New concept of totally endovascular treatment of complex cases of type A and B aortic dissection.
Modern minimally invasive approach to treat aortic dissection.
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Centralization of flow in aortic dissection
1. Endovascular “centralization of flow
concept” is safe and efficient for
treatment of patients with aortic
dissection
Ivo Petrov, MD, PhD, FESC, FACC
Acibadem City clinic, Cardiology center, Sofia, Bulgaria
2. Speaker's name: Ivo Petrov, MD
I do not have any potential conflict of interest
3. Edward Diethrich and Donald Reid at the opening
ceremony of City Clinic 12.12.2012
4. Endovascular experience after 5 years of work:
• 9820 endovascular cases (“Head to toe”) in the cathlab and the
hybrid OR including:
• CTO and Left main Coronary interventions
• EVAR/TEVAR
• TAVR
• Intracranial aneurysms stenting and coiling
• CAS
• Radial approach for complex peripheral cases
• Complex venous interventions (including May-Thurner, CCSVI)
• Renal denervation
6. Treatment of complex aortic
diseases:
One of the biggest challenges of
contemporary vascular medicine
7. Aortic dissection- how far are
we in treatment?
• still high mortality rate despite well-established treatment
guidelines
• incidence may double if pre-morbid risk factors are not better
controlled
• additional tears, critical true lumen compression with end-
organ ischemia can compromise acute and chronic clinical
outcomes after surgical or endovascular treatment in AoD
• patent false lumen is an independent predictor of long term
mortality and aortic events in both type A and type B AD
8. Predictors for worse prognosis in AD:
• age <60 years
• aortic diameter ≥40 mm on initial imaging
• proximal descending thoracic aorta false lumen (FL) diameter ≥22 mm
• elliptic formation of the true lumen
• patent FL or only partially thrombosed FL
• saccular formation of the FL
• presence of one entry tear, large entry tear (≥10 mm) located in the
proximal part of the dissection (3)
• J Vasc Surg. 2014 Apr;59(4):1134-43. doi: 10.1016/j.jvs.2014.01.042 Predictors of aortic
growth in uncomplicated type B aortic dissection.
10. Repeated aortic interventions in Ao dissection:
European Heart Journal doi:10.1093/eurheartj/ehu281 2014
European Heart Journal (2001) 22, 1642–1681 doi:10.1053/euhj.2001.2782, a
11. Our point of complex aortic disease
treatment. Centralization of flow and
decompression of false lumen
• we represent analysis of 1 year f-up (aortic morphological
and clinical outcomes) of 8 patients, all threated with
endovascular uncovered stent implantation combined /or not
with stent-graft implantation or surgical treatment in the
context of complex treatment of type A or type B aortic
dissection
• aim- induction of aortic remodeling by depressurization of
the false lumen and increasing the size of the true lumen by
non-covered stent implantation
• end points- survival, branch patency, true lumen expansion,
false lumen compression
12. Baseline clinical characteristics
• end organ ischemia-8pt
(100%) 20 aortic branches
affected
• mean age- 51.9 ± 16 years
• gender- 7 males and 1 female
• type of dissection- 5pt with
type A and 3pt with type B
• renal failure-6pt (2 in anuria)
38%
33%
10%
19%
Risk profile:
arterial hypertension dyslipidemia diabet smoker
0
1
2
3
4
5
6
2
2
2
4
6
4
Affected by the true lumen compression branches of aorta
13. History of previous treatment and
periprocedural characteristics:
gender type
AD
previous
treatment
Zone of true lumen
compression
additionally stented branches
N=7
patient 1 m A surgery thoracoabdominal
aorta
No
patient 2 m A surgery thoracoabdominal
aorta
No
patient 3 f A surgery aortic arch No
patient 4 m B no previous
treatment
thoracoabdominal
aorta
renal artery, mesenteric superior
artery, left iliac artery
patient 5 m A TEVAR+ bypass
ACC-ACC
crossover right-
left
aortic arch and
descending aorta
right common carotid artery
