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4 Interventional radiology and endovascular procedures
)(
(a) (b)
(c
Figure 1.1 (a) The right vertebral artery is dominant relative to the left (arrows show the right and left
vertebral arteries). (b) There is a large left subclavian artery aneurysm (arrow). (c) In the distal arch there is
a tight stenosis of the true lumen associated with a 90-degree bend in the aorta at the distal arch (arrow).
(d) A large entry tear is seen in the proximal descending thoracic aorta (arrow)
Learning point
The procedure was performed under an epidural anaesthetic, which allowed the immediate detection
of neurological complications such as stroke and paraplegia. The right common femoral was chosen as
the access artery so that additional devices could be placed in the right iliac artery if deployment of the
thoracic aortic stent graft did not restore arterial patency. The right common femoral artery was exposed
surgically, and a guidewire and catheter were inserted easily into the supracoeliac aorta (despite the iliac
artery appearing severely narrowed on CT). Angiography of the visceral arteries demonstrated that the
catheter was situated in the true lumen. Negotiating the catheter in the true lumen around the rightangled bend was difficult but was achieved. The arch angiogram showed that the catheter was still in the
true lumen, and that the primary entry tear was in the proximal descending thoracic aorta. The device
was released under X-ray guidance and post-deployment angiography demonstrated no antegrade
filling of the false lumen, but the right renal and right iliac arteries were still compromised.
d)
An uncovered aortic dissection stent (TXD, Cook Medical, Bloomington, IN) was
placed distal to the stent graft which resulted in perfusion of the right renal artery.
A second TXD stent reaching the aortic bifurcation had to be deployed to restore
ow to the right common iliac artery (Figure 1.2). The patient did well on day one
(a) (b) (c)
Figure 1.2 (a) The stent graft has prevented antegrade flow into the false lumen by covering the entry tear.
(b) Retrograde flow is seen at the lower end of the device within the false lumen (arrow). (c) Good flow is seen
in the right renal artery (arrow) and right common iliac artery after deployment of two bare metal stents
5Case 1 Thoracic endoprostheses for type B aortic dissections
(a) (b)
Figure 1.3 (a) The stent graft has opened the stenosis in the true lumen. (b) Contrast enhancement of
the false lumen at the lower portion of the stent graft (arrow)
with resolution of the chest pain and sensory decit of the right leg. The chest pain
returned on the third post-operative day and CT angiography showed some lling
of the false lumen in the proximal descending thoracic aorta at the distal section of
the cTAG stent graft (Figure 1.3). The true lumen in the region of the proximal TXD
device had fully expanded and the false lumen could not be seen. There was contrast
within the false lumen at the level of the second TXD device in the lower descending
aorta, and the right renal and right common iliac arteries were patent although there
was still some delay apparent in the right nephrogram. No further procedure was
deemed necessary because the primary entry tear had been covered proximally and
therefore the patient was treated with analgesia and hypotensive medication.
However, later that day the patient suffered a cardiac arrest and died despite cardiopulmonary resuscitation. Post-mortem examination showed that the false lumen had
ruptured at the level of the primary entry tear in the proximal descending thoracic aorta.
6 Interventional radiology and endovascular procedures
Discussion
The goals of thoracic endovascular aortic repair (TEVAR) for acute aortic type B dissection include coverage of the proximal entry tear, expansion of the true lumen with
restoration of ow to the visceral vessels, and obliteration of false lumen ow with
subsequent thrombosis [1–5]. When these goals of endovascular therapy are successfully achieved, aortic remodelling should occur with subsequent prevention of
future aneurysmal degeneration of the outer wall of the false lumen. The EuroSTAR
(European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair) and
UK Registry report is the largest group of patients treated with stent grafts to date: 131
patients with aortic dissection (5% proximal, 81% distal, 144% not classied) were
treated with stent grafts and 57% had symptoms of rupture, aortic expansion, or side
branch occlusion. Although no long-term data are available, primary technical success was achieved in 89%, 30-day mortality was 8.4%, paraplegia occurred in 0.8%
of those treated, and survival at one year was reported in 90% of the patients who
completed follow-up [6].
