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C a r d i o p u l m o n a r y I m a g i n g • R ev i ew
Sundaram et al.
Reporting of Cardiac MDCT
FOCUS ON:
Cardiopulmonary Imaging
Review
Baskaran Sundaram1
Smita Patel
Prachi Agarwal
Ella A. Kazerooni
Sundaram B, Patel S, Agarwal P, Kazerooni EA
Anatomy and Terminology for
the Interpretation and Reporting
of Cardiac MDCT: Part 2, CT
Angiography, Cardiac Function
Assessment, and Noncoronary and
Extracardiac Findings
OBJECTIVE. In this part 2 of our two-part article, we aim to describe the evaluation and
interpretation of coronary CTA, cardiac structures, and cardiac functional assessment using
an approach similar to the reporting of catheter angiography and echocardiography.
CONCLUSION. The superb resolution and the isotropic image data acquisition of ECGgated coronary CT angiography (CTA) enable evaluation of the coronary arteries and cardiac
anatomy in any selected plane. The consistent use of standard terminology when reporting
cardiac CT findings is part of a structured and comprehensive coronary CTA report.
E
Keywords: cardiac CT, cardiac function, coronary CT
angiography
DOI:10.2214/AJR.08.1178
Received May 7, 2008; accepted after revision
September 2, 2008.
Gold Medal Exhibit Award for education exhibit at the
2006 annual meeting of the American Roentgen Ray
Society, Vancouver, BC, Canada.
1
All authors: Division of Cardiothoracic Radiology,
Department of Radiology, University of Michigan
Health System, Cardiovascular Center, Rm. 5481,
1500 E Medical Center Dr., Ann Arbor, MI 48109-5868.
Address correspondence to B. Sundaram (sundbask@
umich.edu).
CME
This article is available for CME credit.
See www.arrs.org for more information.
AJR 2009; 192:584–598
0361–803X/09/1923–584
© American Roentgen Ray Society
584 CG gating and recent improve­
ments in MDCT technology
have made possible excellent
imaging of the coronary arteries
[1]. The reported performance of coronary
CT angio­g raphy (CTA) using the current
64-MDCT scanners approaches that of in­
vasive coronary angiography. Coronary
CTA evaluates both the coronary artery
wall and the lumen in a quick, noninvasive,
relatively inexpensive, and robust way. As
in con­ventional catheter angiography of
most other vascular systems in the human
body, it is clear that the extent of coronary
artery disease (CAD) may be under­ap­
preciated with invasive coronary angio­
graphy, which views only the lumen of the
arteries, in comparison with intravascular
sonography and coronary CTA [2, 3].
Coronary CTA can both visualize and deter­
mine the extent of CAD in patients with
normal traditional noninvasive tests, sug­
gesting a role for screening if aggressive
disease management can reduce the rate of
cardiac events and cardiac mortality. It can
also reduce the number of diagnostic cardiac
catheterization procedures in symptomatic
patients and patients with abnormal echo­
cardiography and myocardial perfusion
study results. With improved spatial and
temporal resolution in the future, coronary
CTA has the potential to quantify and
monitor atherosclerotic plaque, particularly
noncalcified and fatty or vulnerable plaque,
providing a CT phenotype of an individual’s
coronary arteries for targeted, patient-
specific risk factor manage­ment and poten­
tial pharmaceutical strategies.
Although invasive coronary angiography
and intravascular sonography provide direct
evaluation of the coronary artery lumen and
wall, respectively, other diagnostic tests
provide predominantly indirect information
about the presence of significant CAD based
on the presence of calcifications (electronbeam CT), wall motion, or perfusion ab­
norm­alities (cardiac stress imaging). In
addition, although risk factor assessment and
management is the primary method for
identifying and reducing cardiovascular risk,
many patients presenting with acute coronary
events are at a low risk for CAD on the basis
of traditional criteria. It is important to note
the high prevalence of atherosclerosis, even
in relatively young asymptomatic indivi­
duals. For example, in one intravascular
sonography study, one in six, or 17%, of
asymptomatic individuals in the age range of
12–19 years had a greater than 0.5-mm
intimal thickness of the coronary arteries,
indicating the presence of preclinical CAD
[4]. Given the prevalence of known CAD, let
alone un­diagnosed and asymptomatic CAD,
interest continues in exploring the most costeffective strategies to both screen for and
diagnose CAD [5, 6].
Depending on the coronary CTA tech­
nique, cardiac function assessment may be
possible. In retrospective ECG gating, dy­
nam­ic information throughout the cardiac
cycle is collected to facilitate cardiac func­
tional assessment, both in a qualitative and a
AJR:192, March 2009
Reporting of Cardiac MDCT
quantitative fashion. Typically, functional
eval­uation of both the left ventricle (LV) and
the aortic valve is performed in our routine
clinical practice. Similar principles may be
extended to assess other cardiac chambers
and valves [7–11]. Also, attempts have been
made to perform myocardial perfusion
assessment using CT [12–16].
We recommend that physicians refer to the
appropriateness criteria outlined by the
American College of Radiology (ACR) and
the American College of Cardiology (ACC)
as a guideline to indications for performing
coronary CTA [17].
Awareness of the findings and standard
descriptions pertaining to coronary CTA,
plaque morphology, characterization, bypass
graft assessment, other cardiac structures,
and cardiac function may help in creating a
structured cardiac CT report. In this article,
we aim to provide a basic foundation for
evaluating coronary CTA findings, non­
coronary cardiac structures, and cardiac func­
tion assessment.
Coronary CTA of Acquired
Coronary Artery Disease
Viewing Methods
The purpose of coronary CTA in the
setting of suspected or known CAD is to
determine the presence and severity of
luminal narrowing and to evaluate lesion
morphology. Distal portions of the coronary
artery smaller than 2 mm in diameter cannot
be evaluated because of the limits of spatial
and temporal resolution of current coronary
CTA data sets. Initial assessment is made
using the axial source images followed by
the postprocessed images. The origins of the
vessels are first evaluated, followed by
evaluation of each coronary artery from its
respective ostium to its most distal extent.
