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show grooves (Figure2B). Both the inow and outow surfaces of the leaets of
the valve that had been implanted in the patient were covered with thrombi that
were directly superimposed on the most supercial layers of valvular collagen
(Figures2C–2F). Some of the grooves in the outow surfaces of the explanted valve
contained platelets, brin strands and erythrocytes (Figure2E), even in areas where
the surface adjacent to the grooves was free of thrombus. In areas of calcication
of surface thrombi (Figure2D), the brin strands were covered by clumps of nely
granular material.
Transmission Electron Microscopic Observations
Observations on ultrathin sections examined by transmission electron microscopy
revealed that the calcic deposits consisted of irregularly shaped masses (Figure3A),
usually 0.25–2.2 μ in diameter, composed of very ne needles or plate-like crystals of
high electron density (Figure3B). These crystals averaged 70 Â in thickness. These
calcic masses were located between brin strands, which were not calcied. The
calcic masses often appeared to be superimposed upon remnants of cells, which
were identied as platelets, macrophages and leukocytes (Figure3C). Most of these
cells showed extensive degenerative and autolytic changes. The larger calcic
masses were extremely dense, and structures associated with these masses were
not discernible. Afew calcic deposits were associated with the most supercial
layers of valvular collagen (Figure 3D). Elastic bers were not calcied, and there
was no evidence of collagen degeneration. Deposits of brin were interspersed with
the most supercial layers of collagen.
DISCUSSION
Ionescu-Shiley pericardial valves have been used for several years with good
clinical results;
valves of this type which have been removed after being implanted in patients,
little information is available on the occurrence of calcic deposits in these valves.
Calcic deposits are known to develop in other types of bioprostheses,
12
however, anatomic studies have been made of limited numbers of
1
12
but the time
and
of onset and the rate of deposition of calcium in bioprostheses are not known.
The host factors and tissue factors that cause calcication of bioprostheses are
poorly understood. It is not known to what extent conclusions derived from studies
of porcine bioprostheses will be applicable to pericardial bioprostheses. Porcine
bioprostheses calcify more frequently and to a greater extent in patients who have
one or more of the following predisposing conditions: younger than 35 years of
1, 3, 4, 7–10, 13–16
age,
chronic renal disease,
1, 2, 10
and infection of the bioprosthesis.
1, 17, 18
Morphologic studies of Ionescu-Shiley valves have been too limited to determine
the importance of these factors in predisposing to calcication of this type of
bioprosthesis. Our patient was young and did have acute renal insufciency, but
had no evidence of infection in the bioprosthesis.
Ultrastructural studies have demonstrated that the two main anatomic sites of
calcication of porcine valvular bioprostheses are collagen brils in the leaets and
surface thrombi and vegetations.
initial deposits of calcium phosphate in thrombi and vegetations are localized in
mitochondria of blood cells and platelets trapped in the brin mesh.
1
Evidence has been presented indicating that the
1
In the present
study, calcic deposits were demonstrated in collagen and in surface thrombi, but
almost all of the deposits were localized in thrombotic material. These deposits were
struct urally simila r to those observed in porc ine bioprostheses.
animals have shown that a thin layer of brin is deposited on the leaets of porcine
bioprostheses within a few minutes after implantation.
brin was observed in two Hancock bioprostheses that had been in place for only 2
and 3 days, respectively, but neither contained calcic deposits.
1
Studies in e xperimental
19
In humans, such a layer of
11
Thus, the changes
140
CASE 413 CALCIFIC DEPOSITS DEVELOPING IN A BIOPROSTHETIC VALVE
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Figure 3 Transmission electron micrographs of valve implanted for 3 days. (A)
Low-magnication view of area near free edge of leaet, showing calcic deposits,
which appear black, and mononuclear cells within the mesh of brin in thrombus
overlying the collagen at the leaet surface. Arrowheads indicate calcic deposit
shown at high magnication in (B). Magnication × 7000. (B) Calcic deposit in
thrombus is composed of very ne needle-like crystals. Magnication × 58,500. (C)
Calcic deposits are localized within cytoplasm of mononuclear cell. Magnication
× 33,500. (D) Calcic deposits (black) overlie collagen brils in area near leaet surface. Magnication × 56,250.