Endovascular repair of aortic disease associated with connective tissue disease is
controversial, although it can be justied in emergencies with careful pre-operative
Expert comment
The presence of a subclavian artery
aneurysm with aortic dissection
and the sudden death of a young
first-degree relative suggest
connective tissue disorder as the
primary pathology in this case.
Genetic screening of first-degree
relatives should be performed.
Expert comment
This patient may have died because
the distal end of the stent graft
did not adequately seal the true
lumen, allowing flow to pressurize
the false lumen. If the stent graft
was longer, a distal seal would have
been achieved because the whole
aortic diameter decreased distally.
However, longer devices are
associated with an increased risk of
paraplegia so the risks have to be
carefully evaluated.
Expert comment
The bare stents, by completely
occluding the false lumen in the
distal thoracic aorta, may have
played a part in the patient’s death.
The continued perfusion of the
false lumen (retrogradely alongside
the distal portion of the device)
through the primary entry tear and
the distal occlusion of the false
lumen by the TXD stents may have
pressurized the false lumen and
ultimately led to aortic rupture.
planning [7]. Care should be taken in elective cases as the long-term durability of
devices relying on oversizing may be compromised by a dilating aortopathy.
Stent-graft sizing is very important in treating patients with type B dissections.
Most of the emphasis on treating complicated type B aortic dissection with stent grafts
has been about the proximal sizing of the device. Too much can cause retrograde type
A dissection and device collapse [8]. It is recommended that oversizing a stent graft
relative to the proximal undissected aorta should be much less in aortic dissection
than for degenerative aneurysm; 5–10% oversizing is considered adequate for dissections whereas aneurysms should be oversized by 15–30%. Balloon dilation is to be
avoided in dissection because of the risk of retrograde dissection. The aortic lumen
may not be the same diameter along its length and, as in this case, this can result in
inadequate sealing of the distal end, allowing retrograde entry of blood into the false
lumen.
Intra-operative evaluation with intravascular ultrasound or transoesophageal
echocardiography might have shown retrograde ow into the false lumen around
the distal end of the stent graft. The ndings of retrograde ow around the device
on digital subtraction angiography were subtle, and the signicance of these was
not appreciated at the time of implantation. Only careful inspection after the death
of the patient showed the real cause of the problem. Unfortunately, intravascular
ultrasound is expensive and is not used in our hospital, and echocardiography is not
used routinely for endovascular thoracic repair of acute aortic dissections.
A bare stent may be used to increase the size of the true lumen and it has been
suggested as a way of overcoming branch vessel compromise. In this case the right
renal and right common iliac arteries, which were compromised even with stent
graft in place, were opened.
Continued or recurrent pain following endovascular treatment of an acute type
B aortic dissection is a sinister sign which should prompt further investigation. The
CT angiographic ndings of continued perfusion of the false lumen at the level of
the device, with no false lumen lling distally at the level of the proximal bare stent,
may represent an unsatisfactory post-operative imaging nding. Use of further stent
grafts rather than TXD devices might have excluded ow from the false lumen and
prevented this fatal complication.
Learning points
●
Endovascular repair in connective tissue disease is not recommended except in cases of emergency.
●
Accurate placement of both the proximal and distal ends of the stent graft is important to prevent
continued filling of the false lumen.
●
Careful intra-operative evaluation following stent-graft placement should be performed (with
two X-ray views or rotational angiography, intravascular ultrasound, or transoesophageal
echocardiography) to exclude retrograde flow alongside the device with continued perfusion of the
false lumen through the primary tear.
●
The use of bare stents distal to the covered stent has been recommended as a means of improving
outcome, however, in the presence of continued false lumen perfusion, occlusion of the false
lumen outflow may cause pressurization resulting in aortic rupture and death.
●
Continuing or recurrent pain after endovascular repair of acute type B aortic dissection is a sinister
sign which should prompt further investigation.
Clinical tip Evaluation of type B dissection with CT angiography
CT angiography provides useful anatomical correlates for endovascular therapy with imaging of the
true and false lumens and entry tear sites.
●
In most cases, the true lumen may be localized by its continuity with the undissected segment of the aorta.
●
The presence of intraluminal thrombus is a good marker of the false lumen, though in patients with
concomitant degenerative aneurysms thrombus may be present in the true lumen.