Various postprocessed images, such as shortaxis views, curved reformations, long-axis
extended views of the lumen, and 3D surfaceshaded volume-rendered images, can be
obtained to evaluate individual coronary
arteries in various projections.
True short- and long-axis coronary artery
images are created, respectively, as images
perpendicular and parallel to the center line
of the artery. The center line of the artery is
automatically identified by most com­
mercially available coronary CTA software
and can be edited to reflect the true center
line of the artery if it is incorrect. The
window width and level are adjusted to suit
reader preference. Three-dimensional volume-
AJR:192, March 2009
r­ endered images help to instantly review the
epicardial surface anatomy of the coronary
circulation; coronary artery dominance;
presence of coronary stents; number and
course of coronary artery bypass grafts
(CABGs), their origin, and anastomosis to
the run-off vessel; the presence of collateral
vessels; and coronary artery anatomic
variations and anomalies.
It is important to be cognizant of artifacts
and pitfalls encountered on coronary CTA
examinations, such as respiratory motion,
cardiac pulsation artifacts, artifacts caused
by beat variability, ventricular ectopic beats,
blooming artifacts from densely calcified
plaque, and misregistration artifacts. Many
artifacts can be prevented by appropriate
patient preparation and postprocessing using
data sets in different phases of the R-R
interval. The ECG editing capability avail­
able with some vendors is a useful tool for
improving a potentially noninterpretable
study to a diagnostic test.
Although purely or partly calcified
plaques are easily visible on coronary CTA
be­cause of high contrast resolution, plaques
that have no coronary artery calcifications—
that is, noncalcified plaques—can be diffi­
cult to appreciate, particularly when they
are small. The attenuation difference be­
tween the arterial wall and the sur­rounding
peri­vas­cular fat can help in identification of
subtle noncalcified plaques. Plaque-related
wall thick­ening may also be apparent when
comparing with either the opposite coro­
nary wall or the adjacent normal arterial
seg­ment. Abrupt change in the lumen di­
ameter due to plaques can also be appreciated
when scrolling through the artery in the
short-axis plane.
Coronary Artery Stenosis and Remodeling
Atherosclerosis in humans begins at birth
and progresses in a nonlinear and largely
unpredictable manner, with plaque disruption
and thrombus formation resulting in an acute
coronary syndrome. Significant obstructive
CAD lesions are predominantly located in
the proximal and mid coronary artery
segments [18]. The prevalence of ostial
involvement is low; in one series, 2.7% of
8,509 patients who underwent CABG surgery
had ostial stenosis of 50% or more [19]. The
severity of stenosis on coronary CTA is
generally described as diameter stenosis
rather than area stenosis, as shown on Figure
1 and detailed in Table 1. Arterial diameter
reductions of 50%, 70%, and 90% correspond
to area reductions of 75%, 90%, and 99%,
respectively (Fig. 2). The critical narrowing
of a lesion (A) may be estimated as the
percentage of ratio between 1 minus actual
(B) lumen diameter and the expected (C)
lumen diameter—A% = 1 – (B / C)—as
illustrated in Figure 3. Because coronary
arteries progressively taper, the expected
diameter of the lumen at the level of the lesion
is determined as an average of the normal
arterial segment proximal to it and the distal
arterial lumen equidistant from the lesion.
Reported ranges of 64-MDCT coronary CTA
sensitivity, specificity, neg­ative predictive
value, and arterial seg­ments that cannot be
evaluated are 73–99%, 93–97%, 95–99%,
and 2–12%, respectively [17]. CAD assess­
ment using 64-MDCT scanners is sig­nif­i­
cantly better and more robust than with earlier
generations of MDCT scanners [20]. A
systematic literature review concluded that
the average sensitivity and specificity for
diagnosing significant CAD (≥ 50% stenosis)
were 95% and 84% with 4-MDCT, 95% and
84% with 16-MDCT, and 100% and 94%
with 64-MDCT scanners [20].
Arterial compensatory remodeling was
described by Glagov et al. [21] as positive or
negative. Positive remodeling refers to exo­
phytic growth of the artery wall at the site of
coronary plaque, which results in unimpres­
sive luminal narrowing even in the presence
of significant CAD (Fig. 4). Negative remodel­
ing refers to endophytic growth of plaque,
which results in lumen decrease [22]. Positive
remodeling is better appreciated with intra­
vascular sonography and coronary CTA than
with invasive coro­nary angiography. Positive
remodeling may have a significant impact in
stenosis estimation. The ratio between the
lumen diameter (edges of the contrast
column) and the artery wall-to-wall (edges
of vascular adventitia) diameter may spur­
iously over­estimate the luminal narrowing.
TABLE 1: Severity of Coronary
Artery Stenosis on CT
Angiography
Degree of Stenosis
Diameter
Reduction (%)
Normal
None
Minimal
1–25
Mild
26–50
Moderate
51–70
Severe
71–99
Occlusion
100
585
Sundaram et al.
A
B
C
D
Fig. 1—Schematic illustrations of coronary artery stenosis.
A–D, Illustrations show progressive narrowing of lumen (L) resulting in mild (A), moderate (B), severe (C), and
complete (D) stenosis.
To avoid this, actual stenosis should be
estimated as the ratio between the lumen
diameter and the expected lumen diameter—
that is, the mean lumen diameter of normal
proximal and distal arteries equidistant from
the lesion. Arterial remodeling assessment
using coronary CTA appears to be reliable
within the spatial resolution limits of the
technology, and comparable to intravascular
sonography [23]. Positively remodeled
lesions are more prone to rupture even when
they are only moderately stenotic [24].