141
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we report apparently represent a very unusual phenomenon of early calcication of
this surface layer. These calcic deposits probably would have become the cause of
clinically signicant bioprosthetic stenosis if our patient had survived longer.
Several factors may have contributed to the early calcication of the bioprosthesis
in our patient: the low cardiac output syndrome, which led to renal insufciency
requiring peritoneal dialysis, and the large amounts of calcium chloride given
intravenously because of the multiple blood transfusions and at times of resuscitative
efforts. Another factor is the presence of proteins in the blood, which function in the
coagulation process and which contain γ-carboxyglutamic acid, an unusual amino
acid capable of avidly binding calcium.
calcied (but not from noncalcied) porcine bioprostheses.
20, 21
This amino acid has been extracted from
20
Its association with
calcication of pericardial bioprostheses has not been investigated.
Uptake of calcium by mitochondria of hypoxic or ischemic cells is known to
occur not only in myocardium but also in other tissues,
22
and the availability of
large amounts of calcium to blood cells incorporated into thrombi may have resulted
in signicant accumulation of calcium in these cells (thus initiating bioprosthetic
calcication) under conditions of hypoxia associated with the low cardiac output
state in our patient. The nding of calcic deposits in necrotic myocardial cells as
in our patient is not unusual; it is frequently observed in patients who have the low
cardiac output syndrome postoperatively.
23
The cotton bers on the surfaces of the cusps of the bioprosthesis may have been
derived from the packing material in the valve container. Such bers were not found
in pulmonary or myocardial vessels. Afatal coronary embolus was produced by
fragments of packing material in a porcine bioprosthesis.
24
The morphologic observations on the unimplanted Ionescu-Shiley valves reveal
marked asym metry in the te xture of the inow and outow surfaces of t he pericardial
tissue leaets. The inow surface is very rough and corresponds to the pericardial
surface that faces the sternum. In contrast, the outow surface is much smoother;
it contains grooves that appear to have been made by a mechanical process and
corresponds to the pericardial surface that faces the heart. These differences, which
were consistently observed in the three unimplanted valves examined, provide
a basis for the identication of the surfaces of Ionescu-Shiley valves; however, in
animal experiments (unpublished observations) we found that the grooves tend to
be obscured (as was the case in the valve from our patient) by the deposition of brin
on the surfaces after the valves are implanted.
REFERENCES
1. Ferrans VJ, Boyce SW, Billingham ME, Jones M, Ishihara T, Roberts WC: Calcic
deposits in porcine bioprostheses: structure and pathogenesis. Am J Cardiol 46:
721, 1980
2. Hetzer R, Hill JD, Kerth WJ, Wilson AJ, Adappa MG, Gerbode F: Thrombosis and
degeneration of Hancock valves: clinical and pathological ndings. Ann Thorac
Surg 26: 317, 1978
3. Rose AG, Forman R, Bowen RM: Calcication of glutaraldehyde-xed porcine
xenograft. Thorax 33: 111, 1978
4. Forfar JC, Cotter L, Morritt GN: Severe and early stenosis of porcine heterograft
mitral valve. Br Heart J 40: 1184, 1978
5. Albert HM, Bryant LR, Schechter FG: Seven year experience with mounted por-
cine valves. Ann Surg 185: 717, 1977
6. Bachet J, Bical O, Goudot B, Menu P, Richard T, Barbagelatta M, Guilmet D:
Early structural failure of porcine xenografts in young patients. In Bioprosthetic
Cardiac Valves, edited by Sebening F, Klövekorn WP, Meisner H, Struck E.
