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Figure 1 Electrocardiogram showing left ventricular hypertrophy and sinus
rhythm.
Figure 2 Chest roentgenogram showing considerable cardiomegaly of the left
ventricular type.
chordae tendineae were normal. The tricuspid and pulmonic valves were normal.
The left ventricular endocardium was diffusely opaque, and the right ventricular
endocardium was focally opaque. Histologic examination disclosed multiple typical
Aschoff bodies in the endocardium of both atria and in the endocardium and
interstitium of both ventricles (Figure4).
COMMENTS
Although each is a fairly common condition, a congenitally bicuspid aortic valve
and rheumatic heart disease have not previously been clearly demonstrated
to be present simultaneously in the same patient. Previous studies
laboratory have shown that congenitally bicuspid aortic valves may occur in as
high as 2percent of the population, and the incidence of rheumatic heart disease
clinically has been reported to be as high as 6percent of the population.
surprising that the two conditions have not been described previously in the same
100
1–3
from this
4
Thus, it is
CASE 243 COMBINED ACUTE RHEUMATIC FEVER AND CONGENITALLY BICUSPID AORTIC VALVE
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Figure 3 Heart. Upper: Opened aorta, aortic valve, and left ventricle. The left ven-
tricular cavity is quite dilated, its endocardium mildly thickened, and its wall, very
thick. Lower. Close-up view of the opened aortic valve. The anterior cusp, the one
containing the raphe, has been severed during the opening of the valve. The posterior cusp, from which no coronary arteries arose, is intact. The anterior leaet of the
mitral valve (shown here) also is thickened by brous tissue. No inammatory cells
were found in histologic sections of any of the four cardiac valves.
patient. One of the reasons for this discrepancy may be different criteria utilized for
dening the congenitally bicuspid condition of the aortic valve and for designating
valvular disease as rheumatic in type. Our criteria for designating an aortic valve
as congenitally bicuspid have been delineatéd elsewhere.
only two aortic valve cusps, only two true commissures, and, in about half of the
cases, a false commissure or raphe also is present. The cusps are oriented either
anteriorly and posteriorly (and if a raphe is present it is always in the anterior cusp)
or right and left (and if a raphe is present it is always in the right cusp). The distance
circumferentially between any two true commissures is always greater than
1
In essence, there are
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Figure 4 Left ventricular endocardium with multiple typical Aschoff bodies. Left:
Low-power (x55) view showing three discrete Aschoff bodies in the thickened endocardium. Right: Close-up (x350) view of one of the Aschoff bodies (hematoxylin and
eosin stains).
between a true and a false commissure. The raphe rarely extends as far cephalad in
the aorta as do the true commissures.
The only unequivocal criterion of rheumatic heart disease is the presence of
Aschoff bodies. Although a number of different stages of Aschoff bodies have been
described,
identied.
of atrial appendages
5
only in the granulomatous stage can an Aschoff body be unequivocally
6
In our laboratory, we have found Aschoff bodies at necropsy or in biopsies
7
or papillary muscles obtained at operation only in patients
with diffuse disease, nearly always stenosis, of the mitral valve. About 5percent of
our patients with fatal mitral valve disease studied at necropsy had Aschoff bodies.
We have never observed an Aschoff body in the heart of a patient with anatomically
isolated aortic valve disease, ie, an anatomically normal mitral valve, and indeed we
have been unable to nd any report demonstrating an Aschoff body in the heart of a
patient with isolated aortic valve disease, irrespective of the number of aortic valve
cusps present. Among approximately 200 adult patients with congenitally biscuspid
aortic valves studied by us at necropsy, only the patient described herein had an
Aschoff body in his heart.
At least two previous authors, however, have mentioned the occurrence of
Aschoff bodies in patients with bicuspid aortic valves. Gross
9
described Aschoff
bodies in 5 of 16 hearts with “so-called congenital bicuspid aortic valve.” It is clear
from study of his paper, however, that his criteria for Aschoff bodies were extremely
loose, indeed unacceptable, and furthermore that several of his patients almost surely
had acquired bicuspid aortic valves rather than congenital malformations. Hall and
8
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10
Ichioka
found Aschoff bodies in ve of eight patients with “bicuspid aortic valves.”