patient 6 m B TEVAR thoracoabdominal
aorta
No
patient 7 m B no previous
treatment
abdominal aorta No
patient 8 m A Surgery aortic arch and
descending aorta
left common carotid artery, left
subclavian artery, brachiocephalic
trunk
14. different “aortic”stents (total number 10) were chosen for
the patients with sizes following the proximal and distal
reference diameter of healthy aorta in 1:1 ratio
“Aortic” stents implanted N=10 diameter
of stent
stent
length
patient 1 two Wallstents 20 55
patient 2 MFM Cardiatis 34 200
patient 3 Zenith Dissection 36 123
patient 4 Zenith Dissection 36 186
patient 5 Zenith Dissection 36/186mm 40 100
patient 6 Sinus XL Flex 24 159
patient 7 Sinus XL Flex 28 80
patient 8 Sinus XL Flex- arcus 36 18
Sinus XL Flex- descending aorta 100 100
15. Procedural protocol and in-hospital results
•Vascular access of choice were: totally percutaneous
(6 pts) or surgical (2pts) femoral access for aortic
stent implantation and percutaneous radial (right or
left) artery 6Fr for angiography and additional side
branches treatment
•general anesthesia (4 pts) due to clinical conditions
•local anesthesia + sedation (4 pts)
•In-hospital major adverse CVE and NVE = 0%
16. Aortic stents for AD. 1 year follow up:
Clinical:
Aorta related mortality 0%
Mortality 0%
Late neurological complications 0%
Normal and normalized kidney function 8/8 (100%)
Device related outcomes:
Device related failure 0%
Aortic stent thrombosis 0%
Side branch stent thrombosis 0%
Preserved covered side branches flow 19/20 (95%)
1. One renal artery arising from false lumen thrombosed
Additional late procedures (3 months later) 1/8 (12,5%)
1. Additional balloon expansion of compressed and invaginated aortic stent
17. Creatinine levels before and after the
procedure
0
100
200
300
400
500
600
700
800
creatinine level before procedure creatinine level after procedure
patient 1 patient 2 patient 4 patient 6 patient 7 patient 8
Gradual normalization of renal function was observed in all
patients with renal failure
18. CTA 1 year later- diameter of true and false lumen
compared to baseline:
Zone of
compression
measured
D of TL before D of TL after D of FL before D of FL after
patient 1 descending
aorta
2 20 25 5
patient 2 descending
aorta
3 28 30 2
patient 3 aortic arch 14 18 53 45
patient 4 abdominal aorta 3,2 27,2 19,8 0
descending
aorta
8,8 43,6 15,8 0
patient 5 aortic arch 10 23 26 19
patient 6 descending
aorta
3,2 48 56 16
abdominal aorta 8 22 28,2 20
patient 7 abdominal aorta 4 19 25,5 0
patient 8 descending
aorta
6
23,8 30 15
19. Results
• measurements based on control CTA scan showed decompression of
the true lumen in all stented zones and statistically significant
decreased size of the false lumen, inducing thrombosis
Before After p-value
True lumen 6.28 ± 4.15 22.63 ± 3.65 < 0.001
False lumen 29.69 ± 9.98 13.25 ± 15.29 < 0.001
20. Case Report
• Year 2002: D.S. 54 -year- old male
• Clinical history: arterial hypertension; smoker; diabetes mellitus
• Admitted in critical clinical condition (hypotensive, anuric,
unconscious, in pulmonary edema)
• Acute De Bakey type I aortic dissection and AoReg III degr. was
diagnosed- Urgent surgical resection of the ascending aorta with
Unigraft No30 implantation was done
• In the immediate post operative period the patient remained in
critical condition and was detected life threatening ischaemia of
the abdominal Ao branches manifested by anuria, subileus,
inferior paraparesis, livedo reticularis of the lumbal area and
lower extremities
21. • Multiple additional tears in the toracoabdominal aorta
causing false lumen expansion and true lumen
compression resulting in life threatening end organ
ischemia
• Implantation of two Wallstents 20х55мм
Extreme true
lumen
compression
22. Final result
Restored and centralized true lumen flow
• Restored abdominal branches flow
• Decreased flow in the false lumen
23. CTA after true lumen flow centralization with
2 Wallstents implantation
