Myocardial performance and its acute response to angiotensin II infusion in fetal sheep adapted to chronic anemia.

Fetal chronic anemia causes lengthening of cardiomyocytes. In adults, severe left ventricular overload may lead to irreversible ventricular dysfunction. We hypothesized that in sheep fetuses with chronic anemia, remodeled myocardium would less successfully respond to angiotensin II (AT II) infusion than in fetuses without anemia. A total of 14 ewes with twin pregnancy underwent surgery at 113 ± 1 days of gestation. After a recovery period, anemia was induced by isovolumic hemorrhage in 1 fetus of each pair. At 126 ± 1 days of gestation, longitudinal myocardial velocities of the right (RV) and left (LV) ventricles were assessed at the level of the atrioventricular valve annuli via tissue Doppler imaging. Cardiac outputs were calculated by pulsed Doppler ultrasound. All measurements were performed at baseline and during fetal AT II infusion. Fetal serum cardiac natriuretic peptide (N-terminal peptide of proatrial natriuretic peptide [NT-proANP] and B-type natriuretic peptide [BNP]) concentrations were determined. Nine ewes successfully completed the experiment. At baseline, ventricular free wall thicknesses, cardiac outputs, and NT-proANP levels were significantly greater in the anemic fetuses than in the controls. The LV isovolumic contraction velocity (IVCV) acceleration and isovolumic relaxation velocity (IVRV) deceleration were lower (P < .05) in the anemic fetuses than in the controls. In the anemic fetuses, there was a positive correlation (R = .93, P < .01) between RV IVRV deceleration and NT-proANP concentration. Angiotensin II infusion increased (P < .05) LV IVCV acceleration in the anemic fetuses. We conclude that in anemic sheep fetuses, myocardial adaptation is associated with impaired LV early contraction and relaxation. However, the LV can improve its contractility with an inotropic stimulus, even in the presence of increased afterload.