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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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8 Pathology ofBiological Prosthetic Cardiac Valves
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a
Fig. 8.14 (a) X-ray showing a calcication starting at the commissures, enough to create tearing and severe acute valve incompetence. X-ray; (b)
histology of a commissure, von Kossa stain
a
a
b
b
b
c
c
Fig. 8.15 (a) Histology; (b) scanning electron microscopy, and (c, d)transmission electron microscopy pictures of unimplanted pericardium.
Note the collagen bers and bundles (b, c) and perfectly xed interstitial cell
d
d
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G. Thiene et al.
Fig. 8.16 (a) Commissural
tearing of pericardial
bioprosthetic valve (IonescuShiley device)and (b) the
same in Hancock pericardial
valve device. (c) Commissural
tearing of monocusp
pericardial valve device. Note
the absence of calcication at
X-rayin all
a
b
c
design with the use of a single sheet of bovine pericardium
mounted on the stent to create a tricuspid valve model and a
second sheet covering the stent to prevent abrasion
(Fig. 8.17). When dystrophic calcication occurred in
second- generation pericardial bioprosthetic valves, mineralization involved all the cups with stenosis, without isolated
commissural calcication and tearing (Fig.8.18).
However, defective glutaraldehyde xation of bovine
pericardium occurred in the second-generation Mitroow
pericardial bioprosthetic valve, accounting for collagen
denaturation (“brinoid necrosis”) and accelerated mineralization (Fig.8.19).
8 Pathology ofBiological Prosthetic Cardiac Valves
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Fig. 8.17 Change of the
design in second-generation
bovine pericardial valve
xenografts. A single sheet is
employed for molding all the
three cusps. Second sheet
covers the stent, to avoid
abrasion
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Fig. 8.18 Second-generation
pericardial valve, gross view
and X-Ray. (a) Prophylactic
early explant: neither
calcication nor tearing at the
commissures. (b) Massive
calcication with stenosisat
distance with calcication of
all the cusps, without tearing
at commissure
a
b
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G. Thiene et al.
Stentless
Stentless bioprosthetic valves (SLBPVs) have represented an
important evolution in the history of surgical treatment of
aortic valve stenosis. The advantage for the use of these
devices, even in patients less than 65years of age, is the lack
of prosthetic frame, to mimic the native aortic valve and to
minimize both commissural hemodynamic stress and postoperative transvalvular gradient. Postoperative regression of left
ventricular hypertrophy occurs. The negative aspect is the
extensive suturing requiring long-time cross-clamping, with
the risk of not optimal myocardial protection and the need of
peculiar skill by the surgeon, with long learning curve.
Stentless bioprostheses are made from the porcine aortic
valve or constructed with bovine pericardium (Fig.8.20); both
are xed in glutaraldehyde and not mounted on a frame. They
are implanted in a free-hand fashion using three separate sutures
to x the valve to the native aortic annulus. This procedure may
be time consuming and therefore such devices have not been
universally accepted as alternative to stented bioprostheses.
In porcine SLBPVs, following the removal of the native
diseased cusps, the commissures remain attached to the porcine xenograft aortic wall and sutured to the recipient one.
The most typical mode of dysfunction of porcine SLBPVs
is usually incompetence while for pericardial SLBPVs is
stenosis.
Porcine SLBPVs degenerate in a peculiar mode, namely,
pinpoint calcication at the commissures, which can lead to
tearing and ever sudden incompetence (Fig.8.21).
Valve tissue degradation may consist also of lipid insudation, tissue disruption, and fraying of collagen bers. Lipid
insudation (“atheromasia”) is well visible at gross examination by a yellowish appearance of the cusps. Histology and
transmission electron microscopy show cholesterol clefts
(Figs.8.22 and 8.23).
In stentless pericardial xenografts the cusps are molded
from a single pericardial sheet, which is then sutured to a
second external pericardial sheet.
In pericardial SLBPVs, calcication phenomenon can be
massive at both cusps commissures and belly, leading to stenosis for cusp stiffening and regurgitation due to cusp tears. In
addition, pericardial SLBPVs may also show focal yellow
spots, like fatty streaks (“atheromasia”). Histology reveals
intrinsic calcication and focal mononuclear cell inltrates,
mostly macrophages positive at immunohistochemistry markers (Fig.8.24).
a
b
d
ec
Fig. 8.19 (a, b) Severe early calcication at gross and X-ay examina-
tion of a Mitroow pericardial valve. Poorglutaraldehyde xation with
collagen denaturation, is well visible both at light (c, d) (haematoxylin-
eosin and Azan Mallory stains) and ultrastructural transmission electron microscopy (e)
Porcine stentless Pericardial stentless
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Fig. 8.20 Stentless porcine
(a) and pericardial bovine (b)
bioprosthetic valves
a
a
b
b
Fig. 8.21 Cryolife-O’Brien porcine stentless valve removed by emergency operation, following an abrupt incompetence due to Ca++ commissural tearing. Gross (a) and X-ray (b) views of the removed cusps with pin point mineralization at the commissures
Mineralization was proven to occur ever in the midterm,
similar to stented valves, particularly at commissural levels
of porcine SLBPVs, as to account for an even abrupt tearing
and valve incompetence (Figs.8.23, 8.24, 8.25 and 8.26).
