Background
—Acute right ventricular (RV) restrictive physiology after tetralogy of Fallot repair results in low cardiac output and a prolonged stay in the intensive care unit (ICU). However, its mechanism remains uncertain.
Methods and Results
—In the first 24 hours after tetralogy of Fallot repair (n=11 patients), serial prospective measurements were performed of cardiac troponin T, indexes of NO production (NO
2
−
and NO
3
−
combined as NOx), and iron metabolism and antioxidants. RV diastolic function was assessed by transthoracic Doppler echocardiography. Patients who had a long stay in the ICU were characterized by restrictive RV physiology (nonrestrictive group [n=7]: 3.0±0.6 days [mean±SD]; restrictive group [n=4]: 10.7±3.1 days). Troponin T peak concentration and the area under its concentration-time curve (AUC) were higher in the restrictive RV group (peak: restrictive group 17.0±2.8 μg/L, nonrestrictive group 10.4±4.6 μg/L,
P
<0.03; AUC: restrictive group 268.8±73.6 μg · h
−1
· L
−1
, nonrestrictive group 136.2±48.3 μg · h
−1
· L
−1
,
P
<0.03). Plasma NOx/creatinine concentrations were higher in the restrictive group than the nonrestrictive group at 2 hours after bypass (restrictive group 1.3±0.4, nonrestrictive group 0.8±0.2;
P
=0.04) but were similar by 24 hours. Iron loading peaked 2 to 10 hours after bypass and was more severe in the restrictive group (peak transferrin saturation: restrictive group 83.9±13.0%, nonrestrictive group 58.3±16.2%,
P
=0.05; minimum total iron-binding capacity: restrictive group 0.59±0.21%, nonrestrictive group 0.76±0.06%,
P
=0.04; minimum iron-binding antioxidant activity to oxyorganic radicals: restrictive group 9.5±22.4%, nonrestrictive group 50.6±11.4%,
P
=0.01).
Conclusions
—After tetralogy of Fallot repair, acute restrictive RV physiology is associated with greater intraoperative myocardial injury and postoperative oxidative stress with severe iron loading of transferrin.