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a Chapter 33 Doppler Echocardiography for Managing Congenital Cardiac Disease 505<br />

Fig. 33.28. Doppler identification of tricuspid regurgitation<br />

in a fetus with complete heart block and heart failuee. Left:<br />

The Doppler sample volume (oblique arrow) was placed in<br />

the right atrium (RA) imaged in the aortic (AO) short axis<br />

plane. Right: Doppler tracing shows prominent reversed<br />

flow (R) during systole indicative of tricuspid incompe<br />

tence. Normal flow patterns were seen during diastole (D).<br />

M-mode echocardiogram (oblique arrow) was used to time<br />

the diastolic and systolic phases of the fetal cardiac cycle.<br />

Horizontal arrow denotes the position of the Doppler sample<br />

volume for the M-mode system. B Doppler baseline, TV<br />

tricuspid valve. (Reprinted from [12] with permission)<br />

Summary<br />

Recent years have witnessed significant progress in<br />

the technique of fetal echocardiography and perinatal<br />

management of fetal cardiac disease. Although 2D<br />

cardiac imaging remains the major tool for this evaluation,<br />

its diagnostic efficacy is significantly enhanced<br />

by the other ultrasound modalities. Specifically,<br />

spectral pulsed Doppler, 2D Doppler color flow<br />

mapping, and color M-mode provide essential tools<br />

for elucidating hemodynamic abnormalities associated<br />

with structural and functional congenital cardiac<br />

disease. This hemodynamic information plays a<br />

crucial role in enhancing the efficacy of investigating<br />

these complex problems. It is not surprising, therefore,<br />

that Doppler echocardiography now plays such<br />

a critical role in the diagnosis, treatment, and surveillance<br />

of fetal cardiac disorders. Future developments<br />

in this area will certainly encompass 3D Doppler flow<br />

evaluation, which has been addressed in Chaps. 7<br />

and 34.<br />

References<br />

1. Mitchell SC, Korones SB, Berendes HW (1971) Congenital<br />

heart disease in 56,109 births: incidence and natural<br />

history. Circulation 43:323±332<br />

2. Benson Jr DW (1989) Changing profile of congenital<br />

heart disease. Pediatrics 83:790±791<br />

3. Zosmer N, Souter VL, Chan CS, Huggon IC, Nicolaides<br />

KH (1999) Early diagnosis of major cardiac defects in<br />

chromosomally normal fetuses with increased nuchal<br />

translucency. Br J Obstet Gynaecol 106:829±833<br />

4. Galindo A, Comas C, Martinez JM, Gutierrez-Larraya<br />

F, Carrera JM, Puerto B, Borrell A, Mortera C, de la<br />

Fuente P (2003) Cardiac defects in chromosomally normal<br />

fetuses with increased nuchal translucency at 10±<br />

14 weeks of gestation. J Matern Fetal Neonatal Med<br />

13:163±170<br />

5. Junker R, Kotthoff S, Vielhaber H, Halimeh S, Kosch A,<br />

Koch HG, Kassenbohmer R, Heineking B, Nowak-Gottl<br />

U (2001) Infant methylenetetrahydrofolate reductase<br />

677TT genotype is a risk factor for congenital heart<br />

disease. Cardiovasc Res 51:251±254<br />

6. McBride KL, Fernbach S, Menesses A, Molinari L, Quay<br />

E, Pignatelli R, Towbin JA, Belmont JW (2004) A family-based<br />

association study of congenital left-sided heart<br />

malformations and 5,10 methylenetetrahydrofolate<br />

reductase. Birth Defects Res Part A Clin Mol Teratol<br />

70:825±830<br />

7. Castaneda AR, Jonas RA, Mayer Jr HE, Hanley FL<br />

(1994) Cardiac surgery of the neonate and the infant.<br />

Saunders, Philadelphia<br />

8. Warnes CA, Liberthson R, Danielson GK, Dore A, Harris<br />

L, Hoffman JI, Somerville J, Williams RG, Webb GD<br />

(2001) Task force 1: the changing profile of congenital<br />

heart disease in adult life. J Am Coll Cardiol 37:1170±<br />

1175<br />

9. Kohl T, Strumper D, Witteler R, Merschhoff G, Alexiene<br />

R, Callenbeck C, Asfour B, Reckers J, Aryee S,<br />

Vahlhaus C, Vogt J, Van Aken H, Scheld HH (2000) Fetoscopic<br />

direct fetal cardiac access in sheep: an impor-

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