Declining cardiac output and placental dysfunction are the key barriers to successful fetal cardiac bypass for
in utero
repair of congenital heart defects. Identifying myocardial dysfunction, especially in the RV that is considered the systemic ventricle in fetal life, may be important for success. We hypothesized that fetal cardiac bypass results in myocardial contractile dysfunction that reduces cardiac output and placental perfusion, leading to placental dysfunction and fetal demise. Three fetuses from mid-term pregnant ewes were subjected to 30 min of cardiac bypass and followed for 120 min after bypass. Piezoelectric crystals (Sonometrics, Ontario, CA) were placed on three axes of the fetal heart and pressure catheters (Millar Instruments, Houston, TX) were inserted in the left and right ventricle (RV). Data were analyzed by repeated measures ANOVA with Fisher’s PLSD post hoc analyses. Representative RV pressure-volume loops in the figure showed that preload increased after bypass, indicated by increased end-diastolic volume (mean 4.1±.7 vs. 4.4±1 mL) and pressure (mean 14.3 ±7 vs. 31.3± 3 mmHg, P<.05). RV contractility decreased after bypass: pre-bypass dPdt
max
(mmHg/sec) - 880±93 vs. 731±102 at 120 min after bypass (P≤.1) and dP/dt
min
- 798±4 vs. 689±11 (P≤.1). Preload recruitable stroke work (slope of regression line) also decreased from 28.5±7 pre-bypass to 22.1±5 at 120 min post-bypass. Increased RV preload and RV contractile dysfunction are evident after fetal cardiac bypass. Minimizing the associated myocardial dysfunction is important for the success of fetal surgery to repair complex congenital heart defects.
This research has received full or partial funding support from the American Heart Association, AHA National Center.
F125Fetal pulmonary venous Doppler flow velocity waveforms in congenital heart defects