●
In the descending thoracic aorta, the false lumen is larger than the true lumen in more than 90% of
cases [9].
●
The orientation and mobility of the dissection flap can be assessed with CTA. If the dissection flap is
concave toward the false lumen, a true lumen pressure deficit can be predicted [10].
Marked compression of the true lumen (true lumen collapse) is evidence of dynamic aortic obstruction
and should raise the index of suspicion for malperfusion syndrome.
7Case 1 Thoracic endoprostheses for type B aortic dissections
Clinical tip Endovascular treatment of malperfusion syndrome
The endovascular management of an acute type B aortic dissection complicated with malperfusion
syndrome involves the following.
●
True lumen access from either a brachial or a femoral approach. Typically, because the type B
dissection is distal to the left subclavian artery, rapid true lumen access is easily obtained through a
right transbrachial approach.
●
Recognition of the entry tear and the proximal zone of fixation.
●
Visualization of all aortic branches before intervention, since changes in flap mobility secondary to
relief of obstruction may alter perfusion of other aortic side branches.
●
Wire access into the distal true lumen of compromised aortic side branches should be secured if the
origin of the branch is uncovered by the dissection
●
If stenting of the proximal descending thoracic aorta and coverage of the entry tear does not restore
flow to the compromised aortic side-branches, uncovered dissection stents can be deployed in the
aorta. If these fail to restore patency, placement of self-expanding stents into the aortic branches
should be performed
Learning point Indications for left subclavian artery (LSA) revascularization
In patients who need urgent TEVAR for acute aortic syndromes it is suggested that revascularization
should be individualized. In selected patients whose anatomy compromises perfusion to critical organs,
routine pre-operative LSA revascularization is strongly recommended. Such configurations include:
●
presence of a patent left internal mammary artery to coronary artery bypass graft
●
termination of the left vertebral artery at the posterior inferior cerebellar artery or other
discontinuity of the vertebrobasilar collaterals
(continued)
8 Interventional radiology and endovascular procedures
●
absent, diminutive, or occluded right vertebral artery
●
a functioning arteriovenous shunt in the left arm
●
prior infrarenal aortic repair
●
planned long-segment (>20cm) coverage of the descending thoracic aorta where critical intercostal
arteries originate
●
internal iliac artery occlusion.
Evidence base Prospective multicenter clinical trial (STABLE) on the endovascular treatment of
complicated type B aortic dissection using a composite device design [11]
●
Prospective single-arm multicentre study.
●
Patients with complicated type B aortic dissection were treated with an endovascular system
consisting of a proximal TX2 thoracic stent graft and distal bare metal dissection stents (Zenith
Dissection Endovascular System; Cook Medical, Bloomington, IN).
●
Indications for enrolment were branch vessel malperfusion, impending rupture, aortic diameter
≥40mm, rapid aortic expansion, and persistent pain or hypertension despite maximum medical
therapy.
●
One-year follow-up results, including clinical and radiographic (CT and X-ray) evaluation, were
available for this study.
●
Forty patients were enrolled in this study.
●
The onset of symptoms was acute (≤14 days) in 24 patients (60%).
●
A majority of patients (77.5%; 31 of 40 patients) presented with impending aortic rupture (indicated
by peri-aortic effusion/haematoma) or branch vessel malperfusion.
●
The 30-day mortality rate was 5% and the one-year survival rate was 90%. Two deaths were
secondary to aortic rupture.
●
Morbidity occurring within 30 days included stroke (7.5%), transient ischaemic attack (2.5%),
paraplegia (2.5%), retrograde progression of dissection (5%), and renal failure (12.5%). Additional
morbidity after 30 days included one case of retrograde progression of dissection and one case of
renal failure.
●
Favourable aortic remodelling was observed during the course of follow-up.
●
Initial data with a composite TEVAR construct have demonstrated favourable clinical and
anatomical results.
References
1. Trimarchi S, Nienaber CA, Rampoldi V, et al. Role and results of surgery in acute ty pe
B aortic dissection: insights from the International Registry of Acute Aortic Dissection
(IRAD). Circulation 2006; 114(1 Suppl): I357–64.
2. Eggebrecht H, Nienaber CA, Neuhauser M, et al. Endovascular stent-graft placement in
aortic dissection: a meta-analysis. Eur Heart J 2006; 27(4): 489–98.
