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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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C. Basso and G. Thiene
Fig. 4.31 Balloon
intervention (a) splitting the
fused mitral commissures (b)
ab
Fig. 4.32 Ballooning split of commissural fusion in mitral stenosis,
complicated by valve disruption with chordal rupture
Fig. 4.33 Surgical specimen of rheumatic mitral incompetence. Note
the retracted cusps and chordae tendineae
ab
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Fig. 4.34 Rheumatic mitral
incompetence. (a) Drawing,
(b) autopsy specimen with
wide orice by retracted
cusps, (c) neovascularization
at histology
45
c
Degenerative Disease
Mitral valve prolapse is currently the hallmark of the leading
degenerative disease, accounting for 2/3 of cases of mitral
incompetence.
It consists of ballooning and “billowing” of cusps and
scallops, prolapsing into the atrial cavity during systole and
resulting in various degrees of valve incompetence
(Figs.4.35, 4.36, 4.37 and 4.38).
At histology the cusp brosa appears inltrated by myxoid tissue with loss of collagen bers (Fig.4.39).
The chordae tendineae may also show myxoid degeneration. They progressively elongate and break suddenly, with
acute valve incompetence (Figs.4.40, 4.41 and 4.42) and
lung edema, requiring emergency intervention (valve
replacement or repair) (Fig.4.43).
The cause of progressive myxoid degeneration may be
the chronic trauma of the leaets, due to congenital defective
disjunction of the posterior leaet to the annulus.
Congenital absence of third-order chordae tendineae has
been postulated (Fig.4.44).
Mitral valve prolapse can be part of the phenotype expression of Marfan syndrome, associated with aneurysm of the
ascending aorta and aortic incompetence (Fig. 4.45).
Ischemic Disease
Acute mitral incompetence with pulmonary edema may
occur in the rst week after myocardial infarction due to
papillary muscle rupture (Figs.4.46, 4.47 and 4.48), involving either the anterior (in the setting of an anteroseptal
infarction) or the posterior papillary muscle (in the setting of
a posterolateral infarction). Simultaneous rupture of both
papillary muscles (Fig.4.49) has never been reported before,
to the best of our knowledge.
The rupture may involve the whole pillar of the papillary
muscle causing abrupt mitral regurgitation and pulmonary
edema or only one head of the papillary muscle, with less
severe mitral valve incompetence (Fig.4.50).
Post-necrotic scarring may cause retraction of a papillary
muscle with chronic mitral valve incompetence (Figs.4.50
and 4.51).
A peculiar degenerative disease of the mitral valve
apparatus is represented by dystrophic calcication of the
annulus, at the insertion of the posterior leaet (Fig.4.52).
Annular mineralization may be huge and soft (Fig.4.53).
The disease may lead to mitral regurgitation, since calcium deposits may hinder the annular sphincteric
contraction.
However, non-Marfan mitral prolapse has not been proved to
be a genetically determined valve disease.
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Floppy mitral valve
Floppy and flailFloppy
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C. Basso and G. Thiene
Fig. 4.35 Mitral valve
prolapse with ballooning of
cusps—scallops and mild
incompetence. (a) drawing,
(b) view from the left atrium
in an autopsy specimen
ab
Fig. 4.36 Much more severe ballooning of the cusps in mitral valve
prolapse of an autopsy specimen
Fig. 4.38 Schematic
representation of progression
of mitral valve prolapse up to
clinical regurgitation and
chordal rupture. LA left
atrium; LV left ventricle
Fig. 4.37 Severe mitral incompetence with hooding and thickning of
the leaets–scallops in an autopsy specimen
LA
LV
ProlapseBillowing
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a
b
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Fig. 4.39 Histology of a prolapsing cusp: note the remarkable replacement of collagen bundles of the brosa by mucoid ground substance
(a); closeup (b)
Fig. 4.40 Drawing of a
chordal rupture in mitral valve
prolapse (a). The mucoid
degeneration involves the core
of the chorda tendinea (b)
a b
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ab
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Fig. 4.41 Mitral valve prolapse in an autopsy specimen of a patient
died by acute pulmonary edema: note the chordal rupture of a prolapsed
cusp
Fig. 4.43 (a) Chordal
rupture of a prolapsing mitral
valve, removed at surgery
(surgical valve replacement).
