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430 A.A. Baschat<br />

coronary vessels and the ventricular cavity (ventriculo-coronary<br />

fistulae) [16]. The plasticity of the coronary<br />

circulation is responsible for the variation in<br />

myocardial vascular territories and blood flow found<br />

in various fetal conditions and illustrates the critical<br />

importance of myocardial oxygenation for proper cardiac<br />

function.<br />

Myocardial metabolism is almost exclusively aerobic<br />

and in the presence of adequate oxygen various<br />

substrates, including carbohydrates, glucose, lactate,<br />

and lipids, can be metabolized [17±20]. In fetal life,<br />

myocardial glycogen stores and lactate oxidation constitute<br />

the major sources of energy while fatty acid<br />

oxidation rapidly becomes the primary energy source<br />

after birth. To maintain metabolism myocardial oxygen<br />

extraction is as high as 70%±80% in the resting<br />

state. Consequently, a coronary atrioventricular O 2<br />

difference of 14 ml/dl exceeds that of most other vascular<br />

beds and allows little further extraction of O 2<br />

unless blood flow is significantly augmented; therefore,<br />

coronary blood flow is closely regulated to<br />

match myocardial oxygen demands.<br />

The regulation of myocardial perfusion operates at<br />

several levels and time frames. The unique parallel<br />

arrangement of the fetal circulation allows for delivery<br />

of well-oxygenated blood through the ductus venosus<br />

to the left ventricle and thus the ascending aorta.<br />

In the fetal lambthe coronary circulation receives<br />

approximately 8% of the left ventricular output at rest<br />

in this manner [21]. This proportion may be higher<br />

in the human fetus and may be further altered by<br />

modulating the degree of shunting through the ductus<br />

venosus [22]. Once blood enters the coronary vessels<br />

from the ascending aorta the pressure difference<br />

to the right atrium becomes the primary driving<br />

force for coronary blood flow. This perfusion pressure<br />

is further subjected to changes in vascular tone and<br />

extravascular pressure. Autonomic innervation of coronary<br />

resistance vessels regulates overall vascular<br />

tone [23, 24], but ventricular contractions are the<br />

main contributor to extravascular resistance with significant<br />

impact on the flow velocity waveform [25±<br />

27]. Myocardial perfusion predominantly occurs during<br />

diastole when the ventricles relax and pose little<br />

extravascular resistance. This diastolic timing of predominant<br />

perfusion is unique to the coronary circulation<br />

and distinguishes it from other vascular beds in<br />

the human body. In the adult, increases above a resting<br />

heart rate of 70 beats per minute result in a disproportional<br />

shortening of diastole. Fetal heart rates<br />

of 120±160 beats per minute place special demands<br />

on dynamic vascular mechanisms to regulate myocardial<br />

blood flow volume.<br />

Efficiency of myocardial oxygen delivery is further<br />

enhanced by active autoregulatory control mechanisms<br />

ensuring optimal myocardial blood flow despite<br />

fluctuations in arterial perfusion pressure [28,<br />

29]. This is achieved through caliber adjustment of<br />

precapillary resistance vessels allowing channeling of<br />

blood flow to areas of greatest oxygen demand [30,<br />

31]. With maximal dilatation of these sphincters myocardial<br />

blood flow may be elevated four times above<br />

basal flow. The increase in blood flow volume that<br />

can be achieved under these circumstances is the<br />

myocardial blood flow reserve. If myocardial oxygenation<br />

cannot be sustained, long-term adaptation<br />

with formation of new blood vessels may be invoked<br />

thus increasing the myocardial blood flow reserve<br />

[32±34]. Such elevated myocardial blood flow reserve<br />

allows marked augmentation of blood flow during<br />

periods of acutely worsening hypoxemia or increased<br />

cardiac work and increases as high as 12 times the<br />

basal flow have been reported [15, 35, 36].<br />

Ultrasound Examination Technique<br />

Ultrasound Setup<br />

The setup of the ultrasound system is of major importance<br />

for successful examination of the fetal coronary<br />

arteries. Gray-scale ultrasound, color-, and<br />

pulsed-wave Doppler are used in a complementary<br />

manner and machine settings need to be optimized<br />

to provide the best spatial and temporal resolution.<br />

Although visualization of coronary vessels can be<br />

achieved using 4-MHz transducers, higher frequencies<br />

are likely to improve resolution and therefore detection.<br />

The dynamic range of the gray-scale image<br />

should be set to an intermediate level that is generally<br />

used in cardiac setups. Zoom magnification of the<br />

area of interest limits the computing power that<br />

needs to be allocated to the generation of the grayscale<br />

image. These two maneuvers will improve the<br />

frame repetition rate and should therefore be applied<br />

before adding color Doppler imaging. When adding<br />

color Doppler imaging the filter should be set to a<br />

high degree of motion discrimination and the color<br />

box and gate are kept as small as possible to optimize<br />

spatial and temporal resolution of this Doppler modality.<br />

The lateral dimension of the color box has the<br />

greatest impact on computing power and therefore<br />

frame rate. The color amplification gain is set to<br />

eliminate background noise on the screen. The persistence<br />

is set to a low level to minimize frame averaging.<br />

The color velocity scale is adjusted to a range<br />

that allows visualization of intra- and extracardiac<br />

flows without aliasing and suppression of wall-motion<br />

artifacts. A useful velocity range for coronary arteries<br />

is between 0.3 and 0.7 m/s for coronary arteries and<br />

between 0.1 and 0.3 m/s for the coronary sinus. Since<br />

initial detection of the coronary arteries relies on col-

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