München, Deutsches Herzzentrum, 1979, pp.341–349
142
CASE 413 CALCIFIC DEPOSITS DEVELOPING IN A BIOPROSTHETIC VALVE
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7. Thandroyen FT, Whitton IN, Pirie D, Rogers MA, Mitha AS: Severe calcication
of glutaraldehyde-preserved porcine xenografts in children. Am J Cardiol 45:
690, 1980
8. Silver MM, Pollock J, Silver MD, Williams WG, Trusler GA: Calcication in por-
cine xenograft valves in children. Am J Cardiol 45: 685, 1980
9. Sanders SP, Freed MD, Norwood WI, Castaneda A, Nadas AS: Early failure of
porcine valves implanted in children, (abstr) Am J Cardiol 45: 449, 1980
10. Fishbein MC, Gissen SA, Collins JJ Jr, Barsamian EM, Cohn LH: Pathologic nd-
ings after cardiac valve replacement with glutaraldehyde-xed porcine valves.
Am J Cardiol 40: 331, 1977
11. Ferrans VJ, Spray TL, Billingham ME, Roberts WC: Structural changes in glu-
taraldehyde-treated porcine heterografts used as substitute cardiac valves.
Transmission and scanning electron microscopic observations in 12 patients.
Am J Cardiol 41: 1159, 1978
12. Ionescu MI, Tandon AP, Mary DAS, Abid A: Heart valve replacement with the
Ionescu-Shiley pericardial xenograft. J Thorac Cardiovasc Surg 73: 31, 1977
13. Kutsche LM, Oyer P, Shumway N, Baum D: An important complication of
Hancock mitral valve replacement in children. Circulation 60 (suppl I): 1–98,
1978
14. Brown JW, Dunn JM, Spooner E, Kirsh MM: Late spontaneous disruption of a
porcine xenograft mitral valve. Clinical, hemodynamic, echocardiographic, and
pathological ndings. J Thorac Cardiovasc Surg 75: 606, 1978
15. Geha AS, Stansel HC Jr, Cornhill JF, Kilman JW, Buckley MJ, Roberts WC: Late
failure of porcine valve heterografts in children. J Thorac Cardiovasc Surg 78:
351, 1979
16. Magil ligan DJ Jr, Lewis JW Jr, Jara FM, Stein PD, Riddle JM, Lee MW: Spontaneous
degeneration of porcine bioprosthetic valves. Ann Thorac Surg 30: 259, 1980
17. Zuhdi N: The porcine aortic valve bioprosthesis: a signicant alternative. Ann
Thorac Surg 21: 573, 1976
18. Magilligan DJ Jr, Quinn EL, Davila JC: Bacteremia, endocarditis, and the
Hancock valve. Ann Thorac Surg 24: 508, 1977
19. Geroulanos S, Gossler W, Walpoth B, Turina M, Senning A: Frühe rasterelek-
tronenoptische Oberächenveränderungen nach orthotoper PulmonalklappenXenotransplantation durch glutaraldehyd-konditionierte Schweineklappen.
Eine experimentelle Studie an Hunden. Helv Chir Acta 46: 91, 1979
20. Levy RJ, Lian JB: Studies on the etiology of calcic aortic valve disease: the role
of the calcium binding amino acid, y-carboxyglutamic acid, (abstr) Circulation
58 (suppl II): 11–54, 1978
21. Levy RJ, Zenker JA, Lian JB: Vitamin K-dependent calcium binding proteins in
aortic valve calcication. J Clin Invest 65: 563, 1980
22. Trump BF, Berezesky IK, Laiho KU, Osomio AR, Mergner WJ, Smith MW: The
role of calcium in cell injury. Areview. Scan Electron Microsc, 2: 437–492, 1980
23. Reichenbach DD, Benditt EP: Catecholamines and cardiomyopathy: the patho-
genesis and potential importance of myobrillar degeneration. Hum Pathol 1:
125, 1970
24. Tubbs RR, Picha GC, Levin HS, Groves L, Barenberg S: Cotton emboli (cellulose
II polymorph, “rayon”) of the coronary arteries. Hum Pathol 11: 76, 1980
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Case 458 Inward Stent-Post Bending of aPorcine
Bioprosthesis in the Mitral Position
Cause of Bioprosthetic Dysfunction
A. Michael Borkon, MD, Charles L. McIntosh, MD, PhD, Michael Jones, MD,
William C. Roberts, MD, and Andrew G. Morrow, MD
Bethesda, MD
Certain clinical and morphologic features are described in a patient with severe
bioprosthetic obstruction 9years after mitral valve replacement. At reoperation,
severe inward bending of the stent-posts was found without signicant
bioprosthetic cuspal abnormalities. “Polymer creep” is considered responsible
for the stent-post deformity.
