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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3655_Библиотеки_им_академика_М_И_Перельмана
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34
%
Surgical pathology
of 181 consecutive stenotic aortic valves
110 M, 71 F, mean age 71 ±
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C. Basso and G. Thiene
a
9
15%
22%
63
TAV BAV RVD
Fig. 4.9 Nowadays, the prevalent aortic valve stenosis is dystrophic
b
senile calcication of a tricuspid aortic valve (TAV tricuspid aortic
valve; BAV bicuspid aortic valve; RVD rheumatic valve disease)
Fig. 4.8 Subendocardial ischemic injury with replacement type brosis (a) and myocytolysis (b)
hood (Fig.4.9). It becomes manifest about 10years earlier
than the senile tricuspid aortic stenosis. The pathogenesis is
probably similar, namely, chronic mechanical stress on a
normal (tricuspid) and abnormal (bicuspid) aortic valve
(Fig.4.10).
Fig. 4.10 Aortic stenosis by bicuspid valve with dystrophic calcication and a raphe
4 Non Infections Pathology ofNative Heart Valves
35
Other Causes ofAortic Valve Incompetence
Aortic valve incompetence may occur even in the setting of
normal aortic cusps, when the sinus portion of the ascending
aorta enlarges because of aortopathy (Figs. 4.11 and 4.12).
The latter, rst reported by Corrigan from Dublin in the
famous article “Permanent patency of the mouth of the aorta”
(Fig.4.13), is another cause of aortic valve incompetence following rheumatic (Fig.4.2), infective endocarditis (Fig.4.14)
and syphilis (Fig.4.15). The free margin of the cusps appears
thickened with a “drum stick” appearance (Fig.4.16).
The tunica media of the aorta shows cystic medionecrosis
with loss of smooth muscle cells and elastic fragmentation of
the lamellar units (Figs.4.16 and 4.17).
Fig. 4.11 Aortic valve
incompetence due to
dilatation of the sinusal
portion of the ascending aorta
and enlarged annulus. (a)
drawing; (b) autopsy
specimen
a b
Aortic valve incompetence may be associated with bicuspid aortic valve in the setting of aortopathy, with dilatation of
the sinusal part of the ascending aorta and the aortic annulus.
Strands (“chordae tendineae”) attached to the commissural
raphe of a bicuspid aortic valve may suddenly rupture and
account for abrupt aortic incompetence with pulmonary
edema (Fig.4.18).
Downward extension of acute aortic dissection may cause
aortic incompetence because of commissural detachment
(Fig.4.19).
Overall, according to surgical pathology experience,
degenerative aortopathy is becoming the prevalent cause of
aortic valve regurgitation (Fig.4.20).
36
ab
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Fig. 4.12 Aortic
incompetence because of
aortopathy and dilatation of
both sinusal and ascending
aorta: angiography (a); the
same, viewed at surgery (b)
C. Basso and G. Thiene
Fig. 4.13 Corrigan, the discoverer of aortic incompetence with normal
semilunar cusps and dilatation of the ascending aorta due to
aortopathy
ab
4 Non Infections Pathology ofNative Heart Valves
37
Fig. 4.14 Aortic
incompetence due to infective
endocarditis with cusp
disruption. (a) drawing; (b)
autopsy specimen
Fig. 4.15 Aortic
incompetence because of
syphilis of the ascending
aorta. Note the paved intima
(a) and the pathognomonic
histologic landmark of plasma
cell vasculitis of the vasa
vasorum in the adventitia (b).
(c) Immunohistochemistry
CD38
ab
c
38
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a c
b d
C. Basso and G. Thiene
Fig. 4.16 Aortic incompetence by aortopathy. The cusps are normal (a), with a drum stick feature (b). The aortic tunica media shows elastic
fragmentation (c) and cystic medial necrosis (d)
Fig. 4.17 Aortic valve
incompetence due to
aortopathy of the ascending
aorta. Note the dilatation of
the sinusal aorta at
angiography (a) and loss of
elastic lamellar units in the
aortic wall (b)
a b
4 Non Infections Pathology ofNative Heart Valves
Fig. 4.18 Sudden rupture of an aortic valve strand (“chorda tendinea”),
detached from a raphe in bicuspid aortic valve
39
cba
Fig. 4.19 Drawings of aortic dissection with detachment of the valve commissures by downward extension of the dissection (a), with aortic
incompetence (b, c)
40
Etiology of Aortic Regurgitation
Surgical Pathology Studies
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C. Basso and G. Thiene
a
Author, Year Country N. RHD%Deg.%I.E.%BAV%Others
Olsen et al.,
1984
Guiney et al.,
1987
Turri et al.,
1990
Michel et al.,
1991
Fig. 4.20 Prevalence of aortic valve incompetence due to aortopathy,
from different surgical pathology experiences. BAV bicuspid aortic
valve; Deg degeneration disease; I.E. infective endocarditis; RHD rheumatic disease
USA 225 46 21 9 20 4
UK 72 26 34 21 9 10
Italy 254 20 59 11 7 3
France 313 38 35 11 5 11
Mitral Valve
Acquired mitral valve disease may be classied as inammatory, degenerative, ischemic, neoplastic, toxic, traumatic,
and functional (secondary).
