.05). Microscopy showed that the amount of micrangii was 45.6 +/- 7.4 vessel/field in the PMR region of the PRM group, significantly much more than that in the non-ischemic region of the PRM group (18.2 +/- 4.7), the ischemic region of the control group (21.4 +/- 5.6), and the non-ischemic region of the control group (17.3 +/- 6.9, all P < 0.05).

CONCLUSION

PMR promotes angiogenesis in the ischemic myocardial wall, thus improving the blood perfusion of ischemic myocardium and global cardiac systolic function.