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Chapter 29
Doppler Ultrasound Examination
of the Fetal Coronary Circulation
Ahmet Alexander Baschat
Introduction
The coronary circulation provides blood to the myocardium.
Matching myocardial blood flow and demand
is critical to ensure cardiac function over a
wide variety of physiologic and pathologic conditions.
For this reason examination of coronary vascular
dynamics in various fetal conditions is becoming
increasingly relevant to the perinatal medicine specialist.
Ultrasound examination of the fetal coronary
circulation has become possible through advances in
ultrasound technology and a better understanding of
human fetal cardiovascular physiology. Although not
yet standard clinical practice, continuing trends in ultrasound
technology and spreading familiarity with
the examination and interpretation is likely to expand
clinical applications in the future [1].
Ultrasound examination of the fetal coronary system
utilizes gray-scale, zoom and cine-loop techniques
and requires optimal spatial and temporal settings
of the Doppler modalities. A proper setup of
the ultrasound system is therefore a necessary prerequisite.
Traditional ultrasound planes used in cardiac
scanning are modified to provide the best visualization
of the coronary vessels. A comprehensive survey
of extracardiac vascular dynamics is often necessary
to provide the clinical context for interpretation of intracardiac
and coronary flow dynamics. This chapter
reviews embryology, functional anatomy, ultrasound
technique, and clinical utility of ultrasound evaluation
of the fetal coronary circulation.
Embryology and Functional
Anatomy of the Coronary Circulation
Oxygenated blood is delivered to the myocardium
through the right coronary artery (RCA) and left
coronary artery (LCA) arising from the right anterior
and left posterior aortic sinuses, respectively, and the
left anterior descending branch (LAD) of the LCA [2,
3]. Venous return from the left ventricle drains
mainly through a superficial system through the coronary
sinus and anterior cardiac veins carrying approximately
two-thirds of myocardial venous return.
The deep system, consisting of arterioluminal vessels,
arteriosinusoidal vessels, and thebesian veins, receives
the remaining venous return and drains directly into
the cardiac chambers [2±4].
In embryonic life endothelial cells migrate from
the septum transversarium in the hepatic region of
the embryo to form epicardial blood islands which
eventually coalesce into vascular networks extending
throughout the epicardium and myocardium [5, 6].
Concurrently, the RCA and LCA originate as microvessels
that penetrate the outflow tracts and acquire a
muscular coat in this process. The primitive coronary
arterial circulation is established when main-stem
coronary arteries and myocardial vascular channels
connect. Venous drainage develops independently of
the arterial system and becomes fully functional
when the coronary sinus, as a remnant of the left
horn of the sinus venosus, becomes incorporated into
the inferior wall of the right atrium and thebesian
veins gain access to the ventricular cavities. The coronary
circulation is completely functional by the fifth
to sixth week of embryonic life and ensures myocardial
blood supply by the time the embryonic circulation
is established.
Coronary vascular development can be modulated
by various stimuli. Such stimuli include local oxygen
tension, mechanical wall stress, and myocardial and
vascular shear forces [6±9]. As a result, the coronary
circulation is subject to great anatomic and functional
variation that is manifested in several ways. Under
physiologic conditions modulation of vascular growth
enables matching coronary vascular development to
myocardial growth [10]. This ensures a balanced relationship
between ventricular mass and vascular density.
Prolonged or progressive tissue hypoxemia may
lead to an exaggeration of this physiologic process
with a subsequent marked increase in vascular crosssectional
area in the coronary circulation [11±14].
Under these circumstances vascular reactivity to
physiologic stimuli is also altered, often resulting in
amplified responses [15]. Similarly, abnormal intracardiac
pressure relationships, such as those found in
outflow tract obstructive lesions, may force the development
of accessory vascular channels between the