Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3695_Библиотеки_им_академика_М_И_Перельмана
.pdf
CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Figure 2 Close-up views of the lonescu-Shiley bioprostheses in the tricuspid (T)
and mitral (M) valve positions. a and a′, from the atrial aspects, the orices of each
are xed in a triangular shape. b, 1 stent (dashed arrow) has burrowed into thê right
ventricular free wall. One stent is encircled by a suture (curved solid arrows). b′,
1 suture (arrows) crosses 2 bioprosthetic cusps holding each rigidly in place. The
Björk-Shiley prosthesis is visible at the upper left. c, another view of the suture
encircling the stent. c′, close-up of the suture inadvertently holding down 2 biopros-
thetic cusps. (Photographs by M.M.M. Moore.)
operator has satisfactorily shown that each cusp of the bioprosthesis is freely mobile,
a requirement to prevent bioprosthetic regurgitation.
REFERENCE
1. Silver MA, Orenburg PR, Roberts WC. Severe mitral regurgitation after mitral
valve replacement with a parietal pericardial bovine bioprosthesis. Am J Cardiol
1983;52:218–219.
170

CASE 724 EXTENSIVE CALCIFICATION OF A BIOPROSTHESIS IN THE TRICUSPID VALVE POSITION
https://t.me/medicina_free
Case 724 Extensive Calcification of a Bioprosthesis
in the Tricuspid Valve Position and Minimal
Calcification of a Simultaneously Implanted
Bioprosthesis in the Mitral Valve Position
Deborah J. Barbour, MD, Charles L. Mcintosh, MD, PhD, and William C.
Roberts, MD
Previous reports describing results of simultaneously implanted and explanted
porcine bioprostheses in the mitral and aortic valve positions
tricuspid valve positions
3
have shown greater degeneration in those bioprostheses
1, 2
and mitral and
in the mitral position than in either aortic or tricuspid valve positions. The reasons
for the more rapid degeneration of the bioprostheses in the mitral position than in
either the aortic or tricuspid valve positions are not clear, but probably are related
to the higher closing pressure on the bioprosthetic cusps in the mitral position. In
contrast to previous observations, a patient who had recently undergone study had
much heavier calcic deposits on the cusps of the bioprosthesis in the tricuspid valve
position than on those of the bioprosthesis in the mitral position. Abrief description
of this patient follows.
T.H., a 38-year-old Greek woman, had a mitral valve commissurotomy at age 19years.
By age 29, anasarca prompted cardiac catheterization (Table 1) and then simultaneous
tricuspid and mitral valve replacements with 31- and 27-mm Hancock porcine bioprostheses
for pure tricuspid valve regurgitation and mitral valve stenosis. She did well for 7years, and
then peripheral edema, dyspnea, anasarca and dizziness occurred. Catheterization (Table 1)
at age 37 revealed severe stenosis of the bioprosthesis in the tricuspid valve position and
moderate stenosis of the bioprosthesis in the mitral valve position, and 105 months after
their initial simultaneous implantation, both bioprostheses were replaced, a 29-mm Hancock
porcine bioprosthesis in the tricuspid position and a Starr-Edwards mechanical prosthesis in
the mitral position. At operation, thrombus was removed from both atria. The bioprosthesis
explanted from the tricuspid valve position had far heavier calcic deposits than did the one
explanted from the mitral position (Figure1).
The cause of the greater degree of calcium on the bioprosthetic cusps in the
tricuspid valve position than on the bioprosthetic cusps in the mitral valve position
Table 1: Hemodynamic data
Age
(yr)
PA
(S/d)
RV
(s/d)
RA
(m)
RA-RV
mdg
LV
(s/d)
SA
(s/d)
PAW
(m)
PAW-LV
mdg Cl
29 115/60 115/18 18 0 105/12 105/65 25 17 1.8
38 32/19 32/4 16 13 95/4 100/60 12 11 2.4
Pressures are in mm Hg.
Cl=cardiac index in liters/min/m
ent; PA=pulmonary artery; PAW=pulmonary artery wedge; RA=right atrium; RV=right
ventricle; SA=systemic artery; s/d=peak systole/end diastole.
From the Pathology and Surgery Branches, National Heart, Lung, and Blood Institutes,
National Institutes of Health, Bethesda, Maryland 20892. Manuscript received and accepted
July1, 1986.
DOI: 10.1201/9781003409281-30 171
2
; LV=left ventricle; m=mean; mdg=mean diastolic gradi-

CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Figure 1 Explanted bioprostheses. Upper panel, radiograph (left) and photographs
(center and right) of the bioprosthesis explanted from the tricuspid valve position;
lower panel, radiograph (left) and photographs (center and right) of the bioprosthe-
sis explanted from the mitral position. The photographs in the center are the atrial
aspect of the bioprosthesis and those at the right, the ventricular aspect.
was not determined. The closing pressure on the bioprosthesis in the tricuspid valve
position was only one-third of that on the bioprosthetic cusps in the mitral position
(32 vs 95mm Hg).
REFERENCES
1. Warnes CA, Scott ML, Silver GM, Smith CW, Ferrans VJ, Roberts WC. Comparison
of late degenerative changes in porcine bioprostheses in the mitral and aortic
valve position in the same patient. Am J Cardiol 1983;51:965–968.
2. Cipriano PR, Billingham ME, Miller DC. Calcication of aortic versus mitral
porcine bioprosthetic heart valves; a radiographic study comparing amounts
of calcic deposits in valves explanted from the same patient. Am J Cardiol
1984;54:1030–1032.
3. Cohen SR, Silver MA, McIntosh CL, Roberts WC. Comparison of late (62 to 140
months) degenerative changes in simultaneously implanted and explanted porcine (Hancock) bioprostheses in the tricuspid and mitral valve positions in six
patients. Am J Cardiol 1984;53;1599–1602.
172

CASE 788 BIOPROSTHESES IN TRICUSPID AND MITRAL VALVE POSITIONS FOR 100 MONTHS
https://t.me/medicina_free
Case 788 Bioprostheses in Tricuspid and Mitral
Valve Positions for 100 Months with Heavier Calcific
Deposits on the Left-Sided Valve Followed by New
Bioprostheses in Both Positions for 95 Months with
Heavier Calcific Deposits on the Right-Sided Valve
Benjamin N. Potkin, MD Charles L. Mcintosh, MD, PhD, Richard O. Cannon III,
MD, William C. Roberts, MD
Previous reports describing results of simultaneously implanted and explanted
bioprostheses in the mitral and aortic valve positions and in the mitral and tricuspid
positions usually, but not always, have shown greater degeneration of the bioprostheses
in the mitral position than in either the aortic or tricuspid valve position, presumably
because of the h igher closing pressure on t he bioprosthet ic cusps in the mitral p osition.
Herein, we describe a patient who had simultaneous bioprosthetic replacement of both
mitral and tricuspid valves. Later replacement of both bioprostheses revealed heavier
calcic deposits on the bioprosthesis in the mitral position after the rst bioprosthetic
replacement and heavier calcic deposits on the bioprosthesis in the tricuspid valve
position after the second bioprosthetic replacement.
E.V., a 62-year-old white woman with systemic hypertension and diabetes mellitus, had
4 cardiac valve operations (Table 1). Congestive heart failure developed during her second
pregnancy and 1 year later, at age 35, she underwent closed mitral commissurotomy for
mitral stenosis. She was nearly asymptomatic for 2 years thereafter and then congestive
heart failure and atrial brillation developed. Because of worsening congestive heart failure,
at age 46 she had simultaneous replacement of both native mitral and tricuspid valves
with Hancock no. 29 and 31 glutaraldehype processed bioprostheses, respectively. She was
asymptomatic for the next 8years when congestive heart failure reappeared at age 54. Left
ventricular cineangiogram now demonstrated 4+/4+ mitral regurgitation and a 22mm Hg
mean diastolic pressure gradient across the bioprosthesis in the mitral position. At age 54,
the 2 bioprostheses, each of which had been in place for 100 months, were excised along with
the diffusely thickened, purely regurgitant aortic valve and all 3 were replaced with Hancock
bioprostheses. The excised bioprosthesis in the mitral position had heavier calcic deposits
than did the bioprothesis in the tricuspid valve position (Figure1). Postoperatively, she again
was asymptomatic. Catheterization, 7 months later, disclosed a 11mm Hg mean diastolic
pressure gradient across the bioprosthesis in the mitral position. Pulmonary hypertension
persisted. Congestive heart failure recurred at age 61years, 86 months after the last operation.
Nine months later or 3 days before death the 3 bioprosthetic valves were replaced because of
refractory congestive heart failure. The bioprosthesis that had been in the tricuspid valve
position had heavier calcic deposits than that present on the bioprostheses that had been in
either the mitral or aortic valve position (Figure2).
This patient is unique in that 2 prostheses had each been in place for 100 months
and 3 other bioprostheses had each been in place for 95 months. When the initially
inserted 2 bioprostheses were explanted, heavier calcic deposits were present in the
bioprosthesis that had been in the mitral valve position compared with the one that
1–4
From the Pathology, Surgery and Cardiology Branches, National Heart, Lung, and Blood
Institute, National Institues of Health, Bethesda, Maryland 20892. Manuscript received
October15, 1987; revised manuscript received and accepted November13, 1987.
DOI: 10.1201/9781003409281-31 173

CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
Figure 1 Radiographs (top) and photographs (bottom) of bioprostheses that had
been in place in the tricuspid (T) and mitral (M) valve positions for 100 months.
Heavier calcic deposits are present in the prosthesis that had been in the mitral
valve position. Additionally, 1 cusp of the prosthesis in the mitral position was torn
(arrow) and this bioprosthesis was severely regurgitant.
Figure 2 Radiographs (top) and photographs (bottom) of bioprostheses explanted
3 days before death and which had been in place in the tricuspid (T), mitral (M) and
aortic (A) valve positions for 95 months. Heavier calcic deposits are present in the
bioprosthesis in the tricuspid valve position than in the bioprosthesis in either the
mitral or aortic valve positions.
174

CASE 788 BIOPROSTHESES IN TRICUSPID AND MITRAL VALVE POSITIONS FOR 100 MONTHS
https://t.me/medicina_free
had been in the tricuspid valve position. When these malfunctioning bioprostheses
were excised and replaced with other bioprostheses that were in place for nearly
the same amount of time, namely 95 months, heavier calcic deposits developed in
the bioprosthesis that had been in the tricuspid valve position compared with that
occurring in either bioprosthesis located on the left side of the heart.
The explanation for the reversal of the heavier calcic deposits in the tricuspid
and mitral valve positions during the 2 time frames (100 months with the initially
inserted bioprostheses and 95 months with the replaced bioprostheses) is unclear. It
is likely that during much of the postoperative period after the initial double valve
replacement the right ventricular systolic pressure, which represents the closing
pressure on the bioprosthesis in the tricuspid valve position, was only mildly elevated
(37mm Hg). In contrast, after the bioprostheses in the tricuspid and mitral valve
positions were replaced, the right ventricular systolic pressure remained elevated
(65mm Hg), probably during the entire 95-month period. During this latter 95-month
period of high right ventricular systolic pressures, heavier calcic deposits developed
on the cusps of the bioprosthesis in the tricuspid valve position than on the cusps
of the bioprosthesis in the mitral valve position. The closing pressure, i.e., the left
ventricular systolic pressure, on the bioprosthesis in the mitral position, however, was
always considerably higher than was the closing pressure on the bioprosthesis in the
tricuspid valve position: 160 vs 37mm Hg after the rst valve replacements and 210 vs
65mm Hg after the bioprosthetic replacements. Thus, factors other than bioprosthetic
closing pressures must have played a role in determining which bioprosthesis in the
atrioventricular valve positions contained the heavier calcic deposits.
Table 1: Patient’s hemodynamic data
Month/year 5/1970 8/1971 6/1979 1/1980 8/1986
Age (yr) 45 46 54 55 61
NYHA FC III I III I III
SA (s/d) 160/95 150/90 112/70 205/90 137/76
RA V (mean) 25 (18) 14 (10) 26 (22) 16 (13) 22 (20)
RV (s/d) 60/9 37/7 75/16 65/7 67/20
PA (s/d) 60/30 37/20 80/40 65/28 68/28
PAW V (mean) 34 (25) 26 (20) 47 (38) 40 (28) 34 (25)
LV (s/d) 155/16 160/12 117/16 210/25 158/17
CO/CI 5.4/3.1 6.3/3.8 2.2/1.4 5.2/3.3 4.0/2.5
LV-SA psg 0 10 0 5 21
PAW-LV mdg 13 8 22 11 10
RA-RV mdg 6 7 8 7 6
MVA/MVI *0.8/0.5 2.8/1.7
TVA/TVI — 2.2/1.3 1.4/0.9 1.4/0.9 1.4/0.9
AR by AA cine (0 to 4+) 0 0 2+/4+ 0 1+/4+
MRby LV cine (0 to 4+) 1+/4+ 0 4+/4+ 0 0
All pressures are in mm Hg. All valve replacements were with Hancock bioprosthesis (size in
parenthesis): mitral commissurotomy, 1959; MVR (29) and TVR (31), 2/1971; MVR (27), TVR
(31) and AVR (19), 6/1979.
* Calculated valve area underestimated because of mild mitral regurgitation.
†
Not possible to calculate valve area because of severe mitral regurgitation.
AA=ascending aorta; AR=aortic regurgitation; AVR=aortic valve replacement; CI=cardiac
index (liters/min/m
ventricular; mdg=mean diastolic gradient; MR=mitral regurgitation; MVA=mitral valve
area; MVI=mitral valve index; MVR=mitral valve replacement; NYHA FC= New York
Heart Association functional class; PA=pulmonary artery; PAW=pulmonary artery wedge
pressure; psg=peak systolic gradient; RA=right arterial; RV=right ventricular; SA=systemic
artery; s/d = systolic/diastolic; TVA = tricuspid valve area; TVI = tricuspid valve index;
TVR=tricuspid valve replacement.
2
); Cine=cineangiography; CO=cardiac output (liters/min); LV=left
†
2.1/1.3 1.3/0.8
175

CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
REFERENCES
1. Warnes CA, Scott ML, Silver GM, Smith CW, Ferrans VJ, Roberts WC. Comparison
of late degenerative changes in porcine bioprostheses in the mitral and aortic valve
position in the same patient. Am J Cardiol 1983;51:965–968.
2. Cipriano PR, Billingham ME, Miller DC. Calcication of aortic versus mitral por-
cine bioprosthetic heart valves: a radiographic study comparing amounts of calcic
deposits in valves explanted from the same patient. Am J Cardiol 1984;54:1030–1032.
3. Cohen SR, Silver MA, McIntosh CL, Roberts WC. Comparison of late (62 to 140
months) degenerative changes in simultaneously implanted and explanted porcine (Hancock) bioprostheses in the tricuspid and mitral valve positions in six
patients. Am J Cardiol 1984;53:1599–1602.
4. Barbour DJ, McIntosh CL, Roberts WC. Extensive calcication of a bioprosthe-
sis in the tricuspid valve position and minimal calcication of a simultaneously
implanted bioprosthesis in the mitral valve position. Am J Cardiol 1987;59:179–180.
176

CASE 806 “QUADRICUSPIDIZATION” OF APREVIOUSLY THREE-CUSPID AORTIC VALVE
https://t.me/medicina_free
Case 806 “Quadricuspidization” of
aPreviously Three-Cuspid Aortic Valve
Jessica M. Mann, MD, and William C. Roberts, MD
Bethesda, MD
Quadricuspid aortic valves have always been described as congenital in origin.
1–4
Surgical manipulation of a previously normal tri-cuspid aortic valve may transform
the latter into a quadricuspid valve. Such was the case in the patient described below.
R.B., a 39-year-old man, was found at age 13years to have discrete subaortic
stenosis with a left ventricular (230/8mm Hg)-to-aortic (96/60mm Hg) peak systolic
pressure gradient of 134mm Hg. The cardiac index was 3.6 L/min/m
2
. When he
was 13years old he underwent resection of a subaortic “membrane” by Dr. Andrew
G. Morrow. At operation, the aortic valve was described as tri-cuspid and each
cusp was normal. The patient was asymptomatic after operation. At age 16, no
peak systolic pressure gradient between the left ventricle and the aortic valve was
present, but an aortic angiogram disclosed 2+/4+ aortic regurgitation. At age 30,
he had several dizzy spells and a Holter monitor disclosed multifocal ventricular
premature complexes and runs of ventricular tachycardia. Serial echocardiograms
showed anterior mitral leaet utter and progressive left ventricular dilatation,
Figure 1 View of the acquired quadricuspid aortic valve from the aorta. The four
cusps are thickened by brous tissue and some degree of commissural fusion is
present. Arrows point out the four commissures. The accessory cusp is posterior and
smaller than the “true” posterior cusp. LM=left main coronary artery; R=right
coronary artery.
From the Pathology Branch, National Heart, Lung, and Blood Institute, National Institutes of
Health.
Reprint requests: Pathology Branch, NHLBI-NIH, Bldg. 10, Room 2N-258, Bethesda, MD
20892.
DOI: 10.1201/9781003409281-32 177

