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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3695_Библиотеки_им_академика_М_И_Перельмана
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Figure 1 Right atrial pressure tracing in patient K. W. showing marked elevation
of peaks of the v- and a-waves.
Figure 2 Pullback pressure tracing from the pulmonary artery (PA) into the right
ventricle (RV), demonstrating the systolic pressure gradient.
over the lower left sternal border, and a harsh systolic murmur was present over
the upper left sternal border in each patient. Electrocardiograms (Figure4) in both
patients revealed low voltage and right axis deviation. In addition, right ventricular
hypertrophy was present in one (C. G.)
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CASE 32 THE NONDISTENSIBLE RIGHT ATRIUM OF CARCINOID DISEASE OF THE HEART
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Figure 3 Simultaneously recorded right atrial (RM) and right ventricular (RV)
pressures showing the tall right atrial v-waves with rapid descent, elevated right
atrial mean pressure, increased right ventricular end-diastolic pressure (e), and
small diastolic pressure gradient (dashed area). Z=z-point, a=a-point.
Figure 4 Electrocardiogram in Patient C. G. Low voltage was present in each of
the 2 patients described herein and is the most frequent electrocardiographic abnormality found in patients with carcinoid heart disease.
At autopsy, both patients had extensive endocardial brosis involving the
tricuspid and pulmonic valves and right atrium (Figures5 to 7). The heart of K. W.
weighed 350 Gm., and that of C. G., 250 Gm.
COMMENT AND CONCLUSIONS
The valvular and mural lesions in carcinoid heart disease are specic and
characterized by the deposition of an unusual type of brous tissue on the
1
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Figure 5 The heart of Patient K. W. Left, the right atrium, tricuspid valve, and right
ventricle are opened. There is marked carcinoid-type endocardial brosis involving
the tricuspid valve leaets and the right atrial wall. The tricuspid valve is incompetent. Right, photomicrograph of section of right atrium showing severe thickening
of its wall by the deposition of brous tissue on the endocardium. The endocardial
surface is toward the left, the epicardial surface is on the right. The thickness of the
superimposed brous tissue at times is greater than that of the right atrial wall.
Elastic tissue stain. Reduced 30 per cent from × 40.
endocardial surface. The deposits, which are devoid of elastic brils, are located
almost entirely on the under or ventricular surface of the tricuspid valve leaets
and on the arterial surface of the pulmonic valve cusps. The underlying valve
leaets and ventricular walls are not involved by this brous process and are
clearly separated from it by the normal endocardial elastic membrane. The brous
plaques frequently bind the posterior and septal leaets of the tricuspid valve to
the underlying right ventricular wall, and the result is a xed regurgitant and
slightly stenotic orice. Tricuspid regurgitation is the most frequent clinical cardiac
lesion resulting from this type of brosis. When the tricuspid valve is involved,
this brosing process almost always involves the right atrial endocardium, as
well. From study of the extensive right atrial deposits at autopsy in the 2 patients
presented, it would seem that the wall of this chamber in these instances is
relatively inelastic and consequently not able to distend or to contract normally.
This reduction in right atrial elasticity or distensibility as a result of the thick
endocardial brous deposits probably signicantly altered the hemodynamic
ndings in the right atrial pulse. Thus, there was in each of these 2 patients a
greater elevation of the right atrial pressures than would have been expected from
the sizes of the tricuspid valve orices observed at autopsy. It is suggested that
even mild tricuspid carcinoid disease may produce signicant elevation of right
atrial pressures, whereas an equal degree of rheumatic tricuspid disease would
not cause right atrial hypertension.
Acknowledgment. Dr. Albert Sjoerdsma, Chief, Experimental Therapeutics
Branch, National Heart Institute, gave permission to report these 2 patients and
reviewed the manuscript.
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CASE 32 THE NONDISTENSIBLE RIGHT ATRIUM OF CARCINOID DISEASE OF THE HEART
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Figure 6 The heart of Patient C. G. a. Exterior view showing a dilated right ven-
tricle (R.V.) and right atrium (R.A.). The apex of the heart is formed by the right ven-
tricle. S.V.C.=superior vena cava. P.T.=pulmonary trunk. b. Opened right atrium,
tricuspid valve, and right ventricle. There is marked brous thickening of the tricuspid-valve leaets with fusion of their commissures, and diffuse carcinoid-type
brosis of the dilated right atrium and superior vena cava. c. Unopened, immobile
pulmonic valve. d. Opened right ventricle and pulmonic valve disclosing marked
carcinoid-type brosis of both tricuspid and pulmonic valve leaets producing
stenotic and regurgitant orices. e. Photomicrograph of section of right atrial wall
which is severely thickened by the deposition of the brous tissue which is devoid
of elastic brils. Elastic tissue stain. × 19.