Inammatory Disease
Rheumatic valve disease has been the leading cause of mitral
valve disease worldwide and is currently conned to thirdworld countries. It is the consequence of an autoimmune
phenomenon, due to streptococcal pharyngitis. Rheumatic
valvulitis affects rst the mitral valve with aseptic verrucae
(Fig.4.21), granulomatous inammation including Aschoff
and Aničkov (“owl” and “spider”) cells, in the absence of
any disrupting lesions like cusp perforation or chordal rupture. The healing process determines valve remodeling with
stenosis by cuspal thickening, commissural fusion, and calcic deposits with intact chordae (valvular stenosis)
(Figs.4.22, 4.23 and 4.24) or with chordal fusion, disappearance, of interchordal spaces and fusion of papillary muscles
with the leaets (subvalvular stenosis) (Figs.4.25 and 4.26).
Both recurrent valvulitis and organization of thrombus
formation at the commissures account for disease progression (Fig.4.27). Histology reveals brosis and neovascularization due to previous valvulitis (Fig.4.28).
Atrial enlargement with thrombus formation, either
within the left atrial appendage or a free-oating ball, source
of systemic emboli (“embolizing rheumatic mitral stenosis”), is a regular occurrence (Figs.4.29 and 4.30).
%
b
Fig. 4.21 (a) Rheumatic valvulitis of the mitral valve with sterile ver-
rucae. (b) Histology
Splitting of fused commissures, accomplished surgically
by a nger, represented historically a mode of palliative
relief of rheumatic mitral stenosis, currently replaced by the
use of transcatheter ballooning in selected cases (Fig.4.31).
However, all these closed-chest and blind procedures imply
the risk of valve apparatus disruption (Fig.4.32).
Pure rheumatic valve incompetence is rare and consists of
chordal and cusp retraction in the absence of commissural
fusion, with the mitral orice remaining patent during ventricular systole (Figs.4.33 and 4.34).
Mitral steno-incompetence is the most frequent disease as
the consequence of post-rheumatic mitral valve remodeling.
Mitral valve involvement by Libman-Sacks endocarditis
in lupus erythematosus or phospholipid syndrome consists
also of sterile verrucae, quite similar to those of rheumatic
disease albeit without the histological hallmark of granulomatous inammation. Also in this setting, the sequelae of the
healing process may account for valve deformity and valve
dysfunction.
ab
ab
4 Non Infections Pathology ofNative Heart Valves
Fig. 4.22 Schematic representation of rheumatic mitral stenosis by
commissural fusion with cusp calcication
Fig. 4.24 Surgical specimen
of mitral rheumatic stenosis,
view from left atrial and
ventricular sides: note the
valve thickening and
commissural fusion (a), with
normal subvalvular apparatus
(b)
41
Fig. 4.23 Rheumatic mitral stenosis in an autopsy specimen: note the
fusion of the commissures and thrombosis
Fig. 4.25 Subvalvular
rheumatic stenosis: fusion of
the chordae tendineae and
commissures, with valve
thickening. a=drawing, (b)
specimen
42
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C. Basso and G. Thiene
a
b
Fig. 4.26 Autopsy specimen with subvalvular rheumatic mitral stenosis (ventricular view): note the fused chordae with disappearance of
interchordal spaces
Fig. 4.27 Rheumatic mitral stenosis with left atrial enlargement and
valve thrombosis (a). Histology of a commissure with thrombus deposition which contributes to progression of commissural fusion (b)
Fig. 4.28 The histological hallmark of chronic rheumatic valve disease is neovascularization
4 Non Infections Pathology ofNative Heart Valves
43
Fig. 4.29 Rheumatic mitral
stenosis: (a) thrombosis of the
left atrial appendage and (b)
free-oating ball thrombus
a b
Fig. 4.30 Rheumatic mitral stenosis with thrombi in the left atrial
appendage and free-oating ball thrombus inside a huge dilatation of
the left atrium
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