CASE REPORTS IN CARDIOLOGY
https://t.me/medicina_free
with a left ventricular diastolic dimension increasing from 66 to 80 mm and the
systolic dimension increasing from 38 to 58mm. He died suddenly at home at age
39. At necropsy, the heart weighed 560 gm. The left ventricular outow tract was not
narrowed. No foci of myocardial brosis or necrosis were present. The aortic valve
was quadri-cuspid with two posterior cusps of unequal size (Figure1). The coronary
arterial system was right-dominant, and all three coronary arteries had wide-open
lumens.
Although there are no photographs to document the appearance of the aortic
valve at operation 26years before death, the surgeon, Andrew G. Morrow, was
an excellent describer of both normal and abnormal cardiovascular ndings at
operation, and consequently there can be little doubt that the aortic valve consisted
of three normal cusps at that time. Aortic regurgitation was noted for the rst time
2 years after operation, and it persisted for the remaining 24years of life. Thus
operative manipulation of the aortic valve during operative resection of discrete
subaortic stenosis can lead to transformation of a tricuspid into a quadricuspid
aortic valve.
REFERENCES
1. Simonds JP. Congenital malformations of the aortic and pulmonary valves. Am J
Med Sci 1923;166:584–595.
2. Robicsek F, Sanger PW, Daugherty HK, Montgomery CC. Congenital quadri-
cuspid aortic valve with displacement of the left coronary orice. Am J Cardiol
1969;23:288–290.
3. Luisi VS, Pasque A, Vernelli F, Aliboni M, Urbano V, Reginato E. Quadricuspid
aortic valve. J Cardiovasc Surg 1984;25:252–254.
4. Matsumoto M, Miki S, Kusuhara K, Ueda Y, Ohkita Y, Tahata T, Komeda M.
Quadricuspid aortic valve associated with severe aortic regurgitation. Jpn Circ J
1984;49:190–191.
178

CASE 811 DEVELOPMENT OF SEVERE STENOSIS IN A CONGENITALLY BICUSPID AORTIC VALVE
https://t.me/medicina_free
Case 811 Development of Severe Stenosis
in a Previously Purely Regurgitant,
Congenitally Bicuspid Aortic Valve
Jay M. Kalan, MD, Charles L. McIntosh, MD, PhD, Robert O. Bonow, MD,
and William C. Roberts, MD
A congenitally bicuspid aortic valve may function normally, it may be stenotic with
or without associated regurgitation or it may be purely regurgitant (no associated
stenosis).
become stenotic (as calcic deposits build up) or it may become purely regurgitant
(because of superimposed infective endocarditis or because of reasons unclear).
Once a bicuspid valve develops some degree of stenosis, its course thereafter is
one of gradually worsening stenosis; once a bicuspid valve develops some degree
of pure regurgitation (without associated stenosis), its course thereafter is one of
gradually worsening regurgitation. Recently, we encountered a man who 8 years
earlier had evidence of severe pure aortic regurgitation (no element of stenosis) and
thereafter he went on to develop severe aortic valve stenosis with virtual loss of
the regurgitation. To our knowledge, conversion from pure aortic regurgitation to
severe aortic stenosis has not been reported. This report records such an occurrence.
forces at about age 25. At age 60, two transient episodes of paroxysmal nocturnal dyspnea
occurred and digoxin therapy was started. He remained without symptoms of cardiac
dysfunction, able to swim and play tennis, until age 70, when aortic valve replacement was
done. At age 62 (1979) his blood pressure was 160/ 70mm Hg. Peripheral signs of aortic
regurgitation were present, including a rapid carotid artery upstroke, water-hammer pulse
and Quincke’s sign. Agrade 3/6 precordial systolic ejection murmur radiated to the neck, and
a grade 3/6 diastolic blow was present and loudest at the left sternal border. Echocardiographic
and catheterization data are shown in Table 1and Figure1. Ejection fraction by radionuclide
angiography was 63% at rest and 52% with exercise. Exercise capacity by exercise stress test
was good. He remained asymptomatic but gradually developed left ventricular hypertrophy
without dilatation (Table 1). At age 70, transient second-degree heart block was seen on
electrocardiogram. The systemic blood pressure was 130/90mm Hg and the carotid upstroke
was delayed. Aharsh, grade 4/6 systolic precordial murmur that radiated to the neck was
present. No precordial diastolic murmur was heard. Cardiac catheterization (Table 1) now
showed a 75-mm Hg peak systolic pressure gradient across the aortic valve (Figure1). The
aortic valve was replaced (August 1987) with a 23-mm Hancock porcine bioprosthesis.
Seven months postoperatively, he is asymptomatic and active, with an ejection fraction by
radionuclide angiography of 70% at rest.
The posterior cusp was mobile but thickened by brous tissue; it contained a single small
deposit of calcium. The anterior cusp, in contrast, was immobile and contained heavy calcic
deposits.
1, 2
Such a valve may function normally for many years and then it may
A.H., a 70-year-old white man, had a precordial murmur when inducted into the armed
The excised native aortic valve consisted of 2 cusps weighing together 5.9 g (Figure2).
From the Pathology, Surgery and Cardiology Branches, National Heart, Lung, and Blood
Institute, National Institutes of Health, Bethesda, Maryland 20892. Manuscript received
May19, 1988; revised manuscript received and accepted June19, 1988.
DOI: 10.1201/9781003409281-33 179
Соседние файлы в папке Библиотека им академика М.И. Перельмана
