Vulnerability of Coronary Circulation After Norwood Operation.
Parole chiave
Astratto
BACKGROUND
We hypothesized that the myocardial oxygen supply-demand balance is impaired in patients after a Norwood procedure and that an abnormal oxygen supply-demand balance is associated with pronounced activation of the renin-angiotensin-aldosterone system and worse clinical outcome after this procedure.
METHODS
To investigate the myocardial oxygen supply-demand balance, the subendocardial viability ratio (SEVR) was measured in 29 hypoplastic left heart syndrome patients after the Norwood procedure, in 27 patients with pulmonary atresia whose pulmonary blood flow was supplied from the aortopulmonary (AP) shunt, and in 30 control patients who were considered to have normal biventricular circulation. The SEVR in Norwood (0.57 ± 0.18) and AP shunt (0.66 ± 0.10) patients was significantly reduced compared with that in controls (0.94 ± 0.25, p < 0.001 vs Norwood and AP shunt).
RESULTS
After controlling for heart rate, the SEVR was significantly lower in Norwood than in AP shunt patients (p < 0.001). Importantly, the SEVR was significantly lower in Norwood patients with poor clinical outcomes (cardiac arrest before second-stage operation, progressive tricuspid regurgitation, or reduction of ejection fraction <0.35) than in the remaining Norwood patients (0.51 ± 0.12 vs 0.69 ± 0.22, p < 0.01). An SEVR of less than 0.52 had a more than 76% probability of having a poor outcome (p < 0.05). Furthermore, a lower SEVR was significantly correlated with more pronounced renin-angiotensin-aldosterone system activation and elevated natriuretic peptides in serum. Multiple regression analysis revealed that increased aortic stiffness and a smaller neoaorta relative to the native descending aorta were independent determinants of reduced SEVR.
CONCLUSIONS
Myocardial oxygen supply-demand imbalance is intrinsic to Norwood circulation but may be improved by technical refinement of aortic reconstruction or afterload-reducing medication with renin-angiotensin-aldosterone system blockade.