Compensatory arterial enlargement is more
common in patients with unstable than in
those with stable angina; unstable angina is
also associated with increased coronary
artery distensibility [25]. The remodeling
index (RI) of a lesion may be reported as a
ratio between the area (including both plaque
and vessel lumen) at the site of maximal (x)
luminal narrowing and the mean (y) area of
the proximal and distal reference sites: RI =
586
x / y (Fig. 5). Inflammation, coronary artery
calcification, and medial thinning are the
primary determinants of positive re­model­
ing, which appears to be a feature of plaque
instability [26].
Plaque Characterization, Morphology, and
Coronary Collateral Circulation
Various techniques are being explored to
characterize coronary plaques and their im­
pact on clinical decision making [27]. Intra­
vascular sonography and invasive coronary
angiography have been used to differentiate
coronary plaques [28], as has coronary CTA
[29–32]. Plaques can most simply be de­
scribed on coronary CTA as noncalcified,
calcified, or mixed. Char­ac­terization of non­
calcified plaques using coronary CTA seems
feasible based on the attenuation values of the
plaque composition for larger and therefore
more proximal plaques [31, 33]. However,
coronary CTA has not yet reliably and
reproducibly been shown to differentiate
among noncalcified plaques that are fibrotic
versus fatty; greater spatial resolution will be
required for this application. In patients with
stable angina, intravascular sonography esti­
mates that approximately one third have
vulnerable plaques [34] that are usually
noncalcified, with a focal lipid core in the
coronary artery wall covered by a thin fibrous
cap along the endoluminal surface. The thin
fibrous cap is usually less than 65 µm thick
and therefore not detectable on coronary CTA,
making differentiation of vulnerable from
nonvulnerable plaque on coronary CTA
difficult [35].
In native coronary arteries, plaque rupture
usually occurs in the proximal left anterior
descending artery (LAD), proximal and distal
right coronary artery (RCA), and anywhere
along the left circumflex (LCX) artery [36].
Knowledge of lesion morphology and the
status of the distal vasculature is necessary to
devise the correct coronary intervention,
either a percutaneous coronary interventional
procedure or bypass graft surgery. Hence, it
may be a good clinical practice to adequately
describe lesion characteristics, such as those
mentioned in Appendix 1 and Figures 4 and
6. The artery segment distal to a lesion can be
described in regard to its size, degree of
luminal opacification, presence or absence of
disease, and collateral vessels. Regarding
lesion characteristics, lesions can be classified
as low-, moderate-, or high-risk for coronary
intervention, according to the criteria of the
American College of Cardiology (ACC)/
American Heart Association (AHA) task
force on lesion morphology [37], which
were subsequently modified by some re­
searchers [38]. Based on fewer lesion char­
acteristics, simplification of the original ACC/
AHA classification for predicting the success
of percutaneous coronary intervention and
complications of coronary lesions was pro­
posed by the Society for Cardiovascular
Angiography and Inter­ventions, which
grades lesions as 1 to 4 [39] (Fig. 7).
Based on appearances on invasive coro­
nary angiography, 22 specific coronary col­
lateral circulation pathways (Appendix 2) are
possible [40]. Collateral circulation and the
direction of blood flow with collaterals are
more readily appreciated on invasive coro­
nary angiography than on coronary CTA.
Collateral circulation may mean that the cir­
culation of one or more coronary arteries is in
jeopardy. “Intercoronary” artery collateral
vessel refers to vascular channels originating
AJR:192, March 2009
Reporting of Cardiac MDCT
A
B
C
D
Fig. 2—CT angiography of coronary artery stenosis.
A, 45-year-old woman with family history of coronary
artery disease and hyperlipidemia who presented
with chest pain. Long-axis reformation image of
proximal left anterior descending artery shows focal
noncalcified plaque (arrow) resulting in minimal
luminal stenosis.
B, 65-year-old man with chronic stable angina. Shortaxis reformation image shows partly calcified focal
plaque (straight arrow) resulting in moderate luminal
narrowing (curved arrow) of mid left circumflex artery
segment.
C, 66-year-old man with chest pain and abnormal
myocardial perfusion imaging. Short-axis reformation
image shows partly calcified plaque in mid right
coronary artery (straight arrow), resulting in severe
luminal narrowing (curved arrow).
D, 75-year-old woman with chronic stable angina.
Curved planar reformation image shows longsegment complete luminal occlusion (arrow) of
proximal and mid right coronary artery segments.
Opacification of distal right coronary artery is
presumably due to blood flow through small
intercoronary collateral vasculature.
from two coronary arteries, and “intracoro­
nary” (bridging) collateral vessel refers to the
dilated adventitial arteries that bypass an oc­
clusion in the same coronary artery.
Coronary Artery Bypass Grafts and Stents
Fig. 3—69-year-old man
with chest pain and negative
myocardial perfusion test.
Visual estimation of curved
planar reformation image
at site of maximum stenosis
(curved arrows) in left
circumflex artery in relation to
equidistant normal proximal
(arrowheads) and distal
(straight arrows) reference
sites suggests mild stenosis.
Semiautomated stenosis
quantification tool also
quantifies diameter stenosis
of 25% (1 – 2.8 / 3.75 mm) and
area stenosis of 45% (1 – 6.5 /
11.65 mm2).
AJR:192, March 2009
Usually the left internal mammary artery
(LIMA) and saphenous vein grafts are used
for CABG; less commonly, other vessels
such as gastroepiploic or radial arteries are
used [41] (Fig. 8A). Arterial grafts have
better long-term patency than saphenous
vein grafts. Graft type, origin, course, and
anastomosis may be reported, and unusual
CABG anatomy (such as T-shaped grafts)
and their anastomoses may be described.
CABG-re­lated complications, such as ste­
nosis, throm­bosis, aneurysm, anastomotic
stricture or dehiscence, twisting, and opaci­
fication of native coronary artery distal to
the anasto­mosis, may be described (Figs.
