Cardiac sympathetic denervation after transmyocardial laser revascularization

Background-Transmyocardial laser revascularization (TMR) has been shown to improve refractory angina not amenable to conventional coronary interventio ns. However, the mechanism of action remains controversial, because improve d myocardial perfusion has not been consistently demonstrated. We hypothesi zed that TMR relieves angina by causing myocardial sympathetic denervation. Methods and Results-PET imaging of resting and stress myocardial perfusion with [N-13]ammonia (NH,) and of sympathetic innervation with [C-11]hydroxye phedrine (HED) was performed before and after TMR in 8 patients with class IV angina ineligible for CABG or PTCA. A mean of 50+/-11 channels were crea ted in the left ventricle (LV) with a holmium:YAG laser. A semiautomated pr ogram was used to determine NH, uptake and HED retention in the LV. Perfusi on and innervation defects were defined as the percentage of LV with tracer uptake or retention >2 SD below normal mean values. All patients experienc ed improvement in their angina by 2.4+/-0.5 angina classes after surgery, P =0.008. Sympathetic innervation defects exceeded resting perfusion defects in all patients before TMR (34.6+/-27.3% for HED versus 9.4+/-10.8% for NH3 , P=0.008). TMR did not significantly affect resting or stress myocardial p erfusion but increased the extent of sympathetic denervation in 6 of 8 pati ents by 27.5+/-15.9%, P=0.03. In the remaining 2 patients, both sympathetic denervation and stress perfusion defects decreased after surgery, Conclusions-TMR causes decreased myocardial HED uptake in most patients wit hout significant change in resting or stress myocardial perfusion, suggesti ng that the improvement in angina may be at least in part due to sympatheti c denervation.