Three of these ve patients were over 65years of age and a fourth was 53. Thus,
three of their patients may have had aortic valve disease of the elderly, probably
degenerative in origin,
also used the loose, nonspecic criteria of Gross and Ehrlich
3
rather than congenital malformations. These authors
5
for identication of
Aschoff bodies. In addition, none of their ve patients had anatomic disease of the
mitral valve. To reemphasize, we have never observed an Aschoff body, using the
criteria dened by Saphir,
6
in a patient without anatomic disease of the mitral valve.
Almost surely in years past there has been an “over-diagnosis” of Aschoff bodies at
necropsy, using loose criteria which may include nonspecic inammatory lesions
of the heart.
Our patient had a classic congenitally bicuspid aortic valve and numerous
classic Aschoff bodies in the heart at necropsy. To our knowledge, this combination
has neither been clearly documented nor illustrated previously.
REFERENCES
1. Roberts WC: The congenitally bicuspid aortic valve. Astudy of 85 autopsy cases.
Am J Cardiol 26:72–83, 1970
2. Roberts WC: The structure of the aortic valve in clinically-isolated aortic steno-
sis. An autopsy study of 162 patients over 15years of age. Circulation 42:91–97,
1970
3. Roberts WC, Perloff JK, Constantino T: Severe valvular aortic stenosis in patients
over 65years of age. Aclinicopathologic study. Am J Cardiol 27:497–506, 1971
4. Marieneld CJ, Robins M, Sandidge RP, et al: Rheumatic fever and rheumatic
heart disease among U.S. college freshmen, 1956–60. Pub Health Rep 79:789–811,
1964
5. Gross L, Ehrlich JC: Studies on the myocardial Aschoff body: Descriptive clas-
sication of lesions. Am J Pathol 10:467–488, 1934
6. Saphir O: The Aschoff nodule (editorial). Am J Clin Pathol 31:534–539, 1959
7. Vermani R, Roberts WC: Incidence and signicance of Aschoff bodies in atrial
appendages removed at operation: An analysis of 800 patients. (In preparation)
8. Roberts WC: Anatomically isolated aortic valvular disease. The case against its
being of rheumatic etiology. Am J Med 49:151–159, 1970
9. Gross L: So-called congenital bicuspid aortic valve. Arch Pathol 23:350–362, 1937
10. Hall EM, Ichioka T: Etiology of calcied nodular aortic stenosis. Am J Pathol
16:761–785, 1940
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Case 267 Clinical Pathologic Conference
A Conversation on Prosthetic Valve Endocarditis
Ernest N. Arnett, MD*, David G. Kastl, MD, A. Julian Garvin, MD, PhD,
and William C. Roberts, MD
Bethesda, MD
Dr. R ober ts:
The starting point for this discussion on prosthetic valve endocarditis
will be a description of a patient with this fatal complication of cardiac valve
replacement.
Dr. Kastl: This 47-year-old man (J.G. #1123701) was in good health until 11
months before death when symptoms of fatigue and exertional dyspnea appeared
four weeks after a dental procedure. Hospitalization four months after onset
of symptoms (seven months before death) revealed anemia, a colonic lling
defect, periodic fever, and Streptococcus bovis in several blood cultures. Penicillin,
20million units intravenously per day, was administered for six weeks; the fever
rapidly disappeared, but murmurs of mitral and aortic regurgitation and signs
of congestive heart failure appeared. Digoxin and diuretic therapy resulted in
transient improvement of the congestive heart failure, and the colonic mass, which
proved to be a benign polyp, was resected. He returned home, but heart failure
quickly returned and he was hospitalized, now in functional Class IV (New York
Heart Association classication), 55 days before death. Digoxin, furosemide, and
aldactone produced a 20 pound weight loss. Subsequently, at cardiac catheterization,
the pressures in mm. Hg were: pulmonary artery wedge mean 35, a wave 35, v wave
55; pulmonary artery 60/35 (mean 50); right ventricle 60/15; and right atrial mean
15, a wave 22, and v wave 17. Multiple blood cultures during that hospitalization
were negative. He was transferred to the National Heart, Lung and Blood Institute
(NHLI) 37 days before death.
The blood pressure was 140/70mm. Hg, cardiac rate, 90 beats per minute, and
respiratory rate, 20 breaths per minute. The jugular venous pressure was elevated,
and the carotid upstroke was rapid but weak. Basilar râles were present in both
lungs. The second heart sound split paradoxically and both third and fourth heart
sounds were present. A Grade 3/6 decrescendo diastolic murmur was present
along the left sternal border, and a Grade 2/6 holosystolic murmur and a Grade 2/6
middiastolic rumbling murmur were present at the apex. The anteroinferior edge of
the liver was palpable 4cm. below the right costal margin. Chest roentgenograms
From the Pathology Branch and Clinic of Surgery, National Heart, Lung and Blood Institute,
and the Laboratory of Pathology, National Cancer Institute, National Institutes of Heaíth,
Bethesda, Md.