587
Sundaram et al.
Fig. 4—Positive remodeling.
A, Schematic illustration shows eccentric bulging
of arterial wall resulting in minimal or no luminal
stenosis despite presence of significant plaque.
B, Arrow in curved planar reformation image of right
coronary artery in 45-year-old woman refers to focal
aneurysmal dilatation in distal right coronary artery
due to partly calcified atherosclerotic plaque.
8B and 8C). Graft false aneurysms are com­
monly located near ana­stomoses, whereas
true aneurysms are loc­ated in the body of the
CABG [41]. False aneurysms develop be­
cause of weakening at the site of valves with
saphenous vein grafts or vessel injury during
surgery. Graft aneu­r ysms are better char­
acterized for the presence of calcification,
dissection and thrombosis, mass effect,
rupture, and fistul­ization into the adjacent
organs. Ab­norm­alities in the feeding vessel
near the origin of a CABG (ascending aorta
for saphenous vein grafts or subclavian
arteries for LIMA grafts) may also be
documented. Graft evaluation with coronary
CTA has high sensitivity and specificity for
stenosis and occlusion, as reported in a recent
meta-analysis [42].
Coronary stents are described by location,
diameter, length, and patency (Fig. 9). Stent
descriptions—such as complete thromb­osis;
in-stent restenosis; excluded side branches;
single, overlapping, or tandem stents; and
contrast runoff in the distal coronary artery
segment—may help to explain the patho­
physiology of the stent-related abnormality.
Fig. 5—59-year-old man
with chest pain, dyspnea,
recent medical history
of viral myocarditis, and
focal apical perfusion
defect. Curved planar
reformation image of distal
right coronary artery
shows atherosclerotic
disease with minimal
luminal narrowing. Arterial
remodeling index may
be estimated as ratio
between area at maximal
stenosis (curved arrows)
and mean area of proximal
(arrowheads) and distal
(straight arrows) normal
reference sites.
588
A
B
Edges of the stents can be assessed for
neointimal hyperplasia. Coronary artery
segments adjacent to stents may need to be
evaluated for dissection and aneurysm
formation. In-stent contrast attenuation
values may be higher than values in the
proximal and distal coronary segments
because of partial volume averaging effects
from high-attenuation stent struts [43].
Hence, the presence of low-attenuation areas
in these stents may be due to in-stent
thrombus. However, these need to be dif­fer­
entiated from strut-related streak artifacts.
Caution should be used in evaluating stents
because many variables make them difficult
to evaluate, including blooming artifact
related to stent struts and calcification in
stents that can obscure plaques. A study
reports that coronary CTA has moderate
sensitivity and high negative predictive
values for detecting in-stent restenosis [44].
Noncoronary Cardiovascular Findings
Pericardium
The pericardial cavity is lined by the 1- to
2-mm-thick fibrous visceral and parietal
pericardium and contains a minimal amount
of physiologic fluid. The CT appearances of
oblique and transverse pericardial sinuses
may be mistaken for mediastinal masses
such as enlarged lymph nodes or broncho­
genic cysts [45]. Pericardial effusions may
be described for their size, for the presence
or absence of septations, and for highattenuation material that suggests hemo­
pericardium; they may also be described by
the presence of gas, calcification, pericardial
nodules or masses, and a pericardial drainage
window or catheter. Cardiac tamponade may
be suspected when there is inward bowing of
the anterior wall of the right ventricle (RV)
or lack of RV expansion on cine imaging.
Cardiac Chambers
The upper and inferior margins of the
heart are called the “acute” margins and the
left heart border is called the “obtuse”
margin, hence the terms “acute” and
“obtuse” marginal coronary artery branches.
Normal LV myocardial thickness (measured
at end-diastole either across the ventricular
septum or the posterior LV wall) is 0.6–1
cm in men and 0.6–0.9 cm in women. LV
wall thickness measurements are commonly
used in routine clinical practice to detect
LV hypertrophy. The ranges of mild,
moderate, and severe hypertrophy are
1.1–1.3 cm, 1.4–1.6 cm, and 1.7 cm or more
for men and 1–1.2 cm, 1.3–1.5 cm, and 1.6
cm or more for women, respectively [46].
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Reporting of Cardiac MDCT
A
C
On CT, the LV myocardial mass can be
measured by summing the volume of muscle
between the endocardial and epicardial
contours; this is time-consuming and is not
used in routine clinical practice. Abnormal
myocardial enhancement with IV contrast
administration, focal thinning, calcification,
fat replacement, or aneurysm formation due
to a prior myocardial infarction scar may be
described. In our current clinical practice,
AJR:192, March 2009
B
Fig. 6—Coronary artery disease.
A, 67-year-old man with multiple cardiac risk factors and
anteroseptal ischemia on stress echocardiogram who has
diffuse heavily calcified multivessel plaques on coronary CT
angiography. Arrows point to severe luminal narrowing at
origin of left main coronary artery.
B, 57-year-old man with exertional angina for 2 years and
abnormal stress echocardiography. Curved planar reformation
images illustrate tandem plaques in proximal to distal left
circumflex artery. Note severe stenosis caused by proximal
plaque (curved arrows), mild stenosis due to subsequent diffuse
plaque (arrowheads), and moderate stenosis by distal plaque
(straight arrows).
C, 76-year-old man with history of hypertension, dyslipidemia,
tobacco use, and family history of coronary artery disease.
Curved planar reformation and short-axis reformation images
from coronary CT angiography show 1.5-cm-wide aneurysm
(arrows) with large amount of intraluminal thrombus. Note
unimpressive luminal reduction due to significant positive
remodeling of arterial wall.
myocardial perfusion study and viability
assessment as done in cardiac MRI are not
routinely performed using coronary CTA.
