Role of MDCT in

Coronary Artery Disease

Swachchhanda Songmen
2071-05-05-05
 Outline
• Normal anatomy
• Anomalies
• Imaging technique of MDCT CA
• Coronary artery disease
• Myocardial perfusion
NORMAL ANATOMY Coronary A
Coronary A:
1st branch of aorta
supply most myocardium &
epicardium

Endocardium & subendocardial tissue

by diffusion & microvasculature
directly from cardiac chamber
RCA: LCA:
• SA nodal 60% • LAD anterior interventricular
• Right marginal branch, diagnonal branch
• AV nodal • LC SA Nodal A 40%; left
marginal A; posterior
• Posterior interventricular interventricular 1/3
branch 2/3
• v
 Variation in CA distribution

• Dominance: supply post interventricular branch

67% RCA; 15% LCA; 18% codominance
• LMCA length
– A: normal 15mm
– B: short 7mm
– C: large 32mm
Anomalies
• Variants in ORIGIN & COURSE of central coronary
segments
• Imp cause of cardiac morbidity & mortality, esp in
adolescent & young adults.
• Rare; 0.5-1%
• Isolated/ aw CHD; SIDS
• Schmid and colleagues evaluated role of MDCT in
coronary anomalies & divided into 2 groups,
depending on origin & course of coronary artery:
– benign or minor coronary anomalies most common;
no clinical relevance
– malignant or major coronary anomalies
Benign coronary anomaly

Independent origin of LAD & CX from left aortic sinus commonest

in left coronary A system; from sinus or common ostium
Benign coronary anomaly

Left CX arising from right aortic sinus from right sinus, ostium or
RCA; commonest benign anomaly; travel benign retroaortic course
Malignant coronary anomaly
• ectopic origin in contralateral side of heart &
then course between aortic root & pulmonary
trunk to other side
• Stm hemodynamically significant & produce
myocardial ischemia or even sudden death
• First & most accepted hypothesis: aorta &
pulmonary arteries reduce lumen of prox origin
of anomalous coronary A during exercise or
body stress.
• Coronary A may originate from pulmonary trunk
Malignant coronary anomaly

• RCA arising from the left aortic sinus: commonest

malignant anomaly
Malignant coronary anomaly

LMCA arising from right aortic sinus: 59% die <20yrs

 Malignant coronary anomaly

Reverse Blant-White- Blant-White-Garland

Garland syndrome syndrome

Ischemia & sudden death in early childhood

 Malignant coronary anomaly
• Commn betn
coronary A with
cardiac chamber/
systemic V
• Coronary A is
dilated &
tortuous
• If large
myocardial
CORONARY ARTERY FISTULA:
CAF draining into right ventricle in a 7-year-old boy perfusion deficits
with dyspnea.
Myocardial bridging
• Congenital anomaly
• Seg of major epicardial CA runs
intramurally thru myocardium
(tunneled A)
• Systolic compression
• Angiography Dx by indirect sign of
systolic compression “milking effect”
• MDCT accurately assess length &
quantify % of compression during
systolic & diastolic phases
• Types:
– Incomplete tunneled A partially
covered
– Complete A fully covered; 3
patterns
 Pattern 1:
no compression in systole & diastole
 Pattern 2:
compression in systole & not in diastole
 Pattern 3:
compression in systole & persisting
partial/complete compression in diastole
Technique of MDCT CA
• Approaches: ECG synchronization cardiac scan
Prospective ECG Retrospective ECG
gated gated
ECG simultaneous Yes Yes
with scan
Basic Scan initiated with Retrospective data
predetermined seg selection
temporal offset
Advantage Less radiation dose Easier
reconstruction,
possible in all phases
Disadvantage Reconstruction in Higher radiation
diff cardiac phases dose
not feasible
1. Prospective ECG gating: data acquisition with heart cycle at a prespecified moment of R-
R interval
2. Retrospective ECG gating: Data continuously acquired & ECG recorded during scan;
reconstruction window can be positioned anywhere within R-R interval, usu during
diastole.
Patient Preparation
• A regular sinus HR is necessary for reliable imaging
of CA by MDCT
• oral and/or IV beta blockers if HR>60 bpm
• orally, 45-60mins before scan (atenolol 50-100 mg;
metoprolol 50-100 mg).
• If HR>60 bpm at time of scan, i.v. metoprolol 5 to 20
mg.
• To dilate CA & avoid vasospasm- s.l. nitrates
(isosorbide dinitrate 2.5-5 mg) or nitroglycerin (0.4-
0.8 mg) immediately before exam
 contraindications
Absolute
• Hypersensitivity to iodinated CM
• Pregnancy

Relative Contraindications
• Irregular rhythm (e.g., AF/flutter, frequent irregular
premature contractions)
• Renal insufficiency (serum Cr >1.5 mg/mL)
• BMI>40 kg/m2
• Hyperthyroidism
• Inability to hold breath for 10sec
• History of allergies to other medications
• Metallic interference (e.g., pacemaker, defibrillator wires)
CT scan protocol
• d/o scanner configuration
• Volume data covering entire heart in inspiratory breath
hold
• Exposure 3-16mSv
• ECG controlled dose modulation system decrease
exposure upto 50%
• Usu centered in mid-diastole (70-75% of R-R interval)