Thus, tissue mineralization is the nightmare also of
SLBPVs. Even pinpoint calcication at the commissure and
belly, especially in porcine devices, may be dangerous
enough to cause abrupt cuspal tearing and sudden incompe-
aortic valve replacement with Toronto porcine stented valve
resulted with an optimal patient survival but suboptimal
valve durability.
Treatment with effective anticalcic agents should
increase long-term durability.
Moreover, nowadays, TAVI with “valve-in-valve” procedure is a valid alternative to surgical prosthetic valve replacement and reoperation in case of SVD.
tence. Lipid insudation contributes to SVD as well. Overall,
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G. Thiene et al.
Fig. 8.22 Cryolife-O’Brien porcine stentless valve. The cusp appears yellow at gross examination (a–c). Coarse calcication at X-ray (d–f) and
lipid insudationat histology with intrinsic calcication (g–i).Von Kossa stain
Fig. 8.23 (a, b)
Transmission electron
microscopy of a porcine cusp
(same case of Fig.8.23). Note
lipid droplet and cholesterol
needles (asterisks)
8 Pathology ofBiological Prosthetic Cardiac Valves
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a
b
c
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Fig. 8.24 Removed cusps of Solo stentless pericardial valve (a) with pinpoint calcic deposits at X-ray (b). Note massive lipid insudation with
cholesterol clefts surrounded by CD68-positive macrophages (c)
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Fig. 8.25 Gross (a, b, c), X-ray (d, e, f) with microscopic histologic
ndings (g, h, i) of a Toronto porcine SLBPV, explanted after 115 mos
because of incompetence due to calcium-related commissural tearing.
The explanted cusps show yellow appearance due to lipid insudation
and commissural tearing (arrow). (a–f) Corresponding X-ray; note the
bright signal at a commissure (d) (arrow), due to calcications with
tearing and incompetence. Histologic sections of the cusps with intrinsic calcium deposits and the cholesterol clefts by lipid insudation (g–i).
Hematoxylin-eosin stain (g, h) and von Kossa stain (i)
ef
bc
8 Pathology ofBiological Prosthetic Cardiac Valves
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a
d
ghi
133
Fig. 8.26 Gross (a–c), radiographic (d–f), and microscopic ndings
(g–i) of a Freedom Solo pericardial SLBPV, explanted after 83 mos
because of stenosis due to calcic dystrophy. (a–c) Gross features of the
cusps: note the thickening due to massive calcications. (d–f)
Sutureless
Sutureless valve devices were introduced in the clinical setting to expedite valve implant even with a thoracoscopy
approach, as to avoid sternotomy.
Unlike with TAVI, in which the native calcic valve is left
in situ, sutureless valve implant procedure consists of cusp
excision, avoiding risk of calcium nodular embolization and
paravalvular leak.
The sutureless Perceval valve model is composed by a nitinol frame, adapted around the pericardial stentless Solo bioprosthesis, and by an anchorage clothed annulus (Fig.8.27).
Corresponding X-ray; diffuse bright signal due to mineralization. (g–i)
Histological sections with von Kossa stain: massive cuspal intrinsic calcium deposits
Since implantation requires collapse of the valve followed
by ballooning (Fig. 8.28), pericardial damage was feared
during this procedure. This phenomenon has been excluded
by scanning electron microscopy studies, detecting neither
collagen periodicity changes nor architectural bers deformation after collapsing and ballooning in vitro (Figs. 8.29
and 8.30).
Thus, collapsing and ballooning during deployment of
Perceval S do not damage the xenograft pericardial collagen.
Collagen crimping appeared unaltered. Neither tear andperforations of the pericardial cusps nor stent deformation fractures have been observed.
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Fig. 8.27 Perceval S sutureless bioprosthetic valve. A self-expandable nitinol network surrounds a pericardial stentless valve
G. Thiene et al.
Ready to implant
Valve is collapsed to a
reduced diameter
First step valve deployment
Fig. 8.28 The two steps of valve implantation valve are as follows:
collapsed to reduce the diameter and then deployed
However, in the mid to long term, both mineralization and
brous pannus (Figs. 8.31 and 8.32) occurred.
Fibrous tissue overgrowth with stenosis took place progressively overtime with a plateau around 20 months after
implant. Structural valve deterioration by mineralization
with stenosis was observed in some patients in the midterm
follow-up as to require redo with bioprosthesis valve replacement. Nowadays, valve-in-valve TAVI procedure is a reliable
alternative to surgical reintervention, avoiding anesthesia,
sternotomy, and cross-clamping.
Effective anticalcication treatment and stent remodeling
will be mandatory to improve long-term durability of
Pericardial sutureless valve bioprosthesis.
Moreover, the implant procedure has to pay attention on
the His bundle, which is only 5–6mm far from the aortic
annulus.
A newly introduced anticalcication treatment is expected
to enhance valve durability, preventing early mineralization.
A second-generation Perceval (Perceval Plus) with antimineralization processing has been manufactured and it is now
in the market.
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