Some reports have shown that delayed
myocardial enhancement on CT correlates
with MRI and nuclear medicine studies and
is predictive of infarct size [12–16].
Chamber morphology may be evaluated
along both the long and the short axes of the
LV (Fig. 10). Horizontal long axis and
vertical long axis are known respectively as
four-chamber and two-chamber views. The
atrioventricular valves and the LV apex are
aligned in plane to form the ideal horizontal
long-axis and vertical long-axis evaluation
planes. The short-axis viewing plane is the
true axial view of the LV, which could be
further divided into basal, mid chamber, and
apical short-axis views. The three-chamber
view is the view in which the LA, LV, and
589
Sundaram et al.
Lesion B (60−80% success during PCI)
Tubular (1−2 cm long)
Moderate to heavy calcification
Eccentric
Total occlusion < 3 months old
Moderately tortuous proximal segment
Ostial location
Moderately angulated segment 45−90°
Bifurcation lesion needs double guidewires
Irregular contour
Some thrombus
Lesion C (< 60% success during PCI)
Diffuse (> 2 cm)
Excessive tortuosity of proximal segment
Extremely angulated segments > 90°
Total occlusion > 3 months old
Degenerated vein grafts, friable lesions
Inability to protect major side branches
Non C lesion
Type 1
(Patent)
C lesion
Type 3
(Occluded)
Type 2
(Patent)
Type 4
(Occluded)
SCAI Types
Lesion A (> 85% success during PCI)
Discrete (< 1 cm long)
Little or no calcification
Concentric
< Total occlusion
Readily accessible
Not ostial in location
Nonangulated segment < 45°
No major branch involvement
Smooth contour
No thrombus
ACC/AHA Types
Lesions
Fig. 7—Coronary artery lesion classifications from American College of Cardiology/American Heart Association (ACC/AHA) [37] and Society for Cardiovascular
Angiography and Interventions (SCAI) [39]. PCI = percutaneous coronary intervention.
A
B
C
Fig. 8—Coronary artery bypass grafts (CABGs).
A, 64-year-old man with history of CABG for multivessel coronary artery disease. Volume-rendered left anterior oblique image of heart shows panoramic view of these
bypass grafts. Curved arrow indicates left internal mammary artery perfusing distal left anterior descending (LAD) artery, straight arrow indicates saphenous vein graft
perfusing left circumflex artery, and arrowhead points to saphenous vein graft perfusing obtuse marginal artery.
B, 55-year-old man with prior CABG who underwent coronary CT angiography to assess saphenous vein graft patency. Curved planar reformation of saphenous vein
graft anastomosed to distal LAD shows occluded coronary artery stent (arrow) in distal portions of graft.
C, 58-year-old woman with prior CABG surgery. Left anterior oblique view of volume-rendered image of right heart shows saphenous vein graft to LAD (arrowhead). Saphenous
vein graft perfusing distal right coronary artery (straight arrow) has focal aneurysmal dilatation (curved arrow) at its proximal anastomosis with ascending aorta.
590
AJR:192, March 2009
Reporting of Cardiac MDCT
RV are seen with both the mitral valve and
the aortic valve in the viewing plane.
Atria
The volume of the right atrium (RA) cham­
ber is minimally larger than that of the left
(LA) (75–80 mL vs 55–65 mL) (Fig. 11). At
its posterosuperior aspect, the RA com­
municates with the superior vena cava, and at
its posteroinferior margin it communicates
with the inferior vena cava (IVC). The IVC
opening is guarded by a semilunaris valve
A
known as the eustachian valve. IVC size at
inspiration is reported to potentially correlate
with cardiac function [47, 48]. The exterior
surface of the RA has a groove known as
the “sulcus terminalis,” which separates the
venae cavae from true RA chamber. The
B
Fig. 9—Coronary artery stents.
A, 55-year-old man with history of coronary artery stent insertion for focal severe luminal stenosis. Short-axis reformation and long-axis reformation images of coronary
CT angiography show widely patent coronary stent (curved arrows) and excluded origin of marginal branch (straight arrows).
B, 67-year-old man with history of coronary stent insertion in left anterior descending artery (LAD). Curved planar reformation image of LAD shows in-stent thrombosis
(arrow) resulting in mild diffuse luminal disease.
A
B
Fig. 10—Traditional cardiac views in 50-year-old man.
A, Three-chamber view shows right ventricle (RV),
left atrium (LA), and left ventricle (LV). Note mitral
(straight arrows) and aortic (AO) (curved arrow)
valves in plane.
B, Short-axis view of RV and LV shows anterior
(arrow) and posterior (arrowhead) LV papillary
muscles.
C, Two-chamber (vertical long-axis) view of LA and
LV shows arrows pointing to mitral valve.
D, Four-chamber (horizontal long-axis) view shows all
four cardiac chambers with tricuspid (curved arrows)
and mitral (straight arrows) valves in plane.
C
AJR:192, March 2009
D
591
Sundaram et al.
A
B
C
Fig. 11—Atria and appendages in 74-year-old woman.
A, Horizontal long-axis view shows all four cardiac chambers. Arrow points to membranous portion of interatrial septum (fossa ovalis).
B, Curved arrow indicates sulcus terminalis and arrowhead points to crista terminalis. Thin pectinate muscles (straight arrow) in right atrial appendage should not to be
mistaken for thrombus.
C, Arrow denotes pectinate muscles in left atrial appendage.
corre­sponding ridge on the interior surface
of the RA is the crista terminalis. The right
atrial appendage (RAA) is a broad-based
structure located anterior to and continuous
with the RA. Pectinate muscles inside the
RA should not be confused with filling
defects such as tumor or thrombus. An
arbitrary boundary between the RAA and
RA is formed by the crista terminalis and
sulcus terminalis. The LA is posteriorly
located and receives oxy­genated blood from
the lungs through the pulmonary veins.