(b) Segmental resection of
prolapsed cusp by chordal
rupture (surgical valve repair)
C. Basso and G. Thiene
Fig. 4.42 Mitral valve prolapse in another autopsy specimen: note the
free-oating cusp due to chordae rupture
4 Non Infections Pathology ofNative Heart Valves
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a
Fig. 4.44 Third-order chordae tendineae: the missed development
may compromise anchorage of the posterior leaet of the mitral valve
a
b
b
Fig. 4.46 Postinfarction papillary muscle rupture in autopsy specimens. Rupture of the anterior (a) and posterior (b) papillary muscles
a
Fig. 4.45 Aortic (a) and mitral (b) valves surgically removed in a
patient with Marfan syndrome, who underwent to mitro-aortic valve
replacement due to incompetence
b
Fig. 4.47 Schematic representation of postinfarction papillary muscle rupture (a). Surgical specimen of posterior mitral papillary muscle rupture (b)
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C. Basso and G. Thiene
a
b
Fig. 4.48 Postinfarction rupture of the posteromedial papillary muscle
of the mitral valve (a). Histology of the ruptured papillary muscle: note
the diffuse myocytolysis (b)
Fig. 4.49 Myocardial infarction with contemporary rupture of both
anterior and posterior papillary muscles of the mitral valve
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51
a
c
d
b
Fig. 4.50 Papillary muscle in chronic ischemic mitral valve incompetence. (a, c) Fibrosis and tethered posteromedial papillary muscle. (b, d)
Rupture of the tip of the posteromedial papillary muscle
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C. Basso and G. Thiene
a
b
Fig. 4.51 Mitral incompetence due to tethered ischemic papillary
muscle. (a) Regurgitation at echo doppler, (b) autopsy specimen of the
same patient
Fig. 4.52 Mild calcication
of the mitral ring with
impaired sphincteric
contraction and valve
incompetence. (a) X-Ray, (b)
gross view of the autopsy
specimen, (c) histology of the
mitral ring
a c
b
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a
a
b
b
Fig. 4.53 Huge, soft calcication of the mitral annulus in an autopsy
specimen. (a) panoramic view, (b) closeup
“Toxic” Disease (See Also Tricuspid Valve
Pathology)
Carcinoid valve disease usually spares the left side of the
heart because serotonin is lysed while crossing the lung circulation, with the exception of a right-to-left shunt as in case
of patent foramen ovale. However, exposure to drugs like
ergotamine, methysergide, and fen-phen may involve the left
heart valves.
Cardiomyopathy
Systolic motion of the anterior mitral leaet accounts for the
so-called systolic click in hypertrophic cardiomyopathy.
Contact of the anterior leaet with septal asymmetric hypertrophy leads to the onset of endocardial plaques as well as
leaet thickening contributing to mitral incompetence
(Fig.4.54).
Functional (“Secondary”) Chronic Mitral
Incompetence
It refers to mitral incompetence in the setting of a normal
mitral valve apparatus (leaets, chordae tendineae, papillary
muscles).
Fig. 4.54 Mitral valve incompetence in hypertrophic cardiomyopathy.
(a) Drawing, (b) panoramic view: note the contact in between the anterior mitral leaet and the ventricular septum, with endocardial brotic
plaque
It may occur in dilated cardiomyopathy due to dilatation
of the mitral annulus (Fig.4.55a) and in ischemic heart disease when the papillary muscles are implanted into an area
of previous myocardial infarction (Fig.4.55b). Tethering of
the mitral leaets occurs in ventricular dysfunction by displaced papillary muscles (Fig.4.56).
Traumatic Mitral Valve Incompetence
Papillary muscle quite rarely may rupture following a blunt
thoracic trauma.
Neoplastic Disease
A huge left atrial myxoma may herniate into the mitral orice, causing severe mitral stenosis and even occlusion
(Fig.4.57). It has been a cause of sudden death in the presurgical, angiographic, and echocardiographic era with cardiogenic shock and pulmonary edema (Fig.4.58). In such cases,
at surgical pathology or autopsy examination, the myxoma
appears hanged with a circular sign of strangulation, because
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