Abstract 17884: Ventricular Sympathetic Innervation in Patients with Transposition of the Great Arteries After Arterial Switch- and Rastelli Procedure, - Impact of Arterial Dissection and Coronary Reimplantation

Abstract

Objectives: Coronary flow reserve is significantly reduced in patients with transposition of the great arteries (TGA) after arterial switch operation (ASO). Dissection of the great arteries and coronary reimplantation may result in partial myocardial sympathetic denervation, with a negative influence on coronary blood flow. Methods: 18 patients with TGA were included in the study; 9 had ASO (age 20.8 + 5.8 years), controls were 9 patients after Rastelli procedure (22.1 + 6.8 years). All patients were fully active and asymptomatic. Sympathetic innervation was measured by positron emission tomography using 11 C hydoxyepinephrine (HED). Results: Myocardial perfusion at rest was homogenous in all patients. Maximal left ventricular myocardial HED retention as a measure of the intensity of innervation ranged from 6.1% to 15.9% (mean 12.74 + 3.8% per minute). Patients with more than one operation had significant reduced maximal HED retention (r=2.99, p<0.001); one patient of each group had HED-retention less than 7% indicating complete denervation. A significant correlation with time after surgery could be found for max. HED retention (r=0.326, p<0.001); max. HED retention was higher in patients undergoing corrective cardiac surgery at an earlier age (r=0.315, p<0.001). No statistical significant difference could be found between patients after ASO and Rastelli procedure. Aortic cross clamp time was inversely correlated with max. HED retention (r=-2.94; p<0.001). Conclusion: Coronary reimplantation and dissection of the great arteries have a negative influence on the sympathetic innervation of the myocardium, but because of reinnervation maximal myocardial blood flow is not essentially altered by this mechanism in older patients. Open heart surgery and prolonged aortic cross clamp time have a negative influence on the norepinephrine content of cardiac sympathetic nerve terminals.