Approximately 80% of the population has
four pulmonary veins: a superior and an
Fig. 12—52-year-old woman with prior myocardial
infarction of inferior wall who developed congestive
heart failure. Cardiac CT reveals large left ventricular
aneurysm (curved arrows) and significant amount
of intraluminal thrombus. Straight arrow indicates
anterior mitral valve leaflet, arrowhead indicates
posterior leaflet.
592
inferior pulmonary vein on both the right
and the left. The right upper and middle lobe
lung parenchyma drain via the right superior
pulmonary veins, the left upper lobe and
lingula via the left superior pulmonary veins,
and the lower lobes each through their
respective inferior pulmonary veins. The
morphology of pulmonary veins and their
ostial size are important for planning ablation
procedures to treat atrial arrhythmias [49,
50]. Variability in pul­monary vein branching,
ostial size, and the distance to the first
tributary of each may be described in studies
performed specifically for ablation mapping
[49, 50]. The left atrial appendage is a long
narrow chamber with a narrow base and
tubular chamber con­figuration that contains
pectinate muscles; the latter should not be
mistaken for thrombus or tumor.
The interatrial septum is a thin structure
of variable thickness that varies both within
a patient and among patients. Along the RA
surface of the septum is a 1- to 2-cm round or
oval craterlike area, the fossa ovalis, where
the foramen ovalis was located in utero. This
crater is covered by a thin portion of the
interatrial septum along the LA surface.
During adult life, there is normally no
communication between the RA and LA.
The prominent oval rim of the fossa ovalis is
known as the limbus ovalis, which is deficient
in its inferior rim. The remaining interatrial
septum is the thick muscular portion, about
1–2 cm thick. The amount of invaginating fat
in the interatrial septum may vary, and in
some patients is extensive. The latter is
known as lipomatous hypertrophy of the
interatrial septum, which could be mis­diag­
nosed as a cardiac mass [51].
The coronary sinus is a short venous
segment that runs in the posterior aortic valve
groove and opens into the RA medial to the
IVC orifice, with the thebesian valve at its
orifice. Most of the cardiac venous return
enters the RA through the coronary sinus ex­
cept venous return from the anterior part of the
heart. Great, middle, and small cardiac veins
can be recognized and evaluated for anato­
my, variations, and abnormalities and de­
scribed, particularly when examinations are
per­formed for anatomic mapping before
place­ment of a biventricular pacemaker. Con­
ventional anatomic and functional classi­fica­
tion of coronary sinuses is nicely describ­ed by
Singh et al. [52], who propose a seg­mental
classifi­cation system of the coronary venous
anatomy based on their epicardial location.
Ventricles
The RV inflow tract is known as a “sinus,”
and the RV outflow tract (RVOT) is known as
the “infundibulum.” The RVOT–pul­monary
artery inflow tract is also known as the
“conus arteriosus,” from which the pul­
monary artery arises. The three components
of the septal portion of the RV are the inflow
tract, the trabecular wall (which typifies the
internal appearance of RV), and the portion
of the septum that contri­butes to the RVOT.
The RVOT is formed by three components,
the conal septum, the septal band division,
and the trabecular septum; the conal septum
is clinically significant because it can be
mal­positioned in patients with con­genital
AJR:192, March 2009
Reporting of Cardiac MDCT
120
Volume (mL)
100
80
3D* method
60
EDV = 115.93 mL (phase 20)
ESV = 31.57 mL (phase 9)
40
SV = 84.37 mL, EF = 72.8%
20
Mass = 69.57 g
0
0
200
400
600
800
1,000
1,200
Trigger Delay (ms)
A
B
C
Fig. 13—55-year-old man with suspected coronary artery disease.
A and B, Short-axis reformations of left ventricle (LV) at end-diastole (A) and end-systole (B) with endocardial (red) and epicardial (green) contours. Note normal systolic
symmetric wall thickening.
C, LV volume curve obtained from retrospectively gated cardiac CT shows ejection fraction of 73%. EDV = end-diastolic volume, ESV = end-systolic volume, SV = stroke
volume, EF = ejection fraction.
dis­orders. Morph­ologic chara­cteristics are
useful in recognizing the anatomic RV in the
context of congenital cardiac diseases such
as transposition of the great vessels. Lateral
to the conal septum, the parietal extension of
the infundibular septum and the infun­dibular
fold constitutes the crista supraventricularis.
Ventricular septal defects commonly occur
in the area between the sinus and the RVOT.
The tricuspid valve is a trileaflet valve that
separates the RV from the RA. RV papillary
muscles connect the RV myocardium to the
caudal aspects of the tricuspid valve via
chordae tendinea.
The anterior leaflet is the largest leaflet and
is notched; the posterior leaflet is smaller and
scalloped. The medial leaflet is known as the
“septal leaflet,” which usually attaches to the
membranous and muscular portions of the
interventricular septum. The moderator band
is a characteristic structure in the RV apex
and is a thick muscular strip that connects
the base of the anterior papillary muscle and
the interventricular septum. The LV cavity is
somewhat narrower and longer than the RV,
measuring 7.5 cm in length and 4.5 cm in
width. It is divided into a large sinus portion
and a small LV outflow tract (LVOT). The
inflow portion has the two-leaflet mitral
valve, and the LVOT has the aortic valve.
Unlike the RV, the inflow and LVOT are
closely related. Near the LV apex, the inter­
ventricular septum has fine trabe­culations.
Two papillary muscles, the antero­lateral and
posteromedial, are connected to the anterior
and posterior mitral valve leaflets through
chordae tendinea. The papillary muscles vary
in size and morphology. They may appear
masslike in cross section, particularly during
AJR:192, March 2009
systole when the myo­cardium thickens [53].
The triangular anter­ior leaflet is the larger
leaflet; the scalloped posterior leaflet is the
smaller (Figs. 10A, 10C, 10D, and 12).
