The new england journal of medicine

case records of the massachusetts general hospital

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Nancy Lee Harris, m.d., Editor Sally H. Ebeling, Assistant Editor
William F. McNeely, m.d., Associate Editor Stacey M. Ellender, Assistant Editor
Jo-Anne O. Shepard, m.d., Associate Editor Christine C. Peters, Assistant Editor

Case 2-2003: A 60-Year-Old Man with Mild

Congestive Heart Failure of Uncertain Cause
Peter M. Yurchak, M.D., and Vikram Deshpande, M.D.

presentation of case
A 60-year-old man was admitted to the hospital because of dyspnea and pulmonary From the Division of Cardiology (P.M.Y.)
vascular congestion. and the Department of Pathology (V.D.),
Massachusetts General Hospital and the
The patient had reportedly been well until seven days earlier, when he began to have Departments of Medicine (P.M.Y.) and Pa-
dyspnea during moderate exertion. Four days before admission, he felt a nonradiating, thology (V.D.), Harvard Medical School—
“heavy” discomfort in the lower retrosternal and epigastric areas when he stooped, both in Boston.

bent over, or walked short distances. There was no orthopnea, sweating, nausea, or
edema.
Two days before admission, he entered another hospital. The blood pressure was
150/70 mm Hg. The pulse was 80 to 90 beats per minute and irregular. Inspiratory
crackles were heard at both lung bases, and a grade 1 systolic murmur was audible. The
abdomen was normal, and there was no peripheral edema. Laboratory tests were per-
formed (Tables 1 and 2). The levels of creatine kinase and creatine kinase MB were nor-
mal twice that day, as was the level of troponin. The levels of urea nitrogen, creatinine,
glucose, calcium, magnesium, electrolytes, aspartate aminotransferase, alanine amino-
transferase, and alkaline phosphatase were normal. An electrocardiogram showed atri-
al flutter with high-degree atrioventricular block and ventricular ectopic beats, as well
as delayed R-wave progression in leads V1 through V4, without abnormal Q waves, and
diffuse, nonspecific ST-segment and T-wave abnormalities. A chest radiograph was said
to have shown cardiac enlargement and lower-lobe infiltrates, findings that suggested
the presence of congestive heart failure. An injection of furosemide was followed by
satisfactory diuresis, with resolution of the retrosternal and epigastric discomfort.
On the second day at the other hospital, another electrocardiogram showed atrial fi-
brillation with a ventricular rate of 48 to 55 beats per minute, with minor T-wave chang-
es. Digoxin, which the patient had been taking for six years, was discontinued. Late that
evening, the patient was transferred to this hospital; at the time of the transfer, he was
receiving verapamil, furosemide, enteric-coated aspirin, a potassium supplement, and
prednisone.
The patient was a sales manager. He had a long history of hypertension, for which he
took verapamil (240 mg daily). Many years earlier, he had smoked cigarettes, and he oc-
casionally drank wine. Six years before admission, he underwent a stress test because of
atypical chest pain; no abnormality was found except for a bout of supraventricular

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 The new england journal of medicine

Table 1. Hematology Laboratory Data. Table 2. Blood Chemical Values.*

Two Days Two Days before On

before On Variable Admission Admission
Variable Admission Admission
Cholesterol (mg/dl)
Hematocrit (%) 40.9 Total 134
High-density lipoprotein 28
White cells (per mm3) Normal 8,700 Low-density lipoprotein 88
Differential count (%) Triglycerides (mg/dl) 90
Neutrophils 76
Lymphocytes 17 Cardiac risk ratio 4.8
Monocytes 4
Eosinophils 2 Glucose (mg/dl) Normal
Basophils 1 Bilirubin (mg/dl)
Platelets (per mm3) 125,000 138,000 Conjugated 0.3
Total 1.5
Mean corpuscular volume (µm3) 85
Protein (g/dl)
Prothrombin time (sec) 15 Total 8.6
Albumin 4.1
Partial-thromboplastin time (sec) Normal
Sodium (mmol/liter) 138
Potassium (mmol/liter) 3.2

tachycardia, and digoxin therapy was begun at that Chloride (mmol/liter) 99

time. The same year, a cardiac ultrasonographic
study revealed slight left atrial enlargement (to 4.5
cm); slight dilatation of the aortic root, without aor-
tic regurgitation; and slight pulmonic regurgitation.
Another stress test, two years before admission,
showed no abnormalities. About one year before
admission, the patient had a brief episode of atrial
fibrillation, which subsided spontaneously.
On more persistent questioning at this hospital,
he recalled several years of fatigue and about five
years of exertional dyspnea accompanied by occa-
sional ankle swelling, episodes of paroxysmal noc-
turnal dyspnea, and palpitations. There was also a
long history of rheumatoid arthritis, which was
managed with prednisone (5 mg daily) and metho-
trexate; about six months before admission, etaner-
cept was substituted for methotrexate. Ruptured
tendons in a hand had been surgically repaired, and
the patient was awaiting an operation on the left
wrist because of a rheumatoid deformity. There was
no history of diabetes mellitus, hyperlipoproteine-
mia, or use of recreational drugs, and there was no
family history of heart disease.
The temperature was 36.9°C, the pulse was 82,
and the respirations were 20. The blood pressure
was 165/85 mm Hg.
On physical examination, the patient appeared
comfortable at rest. His face was ruddy, with telan-
giectases. The jugular venous pressure was 10 cm.
A few crackles were heard at the lung bases. The
heart rhythm was irregular, and a grade 1 systolic
Carbon dioxide (mmol/liter) 26.5
Digoxin (ng/ml) 0.7
Rheumatoid factor (IU/ml) 319
Urea nitrogen Normal
Creatinine Normal
* To convert the values for cholesterol to millimoles per liter,
multiply by 0.