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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.
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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).
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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.
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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.
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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
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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. (fh) 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). (eg) 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.