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7 Pathology ofMechanical Prosthetic Cardiac Valves
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115
Fig. 7.15 (a) TRI-Tech valve leaet, escaped from the aortic position
for valve tab fracture and found at the bifurcation of the left common
iliac artery (b) Close-up of (a). (c) The TRI-Tech valve in the aortic
Another patient, a 53-year-old man who was submitted to
mitral valve replacement with a 31mm TRI-Tech, experienced sudden dyspnea with pulmonary edema, 22 months
postoperatively, and underwent a successful emergency
prosthetic valve replacement. The third patient, a 68-year-old
man, who had undergone 25 mm TRI-Tech aortic valve
position: a leaet is missing. (d) The missing leaet, found in the left
common iliac artery, had a tab asymmetry of 0.41mm
replacement, died suddenly while driving. The escaped leaflet was found in the left common iliac artery (Fig.7.15) with
tab asymmetry of 0.41 mm.
Tab asymmetry, with postoperative risk of fracture of the
pivoting system, leaet escape, and embolization, were
clearly a manufactural error.
implantation and had refused prophylactic prosthetic valve
116
U. Bortolotti et al.
Paravalvular Leak
Apart from prosthetic thrombosis and brous tissue overgrowth, another well-known cause of nonstructural failure of
mechanical valve devices is detachment from the prosthetic
annulus. This complication is most commonly related to
annular disruption by sewing ring sutures, precipitated by
infectious endocarditis or caused by extreme weakness of the
native annulus due to signicant calcication. Technical factors during the surgical procedure may also play a role. As a
consequence, formation of single or multiple regurgitant jets
occurs which may cause both various degrees of hemolysis
and severe valve insufciency (Fig.7.16).
Fig. 7.16 Tilting-disc mechanical valve prosthesis implanted in mitral
position with evident detachment from the native annulus (arrow).
Another periprosthetic leak is indicated by a probe, passing through the
sewing ring-annulus interface (asterisk). The prosthesis had been
implanted using a continuous suture technique. The patient had a mitral
prolapse regurgitation, and the leaks might have been favored by the
weakness of the annulus related to the underlying disease
Further Reading
Bottio T, Casarotto D, Thiene G, Caprili L, Angelini A, Gerosa G.Leaet
escape in a new bileaet mechanical valve: TRI Technologies.
Circulation. 2003;107:2303–6.
Cianciulli TF, Fairman EB, Saccheri MC, Llanos Dethinne SD, Prezioso
HA.Retrieval of a leaet escaped in a TRI-Technologies bileaet
mechanical prosthetic valve. Eur J Echocardiogr. 2007a;9:65–8.
Cianciulli TF, Lax JA, Saccheri MC, Redruello HJ, Belforte SM,
Picone VP, Prezioso HA. Acute mitral valve dysfunction due to
leaet escape in a TRI-Technologies bileaet mechanical valve. Eur
J Echocardiogr. 2007b;8:63–6.
De Martino A, Milano AD, Thiene G, Bortolotti U.Diamond anniver-
sary of mechanical heart valve prostheses. A tale of cages, balls and
discs. Ann Thorac Surg. 2020;110:1427–33.
De Martino A, Milano AD, Thiene G, Della Barbera M, Bortolotti
U.The caged-ball prosthesis 60 years later. Historical review of a
cardiac surgery milestone. Texas Heart Inst J. 2022;49:e207267.
Della Barbera M, Bottio T, Angelini A, Cresce GD, Montisci M, Gerosa
G, Valente M, Thiene G. The pathology of TRI-tech valve leaet
escape. J Heart Valve Dis. 2012;21(2):241–6.
Dikmengil M, Sucu N, Aytacoglu BN, Mavioglu I. Leaet escape
in a TRI bileaet rotatable mitral valve. J Heart Valve Dis.
2004;13:638–40.
Edmunds LH.Thromboembolic complications of current cardiac val-
vular prostheses. Ann Thorac Surg. 1982;34:96–106.
Gerosa G, Carta R, Montisci M, Leoni L, Iliceto S, Rizzoli G, Di Marco
F.How to deal with recipients of valves prone to structural failure in
the 2000s: Padua experience with the TRI Technologies valve. Ann
Thorac Surg. 2006;82:858–64.
Harken DE, Soroff HS, Taylor WJ, Lefemine AA, Gupta SK, Lunzer
S.Partial and complete prostheses in aortic insufciency. J Thorac
Cardiovasc Surg. 1960;40:744–62.
Kliger C, Eiros R, Isasti G, etal. Review of surgical prosthetic para-
valvular leaks: diagnosis and catheter-based closure. Eur Heart J.
2013;34:638–48.