24. 15 years clinical and MSCTA follow up:
Uneventful follow-up,
Normal renal function
Normal ABI, the patient 69 y of age still working
25. clinical case
• NT, 47y male patient with aortic dissection type A, who was operated in
the acute phase
• during the follow up period the patient remained severely symptomatic-
uncontrolled hypertension, worsening renal function, voice lost and
progressive claudication, false lumen expansion. Additional aortic tears at
arch and thoracic aorta level were shown with severe compression of all
brachiocephalic vessels
26. control ct shows partial thrombosis of aortic arch which is supplied by
brachiocephalic trunk; dissection of left common carotid artery with
compressed true lumen and proximal dissection of left subclavian artery;
increasing of the diameter of the false lumen in the desending aorta was
measured as well- compression of the true lumen to 6mm
Extreme true
lumen
compression
27. Interventional procedure: immediate true lumen
flow centralization
• Under local anesthesia
and mild sedation:
• left and right radial 6fr
access, left femoral 10fr
access:
• Sinus xl 6fr 16/40mm in
the brachiocephalic
trunk, Sinus xl 6fr
14/40mm in the left
common carotid artery,
Sinus xl 6fr 14/40mm in
the LSA, 2 overlapping
Sinus xl 36/100mm in the
aortic arch and proximal
descending aorta
28. 1y follow up cta shows excellent centralization of
flow in the true lumen and false lumen progressive
“passivation”
-patient asymptomatic
29. Case report 2 (jump into the future :)
• White male 71 yo
• Admitted in hospital with persistent severe abdominal and peripheral
ischemia with abdominal angina.
• History of pervious surgical treatment for Type A Ao dissection (2 years
before)
30. Case report 2 (travel into the future :)
• White male 71 yo
• Admitted in hospital with persistent severe abdominal and peripheral
ischemia with abdominal angina.
• History of pervious surgical treatment for Type A Ao dissection (2 years
before)
32. Case report 2 (travel into the future :)
• White male 71 yo
• Admitted in hospital with persistent severe abdominal and peripheral
ischemia with abdominal angina.
• History of pervious surgical treatment for Type A Ao dissection (2 years
before)
CARDIATIS MFM
33. Why is Using Max Diameter a
Problem?
• Both AAAs have max diameters of 5.5cm
• “A” ruptured after 18 months of this scan
• “B” is still under observation after more than 3 years
• Max stress of “A” is more than twice that of “B”
• Small Aneurysms are known to rupture
Fillinger et al, Journal of Vascular Surgery April 2003 p726
A B
34. Results: Wall Shear Stress at Systolic Peak
Courtesy of ralfkolvenbach@gmail.com
50. MFM experience in Bulgaria (2011-2015)
(Complex aortic pathology, multiple comorbidities, extremely high surgical risk)
Total patients 21
Sex M/F 21/0
Age 53-76 (65)
AH 18(85,6%)
Dyslipidemia 17(80,9%)
Pervious PCI/PTA 16(76,3%)
Previous TEVAR/EVAR 2(9,5%)
Previous open Ao repair 2 (9,5%)
51.
52. Discussion
• patent and expanding false lumen is an independent predictor for long
term mortality and aortic events in both type A and type B AD
• additional tears, critical true lumen compression and true lumen
obliteration with end-organ ischemia can be life threatening in the
acute/chronic phase
• complicated AD after surgical or endovascular treatment of both type
A and type B AD, can require further intervention to decompress
critical compression of the true lumen, restore blood flow in side
branches or in cases of life threatening organ ischemia
53. Conclusion
The concept of redirection of flow in complex cases
of aortic dissection with non-covered stents
implantation was safe, lead to positive aorta
remodeling combined with side branches flow
preservation and resulted in excellent survival rate.
This example illustrates why. The diagram shows aneurysms.
Now if we used diameter to indicate surgical procedure.
However if you look at the stress.
309,400 N/m2
703,100 n/m2