Neurohormonal stimulation in patients with congenital heart diseases - Influence of age, cardiac defect and hemodynamic

Background: The negative impact of persistant neurohormonal activation on morbidity and mortality due to congestive heart failure is well established in adults while little is known of its role in infants with congenital heart diseases. Methods. We retrospectively analysed 2043 neurohormonal datas from 436 pediatric patients treated in our institution from 1987-1997 (plasmareninactivity = PRA[ng/ml/h] aldosterone = ALDO[pg/ml], norepinephrine = NOR[ng/l], epinephrine = EPl[ng/l], angiotensin converting enzyme = ACE[nmol/min/ml]) Results. PRA, ALDO and NOR were considerably elevated in the first trimenon (PRA = 94 +/- 116. ALDO = 1970 +/- 2380) and in patients with left-to-right-shunts (PRA = 52 +/- 83 ALDO = 990 +/- 1090 NOR = 640 +/- 630). complex cardiac anomalies (PRA = 83 +/- 84, ALDO = 1720 +/- 1970, NOR = 1350 +/- 1700) aortic coarcrations (PRA = 100 +/- 195 ALDO = 2700 +/- 4150) and cardiomyopathies (PRA = 49 +/- 55 ALDO = 910 +/- 1070 NOR = 700 +/- 570). After complete repair and cavopulmonary connection these values are normal in the average in contrast to high values after palliative surgery like pulmonary trunk banding and aorto pulmonary shunt in 129 patients, who had cardiac catheterization, we found no significant correlations of NOR and hemodynamic data but highly significant correlations of PRA and mean atrial pressure (r = -0,57), systemic vascular resistance (r = -0.31). ratio of pulmonary to systemic flow (r = 0.38); pulmonary cardiac index (r = 0,31), pulmonary oxygen saturation (r = 0.39) and mean pulmonary artery pressure (r = 0,36). Patients with a significant neurohormonal activation had a significantly higher incidence of cardiac surgery and higher mortality. Conclusions: Significant neurohormonal stimulation was predominantly found in young infants with heart failure due to left-to-right shunts or aortic coarctation prior ro complete repair The hemodynamic trigger for renin release was arterial hypotension. Neurohormonal stimulation was an important risk factor for mortality and necessity og cardiac surgery.