ECG-controlled dose modulation systems allow alternation of X-ray tube output full
exposure during diastole; during systole output of tube current is decreased.
Contrast Medium Protocol
• nonionic iodinated CM conc 300-400 mg I/mL
• Volume & rate of contrast injection depends on CT
scanner configuration e.g. 64-detector MDCT – inj
80mL at 4-6 mL/sec f/b 40 mL saline at 4 mL/sec
• test bolus scan/ bolus-tracker technique
Postprocessing protocols
• Original cross sectional images insufficient
• Postprocessing MPR, MIP, curved MPR, VR,
stretched MPR for curved vessel, virtual
intravascular US, std angiographic view

Curved MPR
Curved MPR of LAD as stretched MPR; color map to
identify plaque; stenosis inspection & A lumen
analysis
Coronary A Disease
Coronary artery assessment
• All CA can’t be assessed with same image quality.
• Best evaluated almost 100% is LMCA runs along
axis of scan & not significantly affected by cardiac
movements.
• LAD well visualized in 76-96%; not assessable if
severe coronary Ca++.
• Left CX affected by cardiac motion artifacts; 52-
95%.
• RCA most affected by cardiac movement; 71-91%.
• Prox, distal segment, & side branches assessability
of 92%, 71%, & 50%, respectively.
 CA total occlusion
MDCT CA role:
• Identify total occlusion
• Cause- calcified vs noncalcified plaque
• Extension
• Morphology of occluded seg
• Time A was occluded:
– Acute low density thrombus & increase luminal A &
d
– Chronic calcified plaques & N/narrowed lumen
Acute
occlusion:
Hypoechoic
& distended
lumen

Chronic
occlusion:
Echogenic;
lumen not
distended
Calcification of coronary arteries
• Detection of coronary artery calcium indicates that
atherosclerotic dis is present
• The more Ca++ found, the greater the amount of
atherosclerosis .
• However, the amount of calcium underestimates the true
extent of atherosclerotic disease and does not predict the
site of areas of stenosis.
• Agatston and associates in 1990: quantification of CA
calcification
• They scored each lesion in each slice based on maximum
density with particular scale:
– 1 = 130 to 199 HU;
– 2 = 200 to 299 HU;
– 3 = 300 to 399 HU;
– 4 = 400 HU or greater
Calcium score Interpretation
0 No identifiable atherosclerotic plaque; very low
cardiovascular disease; <5% chance of presence
of CAD
A -ve examination
1-10 Minimal plaque burden
Significant CAD very unlikely
11-100 Mild plaque burden
Likely mild or minimal coronary stenosis
101-400 Moderate plaque burden
Moderate non-obstructive CAD highly likely
>400 Extensive plaque burden
High likelihood of at least one significant
coronary stenosis (>50% diameter)
Axial CT prospective ECG-gating for calcium scoring. Calcification (arrows) in LAD & diagonal
branch. Bottom images show cardiac calcium scoring window with areas of pixel values
>130HU in red.
Coronary artery stenosis
• To correctly quantify coronary stenosis
essential to obtain cross-sectional orthogonal
images of selected vessel
• Evaluation of artery cross sections along its
length, assessment of plaque morphology,
quantification of plaque burden, calculation of
remodeling index, & assessment of effective free
lumen diameter & area, stenosis severity, &
geometric parameters
• MDCT CA sensitivity 83-99%; sp 93-99%; NPP 95-
100%
Segmental evaluation of CA usu performed according to
modified AHA classification of 17 coronary segments
Quantitative assessment of stenosis
• Most literature so far used binary cut-off of 50%
stenosis as significant stenosis.
• Society of Cardiovascular Computed Tomography
(SCCT) guidelines on interpretation & reporting of
coronary CTA, recommending that stenoses be
graded in broad ranges rather than assigning a
specific number
Recommended stenosis grading
• Normal - Absence of plaque and no stenosis
• Minimal - <25% stenosis
• Mild - 25% - 49% stenosis
• Moderate - 50% - 69%
• Severe 70% - 99%
• Occluded -100%
Plaque characterization
• Classification based on echogenecity (IVUS) & density
in HU (MDCT)
• Soft Plaques: “softlike” tissue adj to vessel wall with
lower density than enhanced lumen (be identified in
at least 2 independent planes). Mean density value is
14 +/- 26 HU
• Fibrous/Intermediate Plaques: “softlike” tissue adj to
vessel wall with lower density than enhanced lumen
but with greater density than soft plaques (be
identified in at least 2 independent planes). Mean
density value is 91 +/-21 HU
• Calcified Plaques: like soft tissue with higher density
than luminal enhanced area (if it is adjacent) or with
density >130 HU (if separate from lumen). Mean
density value is 419 +/- 194 HU
Plaque burden:
• Plaque burden= [1 - (lumen area/vessel area)] x
100
• +ve>50%.