Lindblom D, Bjork VO, Semb BKH.Mechanical failure of the Bjork-
Shiley valve. Incidence, clinical presentation and management. J
Thorac Cardiovasc Surg. 1986;92:894–907.
Roudaut R, Serri K, Latte S.Thrombosis of prosthetic heart valves:
diagnosis and therapeutic considerations. Heart. 2007;93:137–42.
Starr A, Edwards ML.Mitral replacement: clinical experience with a
ball-valve prosthesis. Ann Surg. 1961;154:726–40.
Weisse AB. The surgical treatment of mitral stenosis: the rst heart
operation. Am J Cardiol. 2009;103:143–7.
Pathology ofBiological Prosthetic
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Cardiac Valves
GaetanoThiene, MilaDellaBarbera, AldoMilano,
StefaniaRizzo, UbertoBortolotti, andMarialuisaValente
8
Stented
At present, approximately 80% of surgical valve replacements are performed employing bioprostheses, obtained
either from the porcine aortic valve or made of bovine pericardium, the latter molded to simulate a tricuspid aortic valve
(Fig.8.1).
Porcine Bioprostheses
Glutaraldehyde xation ensures tissue stabilization by strengthening collagen cross-linking, masking recipient immunological response, and assuring tissue sterilization (Fig.8.2). Porcine
valves are mounted on a stent, which in the initial models was
made by rigid metallic alloys, and then replaced by exible
plastic material such as polypropylene in most recent models;
the stent is covered with a fabric cloth and provided with a sewing ring to facilitate prosthesis implantation (Fig.8.3).
Normal porcine aortic cusps consist of three layers
(Fig.8.4):
(a) “Ventricular,” facing the ventricular cavity with elastic
bers.
(b) “Spongiosa,” with extracellular matrix, mostly ground
substance.
G. Thiene (*) · M. D. Barbera · S. Rizzo · M. Valente
Department of Cardiac, Thoracic, Vascular Sciences and Public
Health, University of Padua Medical School, and Cardiovascular
Pathology Unit, University Hospital of Padua, Padua, Italy
e-mail: gaetano.thiene@unipd.it; mila.dellabarbera@unipd.it;
s.rizzo@unipd.it; marialuisa.valente@unipd.it
A. Milano
Division of Cardiac Surgery, Emergency and Transplant
Department, University Hospital of Bari, Bari, Italy
e-mail: aldo.milano@uniba.it
U. Bortolotti
Section of Cardiac Surgery, Cardio-thoracic and Vascular
Department, University Hospital of Pisa, Pisa, Italy
e-mail: uberto.bortolotti@med.unipi.it
(c) “Fibrosa,” facing the sinus of Valsalva, with collagen
bundles; this layer crimps during ventricular systole and
attens during diastole.
Unfortunately, in the rst-generation models without an
effective antimineralization treatment, structural deterioration of the valve tissue occurred with time so that nearly 50%
of patients required prosthetic valve replacement within
10–12years from implant (Fig.8.5) and almost 100% within
20years.
Causes and mechanisms of structural deterioration of bioprosthetic valves may be divided into host-related and graftrelated (Table 8.1). Among the former, brous tissue
overgrowth consists of exuberant healing at the annulus
invading the orice and overlaying the cusps, thus creating
valve stenosis (Fig.8.6). Lipid insudation from the recipient’s blood may also occur, at times being so great to determine cusp fragility with tearing and prosthetic valve
incompetence, even in the absence of calcication (Fig.8.7).
Among the graft-related causes of structural valve deterioration, inward banding (Fig.8.8a) due to creeping of the
stent, may occur with prosthetic stenosis (Fig. 8.8b).
Occasionally, sudden collapse of the frame by fracture of the
post (Fig. 8.8c) may even cause acute prosthetic valve
incompetence.
Cuspal hematomas are hematic dissections of the porcine
cusps (Fig. 8.9), probably due to blood entering through
stitches at the annulus.
Commissural dehiscence, with detachment of the cusp
commissures from the xenograft aortic wall, results in valve
incompetence (Fig.8.10).
The right cusp of a porcine aortic valve includes a myocardial shelf. An immune reaction with macrophage phagocytosis of the glutaraldehyde-xed pig cardiomyocytes may
cause perforation of the muscle shelf with prosthetic incompetence (Fig.8.11).
Thrombus formation may ll the Valsalva sinuses impairing cusp distensibility and causing valve stenosis (Fig.8.12).
