The cause of B-type natriuretic peptide elevation and the dose-dependent effect of angiotensin-converting enzyme inhibitor on patients late after tetralogy of Fallot repair.

Patients after surgical repair of tetralogy of Fallot (TOF) may experience various complications that result in neurohormonal activation, including plasma B-type natriuretic peptide (BNP) elevation. Right ventricular (RV) dilation is a frequent complication, and few treatments are available. This study aimed to identify the factor or factors leading to BNP elevation and to clarify the effects of angiotensin-converting enzyme inhibitor (ACE-I) on changes in BNP levels in patients with repaired TOF. Plasma BNP levels and hemodynamic data derived from cardiac catheterization were analyzed. In addition, longitudinal BNP levels and ACE-I dosages were analyzed for patients administered ACE-I. For 31 patients with repaired TOF, who mainly had RV dilation, log BNP levels were significantly correlated with the RV end-diastolic volume index (P = 0.02) as well as ventricular volume and pressure (P < 0.01). For 11 patients medicated with ACE-I, BNP levels were significantly lower at the time of maximal ACE-I dosage than at the time of minimal dosage (P < 0.01). Furthermore, BNP levels decreased as the ACE-I dosage per body weight increased (P < 0.01). In conclusion, elevation of BNP in patients after TOF repair could reflect volume and pressure load in the RV end-diastolic phase, and ACE-I may reduce BNP levels in a dose-dependent manner.