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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3676_Библиотеки_им_академика_М_И_Перельмана
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6.5 Case 6.5
6.5.1 History
An 80-year-old male presented with a history of
increasing shortness of breath and no prior cardiac history.
a
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6.5.2 Findings
A non-calcified plaque is seen in the mid-left
circumflex, with positive and negative remodeling and high-grade obstruction of the lumen
(Fig. 6.5a–c). Additionally, there is a complex
plaque in the mid-LAD, adjacent to the ostium
b
Fig. 6.5 (a) cMPR: Mid-left circumflex coronary artery
(LCX) non-calcified plaque causing both positive and
negative remodeling and high-grade obstruction (arrows).
(b) Stretched cMPR: Mid-LCX non-calcified plaque
(arrows). (c) 3D volume rendered: Mid-LCX (arrow). (d)
cMPR: LAD. High-grade obstruction adjacent to the
ostium of D1 (single arrow). Thrombus in the mid-LAD,
with total occlusion of the artery (double arrows), and retrograde flow in the distal LAD. (e) cMPR: D1. Highgrade obstruction in the proximal segment of the artery
(arrow)
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of D1, causing high-grade obstruction. Distal
to D2, there is calcified plaque in the LAD and
a thrombus of undetermined age, with total
occlusion of the artery and retrograde flow
into the distal LAD (Fig. 6.5d). The first diagonal branch is a long vessel of large caliber
and has a mixed plaque in the proximal segment that is also causing high- grade obstruction (Fig. 6.5e). There was no evidence of a
prior myocardial infarct.
6.5.3 Diagnosis
Non-calcified plaque in the mid-LCX, with positive and negative remodeling, causing high-grade
obstruction in the lumen. There is thrombus in
the mid-LAD, which is totally occluded, with
retrograde flow from collaterals into the distal
LAD. There is also high-grade obstruction in the
proximal first diagonal artery.
6.5.4 Discussion
The case depicts the typical findings of progression of disease in the wall of the artery (LCX),
with both positive and negative remodeling causing high-grade luminal stenosis.
6.5.5 Pearls and Pitfalls
Atherosclerosis is a systemic and inflammatory
disease. It is common to encounter multiple
plaques at different stages of disease progression.
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6.6 Case 6.6
6.6.1 History
An 80-year-old male presented with a 2-week
history of chest pain.
6.6.2 Findings
There is a complex plaque in the mid-RCA causing high-grade stenosis (Fig. 6.6a). The atheroma
is causing expansion of the intima, with a donut
sign appearance on the axial slice (Fig. 6.6b).
There is a mixed plaque in the proximal RCA
that is non-obstructive. The patient underwent
stenting of the RCA and subsequent intensive
medical therapy. A 14-month follow-up CTA
demonstrates a patent stent in the mid-RCA, with
decrease remodeling in the adjacent wall and also
diminished soft tissue component in the proximal
plaque (Fig. 6.6d).
6.6.4 Discussion
A lesion causing mild stenosis may rupture suddenly and cause bleeding into the wall of the vessel (plaque hemorrhage), causing high-grade
obstruction and/or occlusion of the vessel because
of thrombosis. Injury to the endothelial lining of
arteries, active uptake by the vascular wall of atherogenic lipoprotein particles, inflammatory and
oxidative reactions, thrombosis, calcification,
and hemorrhage all contribute to arteriosclerosis
and scarring of an artery wall.
6.6.5 Pearls and Pitfalls
We have observed in a number of patients the
CCTA donut sign. It is typical of a complex atheroma, causing high-grade stenosis that is consistent with intramural hemorrhage (acute/
subacute). Since this type of lesion is considered
unstable, it is important to differentiate it from
negative remodeling of an atheroma.
6.6.3 Diagnosis
Complex plaque in the mid-RCA, causing highgrade stenosis.
Fig. 6.6 (a) cMPR: Right coronary artery (RCA), com-
plex plaque in the mid-RCA, causing high-grade obstruction (arrows). There is a mixed plaque in the proximal
RCA that is not flow limiting. (b) Axial RCA. Complex
plaque, with expansion of the intima: donut sign (arrow).
(c) Axial RCA. Proximal to the lesion, the lumen has normal diameter (arrow). (d) cMPR: RCA. 14-month follow up post-stenting of the mid-RCA (arrow)
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a
b
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6.7 Case 6.7
6.7.1 History
A 56-year-old male physician presented with a
family history of CAD and new onset of chest
discomfort during exercise.
6.7.2 Findings
There are scattered mixed plaques throughout the
LAD. There is a non-calcified plaque in the proximal LAD causing high-grade critical stenosis
(Fig. 6.7a–c).
6.7.3 Diagnosis
Non-calcified plaque in the proximal LAD, causing high-grade critical stenosis.
6.7.4 Discussion
The combination of findings, proximal LAD
large non-calcified plaque (potentially vulnerable) causing a critical stenosis, should be communicated immediately to the referring physician.
The patient was sent directly to the hospital from
the outpatient center and underwent a subsequent
angiogram and successful stenting of the lesion
(Fig. 6.7d, e). The patient responded well and is
currently asymptomatic (and very grateful).