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2023
G. Thiene et al. (eds.), Pathology of Cardiac Valve Disease, https://doi.org/10.1007/978-3-031-35498-4_8
117
118
Cells
Cross linking
G. Thiene et al.
a
b
Fig. 8.1 (a) Porcine aortic valve and (b) pericardial aorticvalve, tricuspid molded from a sheet of bovine pericardium
Fig. 8.2 Glutaraldehyde
xation with collagen cross
linking
Bundles of
fibers
GLUTARALDEHYDE
P
cardial
8 Pathology ofBiological Prosthetic Cardiac Valves
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119
Fig. 8.3 Porcine (a) and
pericardial (b) valves, after
being mounted in the stent
Fig. 8.4 (a) Histology of an
aortic porcine cusp with three
layers (ventricularis,
spongiosa and brosa), (b)
note the collagen crimping of
the brosa during systole and
atting in diastole
orcine
stented
a
a
b
Peri
stented
b
120
100
Years Post-PHV Implant
Actuarial Freedom From SVD (%)
80
60
40
20
0
Fig. 8.5 Longevity of porcine and pericardial valve. After 7–8years,
the actuarial Meyer curve freedom from structural valve deterioration
starts to decline
Porcine:
MetaAnalysis - 5,837 patients
CE Pericardial Perimount:
8 studies - 2,902 patients
“Porcine Limits”
0510 15 20
G. Thiene et al.
However, dystrophic calcication of the xenograft cusps
is the major cause of the structural valve deterioration in porcine bioprostheses. Blood calcium of the recipient combines
with phospholipids of the cell membrane debris of the xenograft valve, thus precipitating calcium phosphate formation.
Calcication leads either to cusp stiffness and rigidity with
valve stenosis (Fig.8.13a) or commissural and cusp tearing
with incompetence (Fig.8.13b).
Cusp mineralization accounts for almost 90% of cases of
structural deterioration in porcine bioprosthetic valves recipients. The valve commissures are particularly prone to mineralization as to be the early sites of calcication, being the
structures bearing the maximal mechanical stress during
opening and closing of the cusps (Fig.8.14).
Table 8.1
graft-related causes of structural
valve deterioration
Fig. 8.6 Severe stenosis of
mitral porcine BP valves by
brous tissue overgrowth. (a)
Gross view from the left
atrium; (b) histology.
Weigert-Van Gieson stain
Host-related and
Structural valve deterioration of bioprosthetic valves
Host-related • Fibrous pannus
• Lipid insudation
Graft-related • Stent creeping or fracture
• Cuspal hematoma
• Commissural dehiscence
• Thrombus formation
• Tears, primary
• Mineralization
a b
8 Pathology ofBiological Prosthetic Cardiac Valves
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121
a
b
c
Fig. 8.7 (a) Yellow cusps of a porcine valve, (b) spontaneous tearing at the commissure in the absence of X-ray calcication,(c) insudation with
cholesterol needles and foreign body inammatory. Haematoxylin-eosin stain
122
a
Fig. 8.8 (a, b) Creeping and
(c) fracture with collapse of
plastic stent in porcine
bioprosthetic valves
G. Thiene et al.
b
c
a b
Fig. 8.9 Huge hematoma of the cusps, hindering the orice opening and creating severe stenosis. (a) Gross view of a mitral device from the
atrium; (b) histologyof the hematoma (arrow). Azan Mallory stain
8 Pathology ofBiological Prosthetic Cardiac Valves
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123
a
Fig. 8.10 (a) Commissural dehiscence by detachment from xenograft aortic wall. (b) Closeup
a
b
b
Fig. 8.11 (a) Porcine bioprosthetic valve perforation of the right aortic cusp muscle shelf with valve incompetence. (b) At transmission electron
microscopy, a macrophage phagocytoses a sarcomere from a cardiomyocite
a
Fig. 8.12 Porcine valve sinuses fullled by a thrombus and creating valve stenosis. (a) Gross view; (b) histology. Weigert-Van Gieson stain
b
124
G. Thiene et al.
a
b
Fig. 8.13 (a) Stenosis of bioprosthetic porcine valve by massive dystrophic calcication with stiffened cusps. (b) Calcication may affect only
the commissure and create tearing with even acute incompetence
Pericardial Bioprostheses
Mechanical stress and abrasion of the pericardium by
contact with the stent were considered responsible of com-
Pericardial bioprosthetic valves, made of bovine parietal
pericardium, represent an alternative to porcine bioprostheses. The parietal pericardium consists of a mesothelium
layer, facing originallythe pericardial cavity, compact brosa
with parallel, slightly crimped collagen bers and a few scattered pericardiocytes (interstitial cells) (Fig.8.15).
missural tearing in the rst-generation pericardial devices,
with prosthetic regurgitation both in tricuspid (Fig.8.16a, b)
and monocusp models (Fig.8.16c), even in the absence of
mineralization.
This “Achilles heel” was corrected in the second generation of pericardial bioprostheses, by changing the valve
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