3. Fattori R, Tsai TT, Myrmel T, et al. Complicated acute type B dissection: is surgery still
the best option? A report from the International Registry of Acute Aortic Dissection. JACC
Cardiovasc Interv 2008; 1(4): 395–402.
4. Tsai TT, Trimarchi S, Nienaber CA. Acute aortic dissection: perspectives from the
International Registry of Acute Aortic Dissection (IRAD). Eur J Vasc Endovasc Surg. 2009;
37(2): 149–59
5. Coady MA, Ikonomidis JS, Cheung AT, et al. Surgical management of descending tho-
racic aortic disease: open and endovascular approaches. A scientic statement from the
American Heart Association. Circulation 2010; 121(25): 2780–804.
6. Leurs LJ, Bell R, Degrieck Y, et al. Endovascular treatment of thoracic aortic diseases:
combined experience from the EUROSTAR and United Kingdom Thoracic Endograft registries. J Vasc Surg 2004; 40(4): 670–80.
7. Brown CR, Kitagawa A, Greenberg RK. Endovascular strategies for the management of
aortic connective tissue disorders. J Cardiovasc Surg (Torino) 2012; 53 (1 Suppl 1): 35–42.
8. Dumfarth J, Michel M, Schmidli J, et al. Mechanisms of failure and outcome of secondary surgical interventions after thoracic endovascular aortic repair (TEVAR). Ann Thorac
Surg 2011; 91(4): 1141–6.
9. LePage MA, Quint LE, Sonnad SS, et al. Aortic dissection: CT features that distinguish
true lumen from false lumen. AJR Am J Roentgenol 2001; 177(1): 207–11.
10. Williams DM, Lee DY, Hamilton BH, et al. The dissected aorta. III: Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology. 1997; 203(1): 37–44.
11. Lombardi JV, Cambria RP, Nienaber CA, et al. Prospective multicenter clinical trial
(STABLE) on the endovascular treatment of complicated type B aortic dissection using a
composite device design. J Vasc Surg 2012; 55(3): 629–40
9Case 1 Thoracic endoprostheses for type B aortic dissections
CASE
2
Management of endoleaks after
thoracic endografts
Ali Alsafi
Expert commentary Mo Hamady
Case history
A 72-year-old man (Mr RA) presented to his GP with intermittent central chest pain
on exertion, having had thoracic endovascular aneurysm repair (TEVAR) for a 9.5cm
descending thoracic aortic aneurysm and endovascular aneurysm repair (EVAR)
for a 6.5cm abdominal aneurysm 18 months earlier. His heart rate was 68 beats per
minute, and was irregularly irregular. His blood pressure was 145/75 and his ECG
revealed atrial brillation with no ischaemic changes.
Learning point Classifications of thoracic aortic aneurysms (TAAs)
TTAs are classified according to site of origin and extent.
Stanford classification
●
Type A: aneurysms involving the ascending aorta, regardless of site of origin.
●
Type B: aneurysms distal to the left subclavian artery.
De Bakey classification
●
Type I: Originates in the ascending aorta and propagates distally to involve the descending portion.
●
Type II: originates and is confined to the ascending aorta.
●
Type III: Originates in the descending aorta and extends distally, but may rarely extend retrogradely.
Both systems are somewhat outdated, with detailed anatomical description of site or origin, extent
of aneurysm, visceral artery involvement, the presence of intramural haematoma, and the extent
of potential landing zones being important factors to be considered when planning endovascular
treatment.
Mr RA’s past medical history included peripheral artery disease with aortobifemoral bypass six years earlier, coronary artery disease, atrial brillation, hypertension, hypercholesterolaemia, and recurrent deep vein thromboses (DVTs). He was
taking warfarin, valsartan 80mg, nebivolol 2.5mg, amilodipine 5mg, rosuvastatin
20mg, Calcichew D3, and folic acid 5mg.
Mr RA was referred to the A&E department due to his chest pain. He was haemodynamically stable and his cardiovascular examination was unremarkable. His initial
blood tests were normal apart from chronically low haemoglobin of 9g/dl (for which
he was being investigated) with normal coagulation, renal, and liver function tests.
