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a Chapter 29 Doppler Ultrasound Examination of the Fetal Coronary Circulation 439<br />

calcification die within the first year of life complicated<br />

by cardiac and pulmonary failure, severe hypertension,<br />

renal infarction, peripheral gangrene, and<br />

bowel infarction [76].<br />

Critical Aortic Stenosis<br />

Critical aortic stenosis in fetal life can be associated<br />

with a marked decrease in left ventricular output and<br />

reversal of shunting across the foramen ovale. Under<br />

these circumstances coronary perfusion pressure is<br />

affected by a decrease in arterial pressure and an elevation<br />

of right atrial pressure thereby decreasing the<br />

driving force across the coronary vascular bed. Concurrently,<br />

left ventricular work and therefore myocardial<br />

oxygen demand are increased. Development of<br />

acute heart sparing has been documented in a fetus<br />

presenting with severe left ventricular outflow tract<br />

obstruction and non-immune hydrops due to critical<br />

aortic stenosis. While these findings were ameliorated<br />

initially by transplacental digoxin therapy, visualization<br />

of coronary blood flow became visible at 39<br />

weeks coinciding with shunt reversal across the foramen<br />

ovale [79].<br />

Persistent Left Superior Vena Cava<br />

While Doppler examination of the coronary sinus has<br />

limited utility in the human fetus, substantial dilatation<br />

may result from volume overload from a persistent<br />

left superior vena cava draining into the coronary<br />

sinus [80±82]. The frequency of a persistence of<br />

the left vena cava is 1±2 per 1000 but may be as high<br />

as 9% in the presence of congenital heart defects<br />

[83]. The degree of dilatation is often marked and lies<br />

appreciably above normal reference limits. This dilatation<br />

appears to be predominantly related to vascular<br />

volume changes and is independent of associated cardiac<br />

defects [63]. Other causes of coronary sinus dilatation<br />

in the human fetus may be a coronary arteriovenous<br />

fistula and anomalous pulmonary vein drainage<br />

into the coronary sinus. It is important to note<br />

that because of its close proximity to the insertion of<br />

the atrioventricular valve, a dilated coronary sinus<br />

has been mistaken for an atrial septal defect of ostium<br />

primum type and/or an atrioventricular septal<br />

defect, respectively [84±86]. Coronary sinus dynamics<br />

may be attenuated in fetal conditions associated with<br />

elevated right-heart pressures, severe fetal cardiac<br />

dysfunction, and hydrops. These alterations in dynamics<br />

may indicate elevated coronary sinus pressures<br />

or changes in coronary blood flow [45].<br />

References<br />

1. Abuhammad A (2003) Color and pulsed Doppler ultrasonography<br />

of the fetal coronary arteries: Has the time<br />

come for its clinical application? Ultrasound Obstet Gynecol<br />

21:423±425<br />

2. Williams PL, Warwick R (eds) (1983) Gray's anatomy.<br />

Churchill Livingstone, New York<br />

3. McAlpine WA (1975) Heart and coronary arteries.<br />

Springer, Berlin Heidelberg New York<br />

4. Ganong WF (1989) Review of medical physiology. Appleton<br />

Lange, Norwalk, Connecticut<br />

5. Larsen WJ (1993) Human embryology. Churchill Livingstone,<br />

New York<br />

6. Tomanek RJ (1996) Formation of the coronary vasculature:<br />

a brief review. Cardiovasc Res 31:E46±E51<br />

7. Poole TJ, Coffin JD (1989) Vasculogenesis and angiogenesis:<br />

two distinct morphogenetic mechanisms establish<br />

embryonic vascular pattern. J Exp Zool 251:224±<br />

231<br />

8. Hudlicka O, Brown MD (1996) Postnatal growth of the<br />

heart and its blood vessels. J Vasc Res 33:266±287<br />

9. Skalak TC, Price RJ (1996) The role of mechanical<br />

stresses in microvascular remodeling. Microcirculation<br />

3:143±165<br />

10. Engelmann GL, Dionne CA, Jaye MC (1993) Acidic fibroblast<br />

growth factor and heart development. Role in<br />

myocyte proliferation and capillary angiogenesis. Circ<br />

Res 72:7±19<br />

11. Banai S, Shweiki D, Pinson A, Chandra M, Lazarovici<br />

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endothelial growth factor in cardiac myocytes. Circ<br />

Res 76:758±766<br />

13. Ratajska A, Torry RJ, Kitten GT (1995) Modulation of<br />

cell migration and vessel formation by vascular endothelial<br />

growth factor and basic fibroblast growth factor<br />

in cultured embryonic heart. Dev Dyn 203:399±407<br />

14. Scheel KW, Eisenstein BW, Ingram LA (1984) Coronary,<br />

collateral and perfusion territory responses to aortic<br />

banding. Am J Physiol 246:H768±H775<br />

15. Reller MD, Morton MJ, Giraud GD (1992) Maximal<br />

myocardial flow is enhanced by chronic hypoxaemia in<br />

late gestational fetal sheep. Am J Physiol 263:H1327±<br />

H1329<br />

16. Baschat AA, Love JC, Stewart PA, Gembruch U, Harman<br />

CR (2001) Prenatal diagnosis of ventriculocoronary<br />

fistula. Ultrasound Obstet Gynecol 18:39±43<br />

17. Ascuitto RJ, Ross-Ascuitto NT (1996) Substrate metabolism<br />

in the developing heart. Semin Perinatol<br />

20:542±563<br />

18. Bartelds B, Knoester H, Beaufort-Krol GCM, Smid GB,<br />

Takens J, Zijlstra WG, Heymans HSA, Kuipers JRG<br />

(1999) Myocardial lactate metabolism in fetal and newborn<br />

lambs. Circulation 99:1892±1897<br />

19. Fisher DJ, Heymann MA, Rudolph AM (1982) Fetal myocardial<br />

oxygen and carbohydrate consumption during<br />

acutely induced hypoxemia. Am J Physiol 242:H657±<br />

H661

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