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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3654_Библиотеки_им_академика_М_И_Перельмана
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Collagen wave length (µm)
µm
p=NS
8 Pathology ofBiological Prosthetic Cardiac Valves
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Fig. 8.29 (a) Schematic
representation of collagen
bers wave periodicity length
measurement. (b) Cusp
pericardial tissue, stained with
Picrosirius red and the same
eld seen at polarized light
Fig. 8.30 A 3-hour collapse
of the pericardial valve did
not alter collagen periodicity.
Note the comparison with no
collapse controls. Histogram
displaying collagen wave
length at different collapsing
times, in comparison with
controls (no collapse). All
values are expressed as
mean±standard deviation
a b
Collagen fibers wave periodicity (µm)
25
17.47±2.50
20
15
10
16.51±2.65 16.55±2.8917.01±3.1116.45±2.13
5
0
UNMOUNTED
PERICARDIUM
NO COLLAPASE
VALV E
15 MIN COLLAPSE
VALV E
60 MIN COLLAPSE
VALV E
180 MIN COLLAPSE
VALV E

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G. Thiene et al.
a
d
b
e
c
Fig. 8.31 Fibrous tissue overgrowth(pannus) narrows the orice with stenosis, 59months after implant (a, b). Coarse calcication is also visible
at X-ray (c). Fibrous tissue climbs onto the stent (d), (e)histology of the pannus. Hematoxylin-Eosin stain

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a
d
b
e
c
Fig. 8.32 Severe calcication (a–c) of a Perceval S, 53months after implant. Note the severe calcication at X-Ray (d) and histology (von Kossa
stain). Note brous tissue overgrowth climbing the nitinol strut at gross view(c) and histology(f) (Azan Mallory stain 200x)
f

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The lack of long-distance results represents still a drawback, which does not allow denitive conclusions.
Comparison with transcatheter valve (TAVI) aftermath is
warranted.
Interventional
Transcatheter interventional therapy of valve disease has
expanded therapeutic options. It includes less invasive
approaches such as transcatheter aortic valve implantation
(TAVI), edge-to-edge repair, or even atrioventricular valve
implantation.
TAVI represented a revolutionary approachto repair aortic valve stenosis with minimally invasive treatment.
The procedure consists of implanting a pericardial aortic
valve device through femoral artery. After expansion of the
stenotic aortic valve, which is left in situ, the device is
deployed into the aortic annulus.
Originally, there were three models with different deployment systems (Fig.8.33):
(a) The Edwards Sapien with expandable balloon.
(b) The Core valve with self-expandable nitinol frame.
(c) Cardio Intuity with expandable balloon.
An alternative approach is surgical (Fig.8.34), from the
apex of the left ventricle (“transapical”), or through the
ascending aorta on a beating heart, both without cardiopulmonary bypass. When the interventional bioprosthesis is
implanted in failed bioprosthesis, rather than in a native
valve, the procedure is called “valve-in-valve.”
In any case, the valve is a three-leaet bovine pericardial
bioprosthesis with brosa much thicker than brosa of porcine pericardium (Fig.8.35).
Moreover, experiments with porcine valve showed rupture of the porcine leaets, because of crack of the brosa
with the ballooning, suggesting that porcine valve xenograft
is not suitable to cope with this purpose (Fig.8.36).
The operation is not free from complications, mostly
related to the blind procedure and the leaving in situ the
native calcied valve (Fig.8.37).
Complications consist of the following:
(a) The catheter along abdominal, ascending aorta as well
as the aortic arch may encounter atherothrombotic
plaques (Fig.8.38) with the risk of embolism. The catheter crossing the aortic arch and ascending aorta is at risk
of cerebral embolism and stroke.
(b) Vascular access complications like femoral artery dis-
section or rupture.
(c) Extrinsic calcic vegetations of the native aortic valve,
by forcing to open the orice during device deployment,
may detach nodularcalcic deposits with coronary and
cerebral embolism (Fig.8.39).
(d) The presence of marked calcic deposits at the aortic
annulus may be of obstacle to the deployment of the
device and to achieve perfect adhesion, accounting for
perivalvular leak and aortic regurgitation.
ab c
Fig. 8.33 Three models of TAVI, all employing glutaraldehyde xed pericardial cusps. (a) Sapien, requiring ballooning for deployment. (b) Core
valve with nitinol self-expandable frame. (c) Cardio Intuity with expandable balloons

Bovine
Porcine
BovinePorcine
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ab
Fig. 8.34 Transarterial (a) vs transapical (b) valve implantation (TAVI), the latter from the apex of the left ventricle, both with beating heart and
no need of cardiopulmonary bypass. (c) Sapien in situ after deployment
Fig. 8.35 The thickness of
bovine pericardiumbrosa is
nearly three times than that of
porcine pericardium. Azan
Mallory stain
Pericardium
c
Pericardium
Bovine Pericardial is a strong and resistant tissue
Pericardial Tissue Yield Strength [Newtons]
25
20
15
10
5

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G. Thiene et al.
a
c
b
d
Fig. 8.36 TAVI employing porcine aortic cusps (a, b). The deployment and ballooning create fracture of the thin leaet brosa (c, d). Azan
Mallory stain
Fig. 8.37 The native senile
aortic valve stenosis by
nodular dystrophic
calcication (a) which
appears intrinsic at histology
(b). Azan Mallory stain

ab
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abc
Fig. 8.38 Senile aortic valve stenosis (a) in a patient with severe atherothrombosisof the aorta; (b) panoramic view; (c) closeup of the thoracic
aorta
Fig. 8.39 Embolism of the
right anterior cerebral artery
due to detachment of a
calcic nodule from a native
aortic cusp, occurred during
Sapienbioprosthetic valve
deployment with ballooning.
(a) Panoramic view. (b)
Closeup: note the calcic
embolic fragment occluding
the right anterior cerebral
artery. Arrow indicates the
calcic embolism
(e) Native valve calcic deposits may involve the right and
left brous trigons with the risk of perforation during the
traumatic bioprosthetic valve deployment (Figs. 8.40
and 8.41).
(f) The AV conduction system is just below the aortic annu-
lus (5–6mm at distance) (Fig.8.42). Site of sub-annular
stent insertion should not exceed 2–3mm; otherwise, the
subvalvular nitinol network may compress the His bundle and the left bundle branch, with onset of complete
AV block if a right bundle branch block pre-exists
(Fig.8.43).
Interference with the anterior leaet of the mitral
valve can also occur in the setting of a downward deployment into the left ventricular outow tract (Fig.8.43).
(g) The abovementioned complications are pathognomonic
of TAVI procedure. Of course, other complications like
endocarditis may occur as in any bioprosthetic valve
(Fig.8.44).

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G. Thiene et al.
(h) Thrombus formation, blocking the cusp opening
(Fig.8.45), has been reported, quite similar to that originally observed in surgically implanted porcine
bioprostheses.
(i) Dystrophic calcication at mid to long term can occur
also in the pericardial leaets of TAVI (Fig.8.46). Valvein- valve procedure is now available to treat structural
valve deterioration by calcic degeneration. It has been
already employed for structural valve deterioration of
surgical stented bioprosthetic valves, both porcine and
pericardial.
Fig. 8.40 Calcication in native senile aortic stenosis, extended to the
right and left brous trigones (arrows), at risk of external rupture during
TAVI ballooning and deployment
a
RVOT
PC
LC
b
*
Fig. 8.41 (a) The Sapien prosthesis appears correctly implanted with
no interference with the right and left coronary ostia, the anterior mitral
valve leaet, and the conduction system of the subaortic membranousventricular septum. Note the aortic annulus rupture (probe inside)
at the nadir of the left coronary cusp. (b) View of the left ventricular
outow tract, after removal of the aortic valve prosthesis: note the
amount of calcication distributed along the mitroaortic brous continuity, particularly at the level of the right and left brous trigones. A
perforation (asterisk) is visible at the nadir of the left coronary cusp,
1cm below the coronary ostium (arrow), in correspondence of a calcic deposits which were detached during the TAVI procedure.
LC = left anterior aortic cusp; PC = posterior, noncoronary cusp;
RVOT=right ventricular outow tract
In addition, atrioventricular valves can be a target for
interventional therapy.
Until recently, valve surgical replacement or repair was
the only feasible treatment for mitral regurgitation. Currently,
invasive percutaneous methods include narrowing the orice
by clipping the leaets or implanting bioprostheses into the
native mitral orice or in the lumen of failed bioprosthetic
valves (the valve-in-valve procedure), via a transapical or a
transseptal atrial approach (all in beating heart without extracorporeal circulation), with low complication rate and high
procedural performance.
The most used interventional method of treating mitral
valve incompetence is nowadays the MitraClip device. This
device is a V-shaped, fabric covered clip, which captures the
free edge of both mitral leaets and creates a double orice
valve, a procedure similar to the “Aleri” surgical repair. In
porcine model experimental studies, endothelialization of
the clips occurred as early as 4weeks, with 100% of clips by
17weeks.
Complications may be procedure or device related.
As for procedure-related complications, thromboembolic
events and vascular approach dissection may occur. Devicerelated complications include functional (persistent mitral
regurgitation, mitral stenosis) and structural device failure
(clip detachment with possible embolization, injury of leaflets or subvalvular apparatus, endocarditis).
Transcatheter valve therapies enlarge the limited treatment options also to tricuspid regurgitation and include percutaneous tricuspid annuloplasty, to reduce the orice area
of the tricuspid valve, by edge-to-edge clip repair (Figs.8.47
and 8.48).

de
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Fig. 8.42 (a) Normal AV
conduction system with
distance of His bundle from
the aortic annulus. (b) Safe
subaortic distance of the
bioprosthetic annular stent
should not exceed 2–3mm.
L=left anterior aortic cusp;
R=right anterior aortic cusp;
NC=non coronary aortic
cusp
ac
b
abc
Fig. 8.43 AV block (b, c) by compression of the left bundle branch in
patient with preoperative right bundle branch and sub-annular stent.
The deep implantation of the TAVI device into the left ventricular out-
ow tract (a, d, e) can interferealso the anterior mitral valve leaet. A
=aorta; LV=left ventricle; MS=membranous septum. From Fraccaro
etal., Am J Cardiol. 2011

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Fig. 8.44 Infective fungal
endocarditis in TAVI. (a, b)
At gross examination, note a
prosthetic valve stenosis by
polypous and friable
vegetations that block a
pericardial cusp and extends
along the mitroaortic brous
continuity. (c, d) Histologic
examination shows clusters of
Candida-type yeasts, hyphae,
and pseudohyphae entrapped,
within a brin network
platelets, red cells, and
granulocytes ((c), HE; (d),
PAS; insert, Grocott stains).
From Santos M etal., Eur
Heart J. 2011
G. Thiene et al.
c d
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