Received for publication June9, 1976.
Reprint requests: W. C. Roberts, M.D., Bldg. 10A Rm 3E-30, National Institutes of Health,
Bethesda, Maryland 20014.
*
Present addre ss: Department of Medic ine, The Johns Hopkin s Hospital, Baltimore, Mar yland.
104 DOI: 10.1201/9781003409281-17
CASE 267 CLINICAL PATHOLOGIC CONFERENCE: PROSTHETIC VALVE ENDOCARDITIS
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(Figure1) showed marked cardiac enlargement and electrocardiogram (Figure 2a)
showed left ventricular hypertrophy. The hematocrit was 37 per cent, and the white
blood count 11,900 per cubic millimeter. Simultaneous aortic and left ventricular
pressures were 120/50 and 120/30mm. Hg, respectively. Cineangiography revealed
severe aortic and mitral valve regurgitation, but good left ventricular function.
The aortic valve was replaced with a No. 10A model 2320, Starr-Edwards
prosthesis and the mitral valve, with a 33mm. Hancock xenograft 28 days before
death. Both the excised aortic valve and the excised mitral valve (Figure3) contained
one or more perforations in the cusps. Histologic examination of the excised valves
revealed no evidence of active infection.
During the rst 24hours postoperatively, excessive bleeding necessitated repeat
thoracotomy. Although no specic bleeding sites were found, a large quantity (2,000
ml.) of blood was evacuated from the mediastinum. Oxacillin, 4 Gm. intravenously
per day, and streptomycin, 1 Gm. intramuscularly per day, were started at the time
of the initial operation and continued for 10 and 7 days, respectively. All chest
tubes were removed on the fourth postoperative day. Two days later fever (38.5° C.)
was noted but he otherwise appeared to be doing well. Nine days postoperatively
ventricular brillation occurred, but electroshock was successful in restoring sinus
rhythm. Electrocardiograms following this episode showed diffuse nonspecic
STsegment and T wave abnormalities. Over the ensuing 4 days, he continued to have
frequent ventricular premature beats. On the 17th postoperative day his temperature
rose to 39.5° C., the white blood cell count was 14,500 per cubic millimeter, and blood
cultures were positive for Staphylococcus epidermidis. Oxacillin, 12 Gm. intravenously
per day, was reinstituted. The following day the blood pressure dropped to
95/70mm. Hg and the electrocardiogram (Figure 2b) showed changes of an acute
anterolateral myocardial infarction. On the nineteenth postoperative day, splinter
hemorrhages were noted, the white blood cell count was 17,000 per cubic millimeter,
Figure 1 Posteroanterior chest roentgenogram 4 days before valve replacement.
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Figure 2 Electrocardiograms. a, Four days before valve replacements showing
changes of left ventricular hypertrophy and left atrial enlargement. b, Eighteen days
postoperatively (10 days before death). Q waves are present in Leads I, aVR, aVL and
, the R waves in the precordial leads are of markedly diminished amplitude, and
V
e
the STsegments are elevated in Leads I, aVL and V
through V6. In addition, the P-R
4
interval is prolonged.
and blood cultures again were positive for S. epidermidis, resistant to penicillin but
sensitive to both oxacillin and cephalosporin. On the twenty-rst postoperative day
he lost consciousness, his temperature rose to 39° C., and his systolic blood pressure
fell to 90mm. Hg. During insertion of a catheter into a jugular vein, a collection of
pus was entered, and Gram stain and culture of the aspirated material disclosed
S. epidermidis. Exploration of the mediastinum revealed no focal collections of
pus. Oxacillin was stopped and cephalosporin, 12 Gm. intravenously per day, was
started. Over the next four days consciousness returned, the blood pressure rose to
110/60mm. Hg, but the white blood count was 27,000 per cubic millimeter, and fever
and positive blood cultures continued. On the twenty-seventh postoperative day, his
blood pressure suddenly dropped and he died the next day.
