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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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C. Smuclovisky
6.10.3 Diagnosis
The diagnosis is Churg–Strauss syndrome.
6.10.4 Discussion
Churg–Strauss syndrome is a systemic vasculitis.
The disease was first described in 1951 by Dr.
Jacob Churg and Dr. Lotte Strauss as a syndrome
consisting of “asthma, eosinophilia, fever, and
accompanying vasculitis of various organ systems.” Churg–Strauss syndrome shares many of
the clinical and pathologic features of polyarteritis nodosa. Churg and Strauss discovered that the
presence of granulomas as well as the abundance
of eosinophils distinguished this disease from
polyarteritis nodosa. Another name for Churg–
Strauss syndrome is allergic granulomatosis.
The mechanism behind the changes that produce coronary artery disease in vasculitis involves
immunologically mediated inflammation with
intimal thickening from the accumulation of
fibrous tissue and proliferation of smooth muscle
cells. There is also pathologic evidence that stimulated eosinophils are directly toxic to myocardial cells and arterial wall components.
Aneurysmal dilatation is associated with destruction of the media. The most notable vasculitis to
affect the coronary arteries is Kawasaki’s disease.
Kawasaki’s disease, however, occurs predominantly in children, presenting with fever lasting
several days. It is commonly associated with
strawberry tongue, palmar erythema, rash, or
cervical lymphadenopathy.
Churg–Strauss syndrome usually responds to
prednisone. Initially, high doses of oral prednisone are used in an attempt to get the disease into
remission as quickly as possibly (e.g., using oral
prednisone 40–60 mg/day). After the first month
or so, this high dose of prednisone is gradually
tapered down over the ensuing months. Other
immunosuppressive drugs, such as azathioprine,
mycophenolate mofetil (CellCept), methotrexate,
or cyclophosphamide may be used in addition to
prednisone. High doses of intravenous steroids
(usually methylprednisolone) may be useful for
those patients with severe disease or for those
who are unresponsive to the combination of oral
prednisone used with other immunosuppressive
medications.
6.10.5 Pearls and Pitfalls
Vasculitis should be suspected, particularly in
younger patients, with abnormally dilated coronary arteries and aneurysms.

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6.11 Case 6.11
6.11.1 History
A 76-year-old asymptomatic male presented with
a history of inferior wall ischemia on a nuclear
perfusion scan.
ab
6.11.2 Findings
There is high-grade stenosis in the proximal segment of the RCA and chronic total occlusion in
the mid-segment of the RCA, with retrograde filling of the distal segment. There is non- obstructive
disease in the proximal left circumflex, with critical subtotal occlusion in the ostium of the first
obtuse marginal artery (Fig. 6.11a–e).
cde
Fig. 6.11 (a and b) Curved and stretched MPR RCA:
Proximal segment high-grade stenosis (single arrow).
Mid-segment chronic total occlusion (double arrows). (c)
Angiogram RCA. (d) cMPR LCX: Ostial subtotal occlusion of OM1. (e) Angiogram: LCX–OM1 (arrow)

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6.11.3 Diagnosis
RCA mid-segment chronic total occlusion and
critical subtotal occlusion of the first obtuse marginal artery (OM1).
6.11.4 Discussion
The mid-RCA has a low-density transition zone
that is diagnostic of a totally occluded artery. It is
common to see contrast opacification of the distal
segment from retrograde filling from collaterals.
The thrombus in the occluded segment of the artery
commonly has low density and may contain calci-
fied atheromas. Although the age of the thrombus
in a patient without an acute coronary syndrome
usually cannot be ascertained, these are commonly
referred to as chronic total occlusion (CTO). It may
be challenging with CT to differentiate a subtotal
from a total occlusion. In the subtotal occlusion,
the transition zone is typically shorter, and a small
channel of contrast density is identified.
6.11.5 Pearls and Pitfalls
Due to the timing of the acquisition of a CCTA, it
cannot be determined whether the arterial flow is
antegrade or retrograde.

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6.12 Case 6.12
6.12.1 History
A 77-year-old asymptomatic female with a strong
family history of CAD presented for presurgical
orthopedic clearance. The patient had a prior negative myocardial perfusion scintigram result.
6.12.2 Findings
There is advanced diffuse disease in the proximal
LAD. There is short-segment chronic total occlusion in the mid-LAD. There is diminished contrast density in the distal LAD from retrograde
collateral flow (Fig. 6.12a–d).
6.12.3 Diagnosis
Mid-LAD chronic total occlusion.
abd
6.12.4 Discussion
The mid-LAD has a short low-density transition
zone with a lack of contrast density, indicating a
totally occluded artery. The distal LAD appears
to have diminished caliber and is being opacified
by retrograde flow from collaterals. The findings
were confirmed on an angiogram. The patient
had subsequent bypass surgery to the distal LAD.
6.12.5 Pearls and Pitfalls
The distal segment of an occluded artery commonly appears of small caliber due to the retrograde flow from collaterals and under-filling of
the vessel. Therefore, it cannot be assumed that
the caliber of the artery is too small for bypass
surgery.
c
Fig. 6.12 (a–c) 3D volume rendered, curved, and stretched MPR: Mid-left anterior coronary artery (LAD) chronic
total occlusion (arrow). (d) Angiogram: Confirms the occluded LAD (arrow)