6.7.5 Pearls and Pitfalls
In evaluating cardiac CT, and in the presence of
high-grade stenosis, one should attempt to differentiate stable from potentially unstable disease,
which could lead to a coronary event. As the utilization of cardiac CTA becomes more commonplace (such as in the emergency room setting), the
medical and legal implications become apparent.
ab
cd e
Fig. 6.7 (a) cMPR: LAD. Soft tissue plaque in the proxi-
mal LAD, causing high-grade critical stenosis (arrow). (b)
cMPR-stretched LAD. Same findings as 2.7A. (c) 3D volume rendered. Proximal left anterior coronary artery (LAD)
(arrow). (d) Coronary angiogram: 99% (string sign) proximal LAD stenosis (arrowhead). (e) Coronary angiogram:
PCI with drug-eluting stent placement in the proximal LAD
with excellent results (arrowhead)
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6.8 Case 6.8
6.8.1 History
A 72-year-old asymptomatic male presented with
inferior wall ischemia on a nuclear perfusion scan.
6.8.2 Findings
There is penetration of contrast into the wall of the
proximal RCA. Two additional distal areas of highgrade stenosis are noted in the RCA (Fig. 6.8a, b).
ab
6.8.3 Diagnosis
The diagnosis is ruptured plaque in the proximal
RCA.
6.8.4 Discussion
The case illustrates a fissure in the intimae of the
proximal RCA, with penetration of contrast into
the wall, the classic appearance of a ruptured
plaque. The lesion was considered unstable,
implying the potential to lead to thrombus
Fig. 6.8 (a and b) cMPR: Right coronary artery (RCA).
Ruptured plaque with a fissure in the proximal RCA. There
is penetration of contrast into the wall (proximal arrows).
There are two distal areas of high-grade obstruction (dou-
ble arrows). (c) Coronary angiogram. (d) Post-stenting
coronary angiogram
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formation and potentially an acute coronary syndrome. The patient underwent coronary angiography the following day, with successful ballooning
and placement of sequential drug-eluting stents in
the proximal to mid-RCA (Fig. 6.8c, d).
Most plaque ruptures occur because of disruption of the fibrous cap, which allows contact
between the highly thrombogenic lipid core and
the blood. These modestly obstructive plaques,
which have a greater burden of soft lipid core and
thinner fibrous caps with chemoactive cellular
infiltration particularly adjacent to the shoulder
region, are called vulnerable plaques. The amount
of collagen in the fibrous cap depends on the balance between synthesis and destruction of intercellular matrix and inflammatory cell activation.
6.8.5 Pearls and Pitfalls
Careful observation of atheromas with thin
curved reformatted reconstruction and crosssectional imaging is recommended in order not to
miss a ruptured plaque. Proper windowing and
analysis of Hounsfield density is additionally
necessary to differentiate a complex plaque from
a fissure. Three-dimensional volume rendered
and thick MIP images may obscure the abnormality. Since the lesion is unstable, immediate
therapy (medical/intervention) is warranted to
prevent an acute coronary syndrome.
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6.9 Case 6.9
6.9.1 History
A 57-year-old physician complained of mild
chest discomfort during extreme exercise.
a
d
6.9.2 Findings
There is advanced mixed plaque in the left main
coronary artery, causing high-grade stenosis.
There was also disease in the proximal LAD and
LCX (Fig. 6.9a–d).
bc
Fig. 6.9 (a) A. 3D volume rendered: Left main stenosis (arrow). (b and c) cMPR LM–LAD (arrow). (d) Coronary
angiogram: LM stenosis confirmed on angiography (arrowhead)
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6.9.3 Diagnosis
The diagnosis is high-grade stenosis in the left
main coronary artery.
6.9.4 Discussion
Left main coronary artery disease is defined as
>50% left main diameter narrowing, often characterized by symptoms of unstable angina sometimes with hemodynamic compromise, diffuse
ST depression in inferior and precordial leads on
ECG, and poor prognosis due to sudden death
and massive infarction. CABG is the first-line
therapy, while stenting is commonplace in many
countries as an alternative to surgery. The patient
had a diagnostic angiogram confirming the highgrade left main coronary stenosis and underwent
double bypass surgery.
6.9.5 Pearls and Pitfalls
The left main coronary artery has variable origin,
length, and diameter. Comparison with the diameter of the proximal LAD and circumflex may
prove helpful in assessing the degree of stenosis
in the left main.
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6.10 Case 6.10
6.10.1 History
6.10.2 Findings
There is diffuse coronary artery ectasia, with
multiple aneurysms and LAD, left circumflex,
A 43-year-old male presented with a history of
eosinophilia and cardiac angina.
and RCA chronic total occlusions. There is also a
left coronary sinus aneurysm (Fig. 6.10a–e).
abc
de
Fig. 6.10 (a and b) Aneurysmal dilatation of the left
anterior coronary artery (LAD) with mid-segment chronic
total occlusion and retrograde flow in the distal segment.
(c) 3D volume rendered: Proximal RCA aneurysm and
mid-segment chronic total occlusion. (d) Axial. Left coro-
nary sinus aneurysm (single arrow). Proximal LAD aneu-
rysm (double arrow). (e) Coronal. Thrombosed aneurysm
of the proximal left circumflex coronary artery (double
arrow). (Courtesy of Dr. Martin H. K. Hoffmann, Ulm,
Germany)
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