Dr. Garvin:
Necropsy (A76–45) disclosed no residual pus in the chest. The heart
weighed 660 Gm., and the anterolateral left ventricular wall from midportion to
apex was necrotic. Large vegetations closed the primary orice of the aortic valve
prosthesis, and a brin thrombus was present at the apex of its cage (Figure 4).
Although the aortic prosthesis remained attached, the site of attachment of the
prosthesis was necrotic. Necrosis of the valve anulus, however, was apparent only
after removal of the prosthesis (Figure5). The ring infection extended through the
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Figure 3 Operatively excised aortic (a) and mitral (b) valves. Asingle perforation
is present in the left (L) and right (R) coronary cusp, and multiple ones are present in
the noncoronary (N) cusp. Aperforation is present in the anterior (A) mitral leaet,
and several chordae tendineae from the posterior (P) mitral leaet are absent.
atrial septum into the right atrium and into the adjacent portion of the prosthetic
mitral anulus. Histologic sections from the site of attachment of the aortic prosthesis
revealed numerous colonies of Gram-positive cocci. Examination of subserial
sections of the extramural coronary arteries revealed total obstruction of the lumen
of the left anterior descending coronary artery by a septic embolus (Figure 6).
Sections of myocardium showed numerous foci of suppurating and nonsuppurating
inammation. The lungs were edematous and contained foci of acute inammation.
The walls of the small muscular pulmonary arteries were thick. Both the liver (2,600
grams) and spleen (670 grams) were enlarged, and multiple infarcts were present
in the spleen. Focal collections of mononuclear cells were present in the renal
interstitium, but otherwise the kidneys were normal.
Dr. Roberts:
information previously derived from a study of 22 necropsy patients with fatal
prosthetic valve endocarditis to the present patient.
The above-described patient provides an opportunity to apply
1
To begin this discourse, Dr.
Arnett, how do you dene “Prosthetic Valve Endocarditis?”
Dr. Arnett:
“Prosthetic valve endocarditis” is an infection involving a
prosthetic cardiac valve in a patient in whom no active infective endocarditis was
present at the time of prosthetic valve insertion. In other words, the infection was
acquired after valve replacement. Although the present patient’s valvular disease
resulted from infective endocarditis, the infection was healed at the time of valve
replacement.
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Figure 4 Infected aortic valve prosthesis. a, Prosthesis, viewed from above, in
place, and a′ after removal. Thrombus covers the apex of the cage. b, Excised prosthe-
sis viewed laterally. c, Longitudinal section showing aortic prosthesis in place. The
mitral valve prosthesis has been excised. The aortic “anulus” is necrotic and so is the
adjacent portion of mitral anulus. Alarge vegetation (V) is present in the primary
orice of the prosthesis; its obstructive nature is better seen in d, a view of the prosthesis from the left ventricular (LV) aspect. LA = left atrium.
Dr. Roberts:
cause of this patient’s infective endocarditis, which had involved presumably both
anatomically and functionally normal valves, was Streptococcus bovis. The cause of
the prosthetic valve endocarditis in him, however, was Staphylococcus epidermidis. Dr.
Arnett, could you summarize the organisms found in our previous 22 patients with
prosthetic valve endocarditis?
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Dr. Kastl, in your presentation of this patient, you mentioned that the
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Figure 5 Ring abscess and acute myocardial infarct. a, Longitudinal section of
heart showing the ring abscess involving the entire aortic “anulus” and the portion
of mitral anulus adjacent to the aortic valve. Alarge transmural infarct is present
in the anterior wall of left ventricle (in brackets). Ao=aorta; LA=left atrium; LV =
left ventricle; RV =right ventricle; VS= ventricular septum. b, Histologic section
of the anterior left ventricular wall. The myocardial cells are necrotic and numerous polymorphonuclear leukocytes are present. (Hematoxylin and eosin stain; ×
330). c, Opened right atrium, tricuspid valve, and right ventricle (RV). The aortic
ring abscess has extended through the adjacent atrial septum and is visible in right
atrium (dashed circle). CS=ostium of coronary sinus; STL = septal tricuspid leaet.
d, Histologic section showing colonies of Gram-positive cocci in the necrotic aortic
valve anulus (Brown and Brenn stain; × 880).
Dr. Arnett:
endocarditis, Staphylococcus (epidermidis in 10 and aureus in three) caused the infection
in 13 (59 per cent.) In the other nine patients, nine different organisms caused the
infection. Of these later nine organisms, three were Gram-negative bacteria, and two
were fungi.
Among our 22 previous necropsy patients with prosthetic valve
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