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6.13 Case 6.13
6.13.1 History
6.13.2 Findings
There is advanced diffuse non-calcified and calcified plaque extending from the distal left main
A 45-year-old male presented with exertional
chest pain and reported a normal exercise myocardial perfusion scan result.
to the mid-LAD. There is long-segment tubulartype high-grade stenosis in the proximal and
mid-LAD (Fig. 6.13a, b, and e). There is also
d
e
fgh
Fig. 6.13 (a and b) cMPR LM–LAD. (c and d) cMPR LCX: Diffuse disease with proximal high-grade stenosis. (e) 2D
map: Advanced multi-vessel disease. (f–h) Coronary angiogram

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high-grade stenosis by mostly non-calcified
plaque in the proximal left circumflex (Fig. 6.13c,
d, and e). The RCA has moderate diffuse non-
obstructive disease (Fig. 6.13e).
6.13.3 Diagnosis
Advanced multi-vessel coronary artery disease, with long-segment tubular high-grade
stenosis in the proximal to mid-LAD and shortsegment high-grade stenosis in the proximal
left circumflex.
6.13.4 Discussion
The CTA demonstrates well the extent of disease,
which can be helpful in planning coronary intervention and/or surgical management. It is well
documented in the literature, with intravascular
ultrasound (IVUS) correlation, that conventional
coronary angiography commonly underestimates
the amount and extent of disease in the artery
wall. The angiogram in this case demonstrates
significantly less disease than identified on the
CTA (Fig. 6.13f–h). Percutaneous coronary intervention was not performed in this case due to the
extent of disease in the left main and LAD, which
is also well demonstrated on the CTA. Also based
on the CTA, the angiographer did not deem it
necessary to perform additional IVUS, or flow
wire measurement. The patient had subsequent
bypass surgery to the LAD and left circumflex.
6.13.5 Pearls and Pitfalls
The CCTA provides valuable information to the
angiographer prior to the diagnostic or interventional procedure, thus, contributing to the
decision- making process and management of the
case. It may also potentially shorten the time of
the procedure, save additional costs (e.g., IVUS),
radiation to patient and operator and added risk to
the patient.

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6.14 Case 6.14
6.14.1 History
A 62-year-old male presented with atypical chest
pain and reported a normal exercise myocardial
perfusion scan result.
6.14.2 Findings
There is advanced diffuse non-calcified and calcified plaque involving the left main, and proximal
to mid-LAD, with high-grade stenosis. There is
also high-grade stenosis in the proximal to midramus intermedius branch (Fig. 6.14a–c and e).
The other major coronary arteries had scattered
non-obstructive disease.
6.14.3 Diagnosis
The diagnosis is high-grade stenosis in the left
main coronary artery, left anterior descending,
and ramus intermedius artery.
Fig. 6.14 (a and b)
cMPR LM–LAD:
High-grade stenosis
(arrows). (c and d)
cMPR ramus
intermedius artery:
High- grade stenosis
(arrows). (e) 2D map:
Advanced multi-vessel
disease. (f–h) Diagnostic
angiogram

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Fig. 6.14 (continued)
6.14.4 Discussion
The patient became severely hypotensive during
the diagnostic angiogram. A balloon pump catheter was placed in the aorta, and the patient was
moved to the intensive care unit to await surgical
revascularization.
High-grade left main disease is a major
cause of morbidity and mortality. It is helpful
for the angiographer to previously be aware of
the presence of significant left main coronary
artery disease, since the tip of the angiography
catheter may occlude the lumen of the artery or
unroof a plaque, which may cause significant
adverse or catastrophic cardiac complications.
Awareness of the high complication rate in
such patients has changed the diagnostic procedure: cannulation of the left main coronary
artery and is performed with more caution, and
fewer angiographic views are obtained.
6.14.5 Pearls and Pitfalls
Greater than 50% luminal stenosis in the left
main is considered flow limiting.

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6.15 Case 6.15
6.15.1 History
A 56-year-old male presented with ventricular
ectopy.
6.15.2 Findings
There is high-grade, tubular type, stenosis in the
mid-LAD immediately distal to the ostium of the
second diagonal (Fig. 6.15a–e). There is also
mild non-stenotic fibrocalcific plaque at the
ostium of the LAD.
Fig. 6.15 (a and b) cMPR LM–LAD: High-grade stenosis (arrow). (c and d) 3D and 2D MAP: left anterior coronary
artery (LAD) (arrow). (e–g) Angiogram (arrow). (h) Angiogram post-LAD stenting (arrow)

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6.15.3 Diagnosis
The diagnosis is high-grade (70–80%) tubular
stenosis in the mid-LAD.
6.15.4 Discussion
High-grade obstructing atheromatous plaques are
commonly eccentric. This case demonstrates a
variation, where there is circumferential narrowing
of the lumen in the mid-LAD. Note that there is
diminished contrast density in the stenotic segment
that is estimated at 70–80% and confirmed on angiography (Fig. 6.15e–h).
6.15.5 Pearls and Pitfalls
With tubular stenosis, there is no change in luminal diameter with rotation of the curved multiplanar reconstructed images.
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