Aorta, Pulmonary Arteries, and
Pulmonary Veins
The aortic valve is a three-leaflet structure
with three sinuses. The most common
congenital abnormality of the aortic valve is
an anatomically bicuspid valve [54]; there is
also a rarer quadricuspid aortic valve. Partial
or full fusion of two leaflets results in
functional bicuspid morphology. Valve leaflet
morphology, focal or diffuse leaflet calci­
fication or thickening, vegetations, stenotic
and regurgitant valve orifice areas, leaflet
mobility, and the LVOT (measured just below
the aortic valve) may be described in a cardiac
CT report. An aortic valve stenotic orifice
between the leaflets is calculated as the
narrowest area when the valve is fully open
during LV systole; and the regurgitant orifice,
when the valve fully closes during LV diastole.
Aortic valve calcification may be quantified
on unenhanced calcium scoring CT data
sets—that is, shown to correlate with the
transvalvular gradients and aortic valve area
[55, 56]. The pulmonary valve is a trileaflet
valve with right, left, and nonseptal cusps.
The thoracic aorta included in the dis­
played field of view may be evaluated for
aneurysm and dissection, particularly for
acute syndromes in the context of acute
chest pain. Pulmonary artery filling defects
and morphology, including hypertension,
aneu­r ysms, and stenosis, may be evaluated.
It is not unusual to notice incidental pul­
monary embolism on routine outpatient CT
exam­i­nations, particularly in patients with
malig­nancy [57].
Cardiac Functional Evaluation
The use of retrospective ECG gating for
cardiac CT enables evaluation of wall motion
at rest and the quantification of LV function
without additional scanning time, radiation
exposure, or contrast material. Newer pro­
spective triggering methods allow coronary
CTA to be performed with the x-ray beam on
during end-diastole only at a substantially
lower radiation exposure for the patient;
however, because CT data are collected at
end-diastole, quantitative and qualitative
functional analyses cannot be performed. In
routine clinical practice, functional analysis
is most commonly done to evaluate the LV
and aortic valve; if needed, the same
principles and techn­ique can be extrapolated
for other cardiac chamber and mitral valve
function assessment [7–11]. Precise eval­
uation of LV function is important for the
diagnosis, therapy, and follow-up of patients
with cardiac disease [58].
LV Function
Ventricular volumes at end-diastole and
end-systole (EDV and ESV), ejection frac­
tion, stroke volume, and cardiac output can
be calculated. The endocardial borders
traced on short-axis reformations selected
at both end-diastole and end-systole are
used to determine LV volume. The contours
are automatically drawn to consistently
include or exclude the papillary muscles in
the LV volume and are manually adjusted as
needed (Fig. 13). The most basal slice is the
one just anterior to the atrioventricular ring
593
Sundaram et al.
A
B
C
D
E
F
Fig. 14—Schematic diagrams representing normal left ventricular (LV) function and dysfunction of left anterior descending artery territory.
A and B, During normal LV diastole (A) and systole (B), note respectively concentric and symmetric myocardial relaxation and thickening.
C and D, Note relative less or delayed systolic anterior LV wall thickening (hypokinesis, C) and absent systolic anterior LV wall thickening (akinesis, D).
E and F, Drawings show paradoxical outward motion of anterior LV wall (dyskinesis) during systole (E) and diastolic anterior LV wall deformation (aneurysm, F).
displaying myocardium in at least 50% of
the perimeter, and the most apical slice is
the last slice with a contrast-opacified
lumen. LV volume calculation is made using
Simpson’s rule: the sum of all crosssectional areas A multiplied by section
thickness S…, as follows [59]:
LV vol = ∑ A × S.
Ejection fraction, stroke volume, and cardiac
output are derived from the ventricular
volumes and are calculated as follows:
Ejection fraction (%) =
(EDV − ESV / EDV) × 100,
Stroke volume (mL) = EDV − ESV,
Cardiac output (mL/min) = stroke volume ×
heart rate.
An LV volume curve and the global par­
ameters of CT-derived LV function are
depicted in Figure 13; they are generated
594
when images of the heart are reconstructed at
10–20 partitions of the R-R interval. Several
studies have compared 4-, 8-, and 16-MDCTderived global function para­meters with
measurements from the current reference
standard for cardiac function, MRI [60–64],
as well as echocardiography [65, 66], cine­
ventriculography [67–69], and SPECT [64].
CT has good agreement with MRI, slightly
overestimating ESV and underestimating
ejection fraction by 1–7% [59–64, 70]. This
has been attributed to partial volume
averaging resulting from the limited temporal
resolution achieved by the current scanners.
The use of faster scanners with improved
temporal resolution is expected to improve
agreement with MRI. Normal reference
values for global LV function as used for
MRI [71] are depicted in Table 2.
LV wall motion is assessed for endocardial
excursion and the extent and timing of
systolic LV myocardial thickening. Wall
motion may be reported as normal, hypo­
kinetic, akinetic, dyskinetic, or aneurysmal
(diastolic LV deformation) [72] (Figs. 14,
S15, and S16; supplemental cine images may
be viewed at www.ajronline.org). Abnormal
wall mo­tion is related to loss of normal
functional myocardium and insufficient
myocardial per­fusion and corresponds to
diseased coron­a ry artery territories. Regional
function may be reported using the
17-segment model of the AHA [73], with six
segments each in the basal and mid LV
section, four segments in the apical section,
and one segment repre­senting the LV apex.