Troponin I at 24 hours was not elevated.
A chest radiograph in the A&E department revealed a widened mediastinum and
a descending thoracic aortic endograft in situ (Figure 2.1).
A subsequent CT angiogram revealed an increase in TAA sac size, which now
measured 12.2cm. This was secondary to a type II endoleak from intercostal
12 Interventional radiology and endovascular procedures
Figure 2.1 Chest radiograph at presentation
to A&E, showing a widened mediastinum and a
thoracic aortic endograft.
Expert comment
Mr RA should have had a closer
follow-up; this would have
identified the endoleaks and the
enlargement of the TAA prior to
the patient developing symptoms.
After TEVAR, patients should be
followed up for life, initially with
a post-TEVAR CTA, followed by a
repeat at 30 days, 6 months and
yearly thereafter in the absence
of complications and symptoms.
Symptoms should prompt earlier
imaging and closer follow up.
arteries. He also had type Ib and type II endoleaks of the abdominal aortic aneurysm (AAA), causing enlargement of the aneurysm sac which now measured
7.7cm (Figure 2.2). As Mr RA was stable, he was discharged with a view to being
discussed by the vascular multidisciplinary team (MDT) for management of his
endoleaks.
Learning point Endoleaks [1]
Endovascular aneurysm repair aims at excluding the aneurysm sac from circulation by means of a
covered stent graft. Persistent blood flow into the aneurysm sac following treatment is known as an
endoleak, and it may result in increasing aneurysm size thereby increasing the risk of rupture. Five
types of endoleaks have been described.
●
Type I: this is the result of an incomplete seal of the aneurysm sac and is regarded as treatment
failure. This usually presents early but may be delayed in cases of stent migration. Type I endoleaks
are sub-classified into type Ia, where the leak is proximal, and type Ib, where it is distal.
●
Type II: this is the result of retrograde blood flow through patent vascular channels, feeding the
aneurysm sac directly, often from intercostal arteries, lumbar arteries, or inferior mesenteric artery.
●
Type III: this is due to device malfunction, rupture, fatigue, or breakdown. More often, however,
type III endoleaks result from junctional separation of two stent-graft components.
●
Type IV: this is secondary to stent-graft porosity while patients are anticoagulated during the peri-
procedure period.
●
Type V: this is said to be present when the aneurysm sac expands without an apparent endoleak
and may be due to graft ultrafiltration or slow flow, which is not detectable on standard imaging.
Type V endoleaks are also known as ‘endotension’ and are considered significant, mandating further
action.
Types IV and V are increasingly historical as stent-graft technology improves.
After MDT discussion, Mr RA went on to have a stress echocardiogram, which
showed no ischaemia, and was subsequently admitted for treatment of his endoleaks.
A planning CT showed stable appearances of the aneurysms, and was followed by
bilateral subclavian angiography using a brachial artery approach; the thyrocervical trunk was identied as the origin of the vessels feeding the TAA sac. Several
thyrocervical trunk branches were accessed with a microcatheter and embolized
with Onyx; however, there was persistent lling of the feeder vessels via other
(a)
(b)
(c)
13Case 2 Management of endoleaks after thoracic endografts
(a)
(b)
(c)
Figure 2.2 3D volume render from the admission CT angiogram with axial images demonstrating the
thoracic and abdominal endoleaks: (a) intercostal vessels feeding the TAA sac (type II endoleak); (b) TAA
endograft with contrast in the TAA sac; (c) AAA endograft with contrast in the enlarged aneurysm sac.
tributaries (Figure 2.3). A CT two days later showed persistent opacication of the
aneurysm sac from intercostal arteries. A second attempt at embolizing the feeder
vessels again via a right brachial artery approach was abandoned due to challenging
anat omy.
Following further MDT discussion, the TAA sac, which occupied most of the left
hemithorax, was directly punctured under ultrasound and 3D rotational uoroscopy
guidance, where a 6Fr catheter was inserted, permitting selective catheterization of
the two feeding branches, followed by embolization using Onyx. The outow vessels
were also embolized and the aneurysm sac lled with embolic material and thrombin (Figure 2.4). A follow-up CT three months later showed a reduction in TAA size
to 10cm with resolution of the type II endoleak (Figure 2.5).
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