The morphologic features of late bioprosthetic valve failure have been well
described.
1–5
In most patients, bioprosthetic failure was the result of cuspal
calcication and collagen disruption. Deterioration of the other components of the
bioprosthesis infrequently has been responsible for failure. Recently, permanent
inward stent-post deformity producing secondary valvular orice obstruction and
valvular failure has been reported after aortic valve replacement with Hancock
bioprostheses and is believed to have resulted from stent-post compression from
a narrow aortic root.
may result also from “polymer creep,” an aging characteristic of polypropylene.
6, 7
Experimental studies have shown that stent-post deformity
8
Stent-post deformity has not been described previously in the mitral position. Such
was the case, however, in the case described herein.
CASE REPORT
A 50-year-old white woman underwent closed mitral commissurotomy in
September, 1960, and was well thereafter until November, 1969, when congestive
heart failure reappeared and repeat cardiac catheterization was performed (Table 1).
On Nov. 3, 1970, she underwent aortic valve replacement with a No. 8 Starr-Edwards
Model 2310 prosthesis and mitral replacement with a No. 29 Hancock bioprosthesis.
The postoperative course was uncomplicated, and she was discharged receiving
warfarin sodium. Cardiac catheterization (Table 1), 7 months after operation,
disclosed a residual mean gradient across the Hancock mitral bioprosthesis of 7mm
Hg and a calculated mitral valve orice area of 2.4cm
2
. She was symptomatically
improved (New York Heart Association Functional Class II). In September, 1979, she
began to have increasing symptoms of congestive heart failure. AGrade 2/6 systolic
ejection murmur was heard at the right upper sternal border and a Grade 2/6
holosystolic murmur at the apex and axilla. These murmurs were unchanged from
prior examinations. No diastolic murmur was heard. Repeat cardiac catheterization
From the Clinic of Surgery and the Pathology Branch, National Heart, Lung and Blood
Institute, Bethesda, Md.
Received for publication March2, 1981.
Accepted for publication May19, 1981.
Address for reprints: Andrew G. Morrow, M.D., National Heart, Lung and Blood Institute,
Bethesda, Md. 20205.
144 DOI: 10.1201/9781003409281-23
CASE 458 INWARD STENT-POST BENDING OF APORCINE BIOPROSTHESIS
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Table 1: Hemodynamic data
Immediately
preoperatively
Rhythm Atrial brillation Sinus Atrial brillation
Pressures (mm Hg):
Right atrium (mean) 5 2 11
Right ventricle (s/d)* 53/5 38/6 108/10
Pulmonary artery (s/d) 53/25 38/18 108/10
Pulmonary artery
wedge (PAW)
Left ventricle (LV) (s/d) 170/8 170/12 190/14
Aorta (s/d) 160/80 155/77 190/86
PAW/LV mdg=mean
diastolic gradient
Cardiac output (L/min) 3.4 5.4 3.3
Mitral valve area (cm
*s/d=systolic/diastolic.
2
) — 2.4 1.0
m=26
v=36
8 7 11
Months preoperatively
7 106
m=15
a=16
v=22
m=32
v=46
Figure 1 Mitral bioprostheses removed from the patient 107 months after implantation. A, Ventricular aspect. The stent-posts are bent inward, producing secondary
valve orice obstruction. Valve leaets are thin and pliable. B, Atrial aspect. There is
a pinhole leaet perforation (arrow).