Remodeling index
• Remodeling index= area at max luminal
narrowing/ mean area of prox coronary seg
• Plaques that form intracoronary thrombus have
higher plaque burden & RI than stable ones.
Coronary artery aneurysm
• CA diameter > 1.5X D of normal ad seg
• Cardiac gated CTA
– Aneurysmal dilatation well-depicted
– Calcification frequently present in atherosclerosis
– Detects mural thrombus
• Invasive angiography may underestimate luminal
diameter if mural thrombus present
Coronary stent assessment
• Rate of coronary stent restenosis 20-35% for
bare metal stents & 5-10% for DES
• Restenosis cause: (1) neointimal or myointimal
proliferation and (2) mechanical reasons.
• Patent: hyperattenuation of stented CA seg &
distal seg

Patent stainless steel stent at

LAD mid segment
• 2 main factors for interpretation of MDCT scans
of stented segments:
1. type of stent (strut thickness and material):
Excessive radiopacity of implanted stents causes
blooming, increasing thickness on stent struts &
obscuring part of stent lumen (Au & Tantalum>
stainless steel & Co)
2. stent diameter: Diameter at least 3.5 mm
A, Axial CT image of a gold-coated stent in the left anterior descendent artery. Because of
artifacts caused by the dense stent material, the assessment of the lumen within the
stent is not possible. B, Curved multiplanar reformatted image showing a stainless-steel
stent in the circumflex artery without evidence of in-stent restenosis.
absence of contrast enhancement in the stent lumen
CABG assessment
• Better visualization of bypass grafts and graft
anastomosis with assessment of patency &
detection and grading of stenosis
• Easier to image than native coronary arteries
owing to a straighter course, larger diameter,
and fewer cardiac motion artifacts
• Sensitivity 92% for patency, accuracy 88%
(Engelman)
• With newer machines, high diagnostic
accuracy can be used in clinical routine as
reliable, noninvasive Dx tool in susp CABG dysFn
VR patent left internal mammary artery (LIMA) Curved MPR: patent prox course &
double-jump graft to the LAD (arrows), to a diagonal occlusion (arrows) of distal segment and
branch (DG) (dotted arrows), and to an intermediate distal graft anastomosis of a left internal
ramus branch (IR) (double arrows). mammary artery (LIMA) graft to LAD
Myocardial perfusion by MDCT
• SPECT predominant technique to study regional
distribution of CA flow others e.g. PET, EBCT,
stress echo, MRI
• But none give associated coronary anatomy
information
• MDCT for myocardial perfusion assessment while
simultaneously appraising coronary arteries
• MDCT performed
– at rest necrosis +nce
– with pharmacologic stress ischemia (adenosine,
dipyridamole)
– as a delayed scan determine viability of particular
myocardial perfusion defect
Using cardiac
review
software, heart
is reoriented in
a strict axial
plane, & short
& long axis
images of LV
created, based
on AHA 17-seg
model of LV
recommended
for all cardiac
imaging
modalities
3 patterns-
• normal myocardium: enh homogenously in both
rest & stress scans
• myocardial perfusion defect:
– Ischemia: defect in stress; disappears in rest
– Necrosis: defect in stress & rest
Pattern of defect intramural, transmural,
subendocardial
• myocardial viability:
– Negative: accumulates in nonviable tissue
hyperenh
– Positive: hypoenh
Normal myocardium. The normal myocardium enhances homogeneously in both rest and
stress MDCT (A and B)
Subendocardial myocardium ischemia. Rest MDCT (A) show normal enhancement of the left
ventricle myocardium. A subtle myocardial perfusion defect is presents in the stress MDCT
image (B) (arrow).
Myocardial necrosis. MDCT (A and Bimages perfusion defect in inferior-lateral wall, in both
rest and stress images. Hypoattenuation is increased in the stress images due to ischemic
changes (arrow).
Transmural (solid arrows) and intramural (dashed
arrows) infarction areas on an early MDCT image. B, On
a late image, the contrast material accumulates in
nonviable tissue, showing a typical hyperenhancement
(negative viability)
THANK U!
 Questions
1. Important branches of Right & left coronary artery
2. coronary artery dominance
3. classify coronary artery anomalies
4. Malignant coronary anomaly
5. Myocardial bridging
6. Prospective versus retrospective ECG gated MDCT CA
7. Patient preparation & protocols
8. Coronary artery total occlusion: role of MDCT CA
9. Calcification of coronary artery with Agatston scoring
10. Quantitative assessment of coronary artery stenosis
11. Plaque characterisation
12. Coronary stent assessment
13. CABG graft assessment
14. Myocardial perfusion by MDCT
Limitation of MDCT CA:
• limited spatial resolution in comparison with
IVUS cannot detect early stages of dis

Advantage of MDCT CA
• depicts CA wall expansive remodeling process
that occurs in earlier phases of dis to preserve
normal luminal size (positive remodeling).
• This phenomenon cannot be detected by CA,
which only diagnoses the coronary artery
stenosis in the advanced stages, when the
lumen is reduced (negative remodeling).