Stress imaging, com­monly used in
echocardiography and MRI, is impractical
with cardiac CT because of the radiation
dose and the need for ad­ditional IV
administration of iodinated con­trast material
[59]. Thus, only wall motion abnormalities
AJR:192, March 2009
Reporting of Cardiac MDCT
TABLE 2: Reference Values of Global Left Ventricular Function for All Ages
Area of Function
End-diastolic volume (EDV) (mL)
All
142 ± 21
Men
Women
156 ± 21
128 ± 221
EDV/BSA (mL/m2)
78 ± 8.8
80 ± 9
75 ± 8.7
End-systolic volume (ESV) (mL)
47 ± 10
53 ± 11
42 ± 9.5
ESV/BSA (mL/m2)
26 ± 5.1
27 ± 5.5
24 ± 4.7
Stroke volume (SV) (mL)
95 ± 14
104 ± 14
86 ± 14
SV/BSA (mL/m2)
52 ± 6.2
53 ± 6.1
50 ± 6.2
Ejection fraction (%)
67 ± 4.6
67 ± 4.5
67 ± 4.6
127 ± 19
146 ± 20
108 ± 18
69 ± 8.1
74 ± 8.5
63 ± 7.5
Left ventricular mass (g)
Mass/BSA (g/m2)
Note—Adapted from [71]. BSA = body surface area.
from high-grade lesions that lead to impaired
perfusion even at rest or fixed abnormalities
from prior myocardial infarctions with myo­
cardial damage are usually detected.
Aortic Valve Function
With ECG-gated MDCT, aortic valve
leaflet motion can be evaluated dynamically.
This trileaflet valve opens during systole
with effacement of the sinuses and closes
during diastole with complete coaptation of
the leaflets (Fig. S17). When evaluating a
native aortic valve, note the number of
leaflets (Figs. S18 and S19), valve stenosis
(Fig. S19), regurgitation (Fig. S20; supple­
mental images are available at www.
ajronline.org), the presence or absence of
calcification, and valve vegetation. Cine
images are useful to evaluate the precise
architecture of the valve and the patterns of
commissural fusion [74]. Incomplete co­
aptation of the leaflets may represent valve
dysfunction, and the diastolic regurgitant
aortic valve orifice area is reported to cor­
relate well in grading known aortic incom­
petence as defined by trans­eso­phageal echo­
cardiography [75].
Noncardiovascular Findings
Noncardiac findings on coronary CT can
be seen in 25–61% of patients, of which
5–41% may be significant or potentially
significant findings [76–81], similar to earlier
reports of calcium scoring electron-beam CT
examinations [78, 80, 82]. A patient with
absolutely normal coronary arteries could
have a potentially life-threatening finding in
the thorax accounting for chest pain, such as
acute pulmonary embolism, acute aortic
syndrome, or a relatively benign finding such
as a large hiatal hernia. Few studies have
reported the rate of incidental findings of
AJR:192, March 2009
lung cancer first detected on coronary CT
[76, 77]. It is therefore important to evaluate
all the structures surrounding the heart and
included in the acquisition. A systematic
approach to analyzing the noncoronary
findings is helpful; whether a field of view is
reconstructed for the heart only or for the
entire width of the thorax, findings in the
imaged field of view may have a major impact
on patient management.
Conclusion
Cardiac CT is increasingly integrated in
clinical practice for elective and emergent
evaluation of suspected CAD. In this article,
we have reviewed our understanding of
CAD, and the usefulness of coronary CTA in
the diagnosis and characterization of CAD.
We have illustrated accepted descriptions
relevant to coronary artery disorders, cardiac
anatomy, and cardiac functional assessment
that may be useful to interpret cardiac CT
examinations, with the aim of providing a
comprehensive cardiac CT report that is
concise, structured, and informative about
the question posed by the nonradiology
physician colleague.
Acknowledgment
We sincerely thank Anne Phillips, med­
ical illustrator, Department of Radiology,
University of Michigan, Ann Arbor, MI, for
creating the schematic illustrations in Fig­
ures 1 and 4A.
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Appendices appear on next page
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Sundaram et al.
APPENDIX 1: Potential Descriptions of Characteristics of Native Coronary Artery Disease
Lesion Characteristics
• Calcifications (minimal, moderate, severe)
• Length
• Eccentricity
• Osteal involvement
• Ulceration
• Irregularity
• Tortuosity
• Vessel wall remodeling
• Intraplaque hypodensity
• Thrombus or embolus
• Acute or chronic occlusion
• Bifurcating lesions
• Tandem lesions
• Coronary artery aneurysm
APPENDIX 2: Coronary Collateral Circulation Pathways
Right Coronary Artery Occlusion
• Left anterior descending (LAD) artery to posterior descending artery (PDA) via ventricular septal branches
• Distal left circumflex (LCX) artery to distal right coronary artery (RCA)
• Obtuse marginal (OM) to posterior left ventricular (LV) branch of RCA
• Proximal acute marginal (AM) artery or conus branch to distal AM
• Kugel’s artery: proximal RCA or left main (LM) coronary artery to atrioventricular (AV) nodal branch
• Distal LAD to PDA
• Distal LCX or its left atrial (LA) branch to AV node branch
• AM to PDA
• Sinoatrial node branch to LA circumflex branch, then to distal RCA
• Right ventricular (RV) branch of LAD to AM
Left Anterior Descending Artery Occlusion
• AM to LAD
• Proximal ventricular septal branch of LAD to distal septal branch
• OM to LAD
• Conus branch of the RCA to LAD
• Diagonal branch to distal LAD
• PDA to LAD via apex
• PDA to LAD via the septal branches
Left Circumflex Artery Occlusion
• LA LCX branch to distal LCX
• Proximal OM to distal OM
• Diagonal artery to OM
• Distal RCA to distal LCX
• Posterior LV branch of the RCA to OM
Adapted from [40].
F O R YO U R I N F O R M AT I O N
• A data supplement for this article can be viewed in the online version of the article at: www.ajronline.org.
• This article is available for CME credit. See www.arrs.org for more information.
• The reader’s attention is directed to part 1 of this article, titled “Anatomy and Technology for the Interpretation
and Reporting of Cardiac MDCT: Part 1, Structured Report, Coronary Calcium Screening, and Coronary Artery
Anatomy,” which appears on page 574.
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