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Figure 7 Photomicrographs of right-sided cardiac valves in patient C. G. Left, tri-
cuspid valve (T.V.). The superimposed atypical brous tissue is deposited only on
the undersurface of the leaet, binding it to the underlying right ventricular (R.V.)
wall. Right, pulmonic valve (P.V.). The cusp itself is normal and sharply outlined by
its black-staining elastic membrane, but the superimposed brous tissue is adherent to its entire arterial surface and lls much of the sinus. Asmall deposit also is
present on the pulmonic trunk (P.T.). The surface of the pulmonic valve cusp which
has the initial contact with blood ejected from the right ventricle is free of brous
deposits. Elastic tissue stains. Reduced 20 per cent from × 15.
REFERENCE
1. Roberts, W. C., and Sjoerdsma, A.: The cardiac disease associated with the carci-
noid syndrome (carcinoid heart disease), Am J Med 36:5–34, 1964.
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CASE 35 PULMONARY ARTERIOVENOUS FISTULA AND RHEUMATIC CARDIAC DISEASE
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Case 35 Pulmonary Arteriovenous Fistula
and Rheumatic Cardiac Disease
Costan W. Berard, M.D*, William C. Roberts, M.D.** and Richard L. Kahler, M.D.***
Bethesda, MD
The occurrence of peripheral cyanosis (normal arterial oxygen saturation)
in patients with severe acquired cardiac valvular disease is not uncommon.
However, the occurrence of central cyanosis (reduced arterial oxygen saturation)
in these patients is distinctly unusual and suggests the presence of a right-to-left
(venoarterial) shunt or extreme pulmonary disease. Apatient with severe rheumatic
valvular disease was noted to have generalized cyanosis and was found to have a
pulmonary arteriovenous stula. Areview of published reports of pulmonary A-V
stulas revealed only 2 other patients with coexistent cardiac valvular disease,
consequently prompted this report.
CASE REPORT
M.P. (#05-45-49), a 50-year-old white woman who had had acute rheumatic fever
during late childhood, was told during her twenties that she had a “heart murmur.”
She was asymptomatic until age 47, when exertional dyspnea appeared. Thereafter,
symptoms of cardiac decompensation rapidly progressed despite digitalization
and diuretic therapy, and, in the 6 months before admission, she became markedly
incapacitated, bedridden, and cachectic (35 kilograms).
On admission, she was dyspneic and tachypneic (42 per minute) while sitting
up in bed. Her lips and nail beds were cyanotic but there was no digital clubbing
or cutaneous or mucosal telangiectasia. The blood pressure was 100/70mm. Hg,
and the heart was enlarged. AGrade 3/6 pansystolic blowing murmur and a Grade
3/6 diastolic rumble were audible over the cardiac apex. Agrade 4/6 high-pitched
decrescendo diastolic blowing murmur was heard at the lower left sternal border.
No murmur was heard over the back. The liver was enlarged, but there was no
peripheral edema.
The hematocrit was 46 per cent, and the hemoglobin was 14.3 Gm. per cent.
Chest roentgenograms (Figure 1) showed a mass, 6-by-3 cm. in size, in the left
lower lung eld, cardiomegaly, and calcium in the region of the mitral valve.
The electrocardiogram revealed atrial brillation, right axis deviation, and right
ventricular hypertrophy. Femoral arterial hemoglobin oxygen saturation was 76
per cent while the patient was breathing room air, and rose to 84 per cent after the
patient breathed 100 per cent oxygen for 10 minutes. Before cardiac catheterization
studies and angiocardiography could be performed, the patient developed acute
pneumonia and died.
1, 2
and
From the Department of Pathologic Anatomy, National Cancer Institute, the Laboratory of
Pathology, Clinic of Surgery, and the Cardiology Branch, National Heart Institute, National
Institutes of Health, Bethesda, Md.
Received for publication April22, 1965.
*
Department of Pathologic Anatomy, National Cancer Institute.
** Laboratory of Pathology, Clinic of Surgery, National Heart Institute.
Cardiology Branch, National Heart Institute.
***
DOI: 10.1201/9781003409281-5 35
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Figure 1 Chest roentgenograms. Posteroanterior view (left), lateral view (middle),
and anteroposterior tomogram (right). The pulmonary A-V stula is designated by
the arrows.
Figure 2 Photograph of the left atrium (L.A.), mitral valve, and the left ventricle
(L .V.). The insert shows the unopened diseased mitral valve as seen from the left
atrium.
At autopsy (A64–127), the mitral valve was rigid and calcied, and showed
evidence of being both insufcient and stenotic (Figure2). The aortic valve leaets
were thickened and slightly retracted. The left atrial appendage contained old
and recent thrombus. In the lingular portion of the left upper lobe, immediately
posterolateral to the heart, there was a saccular pulmonary A-V stula (Figures3
and 4). Histologic sections of the lungs showed no changes indicative of hypertensive
pulmonary vascular disease.