(Table 1) on Sept. 19, 1979, demonstrated severe stenosis of the bioprosthetic mitral
valve (mean mitral gradient 11mm Hg and calculated orice area 1.0cm
Hancock bioprosthesis was replaced with a Starr-Edwards valve. The postoperative
course was uneventful, and she remains well.
The cusps of the bioprosthesis removed at operation were thin and delicate and
a small tear was present adjacent to one commissure. The stent-posts were indented
inward and appeared to result in bioprosthetic obstruction (Figure1).
COMMENTS
The exible stent was developed in 1970 by Reis and associates
valve durability by diminishing stress on the bioprosthetic cusps. In most instances
2
). The mitral
9
to improve Hancock
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Figure 2 Mechanism of stent-post deformity due to left ventricular compression
from bioprosthesis-ventricular disproportion.
leaet calcication and collagen disruption result in bioprosthetic dysfunction.
Deterioration of the Stellite ring, polypropylene stent, or Dacron cloth covering has
seldom been implicated as a primary mechanism of bioprosthetic valve failure.
In two recently reported cases there was permanent inward stent-post deformity
causing signicant valve orice obstruction after aortic valve replacement with
Hancock bioprostheses. In both cases, the bioprosthesis was compressed by a small
aortic root and was associated with bioprosthetic thrombosis
Stent-post deformity producing obstruction and requiring reoperation has
not previously been reported after mitral valve replacement. Spray and Roberts
observed stent-post deformity associated with bioprosthetic failure due to leaet
degeneration, but they did not discuss its signicance. Pohlner et al
6
or severe hemolysis.
8
demonstrated
7
1
that polypropylene may be subject to “polymer creep” from persistent cyclic fatigue,
producing permanent inward stent-post migration and bioprosthetic failure.
Possibly, “polymer creep” may have been responsible for the secondary valve orice
obstruction in our patients, as cardiac catheterization documented worsening of
the bioprosthetic stenosis and no cuspal abnormalities were identied that could
account for this degree of obstruction.
Left ventricular compression may also result in stent-post deformity owing to
bioprosthesis-ventricular disproportion if proper care is not taken in sizing not only
the mitral valve anulus, but also the ventricular cavity, as demonstrated in Figure2.
It is unlikely that this was the mechanism of stent-post deformity in the patient
presented because obstruction developed late and the ventricular cavity at both
operations was of adequate size.
REFERENCES
1. Spray TL, Roberts WC: Structural changes in porcine xenografts. Am J Cardiol
40:319–330, 1977
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CASE 458 INWARD STENT-POST BENDING OF APORCINE BIOPROSTHESIS
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2. Ferrans VJ, Spray TL, Billingham ME, Roberts WC: Structural changes in glu-
taraldehyde-treated porcine heterografts used as substitute cardiac valves. AM J
CARDIOL 41:1159–1184, 1978
3. Ferrans VJ, Spray TL, Billingham ME, Roberts WC: Ultrastructure of Hancock por-
cine valvular heterografts. Pre-and postimplantation changes. CIRCULATION
58:Suppl 1:10–18, 1978
4. Hezter R, Hill JD, Kerth WJ, Wilson AJ, Adappa MG, Gerbode F: Thrombosis
and degeneration of Hancock valve. Clinical and pathological ndings. ANN
THORAC SURG 26:317–322, 1978
5. Fishbein MC, Gissen SA, Collin JT, Barsamian EM, Cohn LH: Pathologic ndings
after cardiac valve replacement with glutaraldehyde-xed porcine valves. AM J
CARDIOL 40:331–337, 1977
6. Salomon NW, Copeland JG, Goldman S, Larson DF: Unusual complication of the
Hancock porcine heterograft. Strut compression in the aortic root. J THORAC
CARDIOVASC SURG 77:294–296, 1979
7. Magilligan DJ, Fisher E, Alam M: Hemolytic anemia with porcine xenograft aortic
and mitral valves. J THORAC CARDIOVASC SURG 79:628–631, 1980
8. Pohlner PG, Thompson FJ, Hjelm E, Barratt-Boyes BG: Experimental evaluation
of aortic hemograft valves mounted on exible support frames and comparison
with glutaraldehyde-treated porcine valves. J THORAC CARDIOVASC SURG
77:287–293, 1979
9. Reis RL, Hancock WD, Yarbrough JW, Glancy DL, Morrow AG: The exible stent.
J THORAC CARDIOVASC SURG 62:683–689, 1971
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Case 491 Acquired Cor Triatriatum (Left
Ventricular False Aneurysm)
Complication of Active Infective Endocarditis of the Aortic
Valve with Ring Abscess Treated by Valve Replacement
Bruce M. McManus, MD, PhD,* Nevin M. Katz, MD, Brian D. Blackbourne, MD,
John S. Gottdiener, MD, Robert B. Wallace, MD, and William C. Roberts, MD
Bethesda, MD, and Washington, D.C.
Cor triatriatum is a congenital anomaly in which the left atrium (LA) is essentially
partitioned into two chambers with a small orice between them. The cephalad
chamber receives the pulmonary veins and the caudal chamber is connected to
the mitral valve. The concept of “cor triatriatum” as an acquired condition is new.
Recently, however, we studied the heart of a 31-year-old opiate addict who had
Figure 1 M-mode echocardiograms. Left, Preoperative view showing a Swan-
Ganz (S-G) catheter in the right ventricular outow tract, a hyperdynamic ventricular septum (VS) and left ventricular free wall (LV), and vibratory movement (arrow)
of the anterior mitral leaet and ventricular septum. Middle, Preoperative view at
the level of aortic valve and left atrium revealing “shaggy” thickenings (arrow) of
the aortic valve cusps and echo-dense zones between right ventricular outow tract
(RV) and aorta (Ao), and between Ao and left atrium (LA) that are believed to represent aortic valve ring abscess. Right, Postoperative view at the level of aortic valve
and left atrium showing the bioprosthesis in aorta and increased echo densities
behind the aorta. The latter may represent a portion of the false aneurysm.
From the Pathology Branch, National Heart, Lung and Blood Institute, National Institutes of
Health; the Departments of Surgery and Medicine, Georgetown University; and the Medical
Examiner’s Ofce, Washington, D.C.
Received for publication March29, 1982; accepted Apr. 20, 1982.
Reprint requests: William C. Roberts, M.D., Pathology Branch, NIH-NHLBI, Bldg. 10A, Room
3E-30, Bethesda, MD 20205.
*
Present address: Department of Pathology, University of Nebraska Medical Center, Omaha,
NE 68105.
148 DOI: 10.1201/9781003409281-24
CASE 491 ACQUIRED COR TRIATRIATUM (LEFT VENTRICULAR FALSE ANEURYSM)
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three chambers at the atrial level rather than two. He had developed Staphylococcus
aureus endocarditis of the aortic valve resulting in severe aortic regurgitation (AR),
causing severe congestive heart failure and associated with hemorrhagic pericardial
tamponade. At operation, each of the three aortic valve cusps was virtually destroyed
by the active infection. Aring abscess was found at operation and the mouth into it
was just caudal to the junction of the left and posterior cusps. The cusps were excised
and the mouth into the ring abscess was debrided. Aporcine bioprosthesis (23mm
size) was inserted at the level of the “anulus.” The patient died of a narcotic overdose
75 days after an otherwise uneventful clinical postoperative course. Amurmur of
AR was never present postoperatively and he had received antibiotics for 6 weeks
after operation. Echocardiograms recorded 2 days before and 18 days after operation
are shown in Figure1.
At necropsy, an opening was found just caudal to the ring of the bioprosthesis
that led into a large chamber situated adjacent to both atria (Figures2 and 3). This
Figure 2 D rawings of the fa lse aneurysm a nd its likely mec hanism of development.
149
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