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CASE 35 PULMONARY ARTERIOVENOUS FISTULA AND RHEUMATIC CARDIAC DISEASE
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Figure 3 Diagram of the pulmonary A-V stula. A: Pulmonary artery. V:
Pulmonary vein. F: Pulmonary A-V stula. The diameter of the pulmonary vein is
greater than that of the pulmonary artery.
Figure 4 Photograph of the pulmonary A-V stula in the lingular portion of the
left upper lobe. Left: The stula is shown before removal of its medial wall. Right:
Close-up view showing the quadrilocular stula.
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DISCUSSION
The majority of patients with pulmonary A-V stula have central cyanosis, digital
clubbing, polycythemia, and a localized continuous murmur over the chest.
The present patient, however, like 2 previously reported patients with coexistent
cardiac valvular disease and pulmonary A-V stula
1, 2
did not have clubbed digits,
polycythemia, or a thoracic murmur which could be denitely attributed to a shunt
through the stula. Although occasionally an individual with a pulmonary A-V
stula has no detectable thoracic murmur,
2
it is more likely that in the present patient
a murmur was produced by the shunt but was masked by the cardiac murmurs.
REFERENCES
1. Gagnon, E. D., Johnson, R., Siniard, L. C., and Page, A.: Two cases of pulmonary
arteriovenous aneurysm with associated rheumatic aortic stenosis in one of them,
Canad MAJ 79:906, 1958.
2. Steinberg, L: Pulmonary arteriovenous stulas of the medial basal segment of the
right lower lobe: Anote on absence of vascular bruits, Dis Chest 33:86, 1958.
3. Moyer, J. H., Glantz, G., and Brest, A. N.: Pulmonary arteriovenous stulas, Am J
Med 32:417, 1962.
3
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CASE 38 INTESTINAL INFARCTION FROM MESENTERIC ARTERIAL INSUFFICIENCY
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Case 38 Intestinal Infarction Resulting from
Nonobstructive Mesenteric Arterial Insufficiency
With a Note on Hepatic Hypoglycemia as a Possible
Aid in Diagnosis
Robert K. Brawley, MD; William C. Roberts, MD; and Andrew G. Morrow, MD
Bethesda, MD
GASTROINTESTINAL hemorrhage and necrosis may result from intestinal
ischemia secondary to inadequate cardiac output and increased splanchnic vascular
resistance.* A variety of conditions, including severe congestive heart failure,
acute myocardial infarction, shock, cardiac arrhythmias, and extensive operative
procedures, may precipitate intestinal ischemia. The clinical manifestations which
accompany this process are determined by the degree of mesenteric vascular
insufciency and range from transient abdominal angina, nausea, and diarrhea
to signs of a perforated viscus. The abdominal symptoms and signs resulting
from intestinal ischemia are, however, often obscured by the presence of serious
disturbances of the nervous and cardiovascular systems. Detailed descriptions of
patients who have developed severe abdominal pain secondary to nonobstructive
mesenteric arterial insufciency are unusual. This report describes the clinical,
operative, and pathologic ndings in such a patient, who had rheumatic mitral
stenosis and congestive heart failure.
REPORT OF CASE
Clinical Summary.—A 41-year-old woman, who had acute rheumatic fever at age
nine, had been found to have a precordial murmur during her rst pregnancy at age
25. At age 32 she was treated with digitalis because of increasing exertional dyspnea,
fatigue, and orthopnea. At age 37 (1960) a diagnosis of mitral stenosis was made, and a
closed mitral commissurotomy was performed. At operation the valve was found to
be heavily calcied, markedly stenotic, and a mild regurgitant jet was also palpable.
The patient improved only transiently after this procedure and a year later again
developed severe cardiac decompensation, despite digitalis and diuretic therapy.
Thereafter, she was hospitalized on numerous occasions, and in December1963 was
admitted to the National Heart Institute. She was dyspneic, afebrile, and in atrial
brillation with a ventricular response of 110 beats per minute. The blood pressure
was 110/80mm Hg. The trunk, arms, and legs were covered with a maculopapular
rash. The jugular veins were distended, and the heart enlarged. Agrade 3/6 blowing
pansystolic murmur and a grade 2/6 rumbling diastolic murmur were audible at
the cardiac apex. The liver was enlarged and tender; the legs and sacrum were
edematous. The hematocrit value was 50%; white blood cell count (WBC), 8,300/cu
Submitted for publication Dec 7, 1965.
From the Cli nic of Surgery, Nationa l Heart I nstitute, National Institutes of Healt h, Bethesda.
Reprint requests to National Heart Institute, National Institutes of Health, Bethesda, Md
20014 (Dr. Morrow).
References 1–10, 18, 19.
*
DOI: 10.1201/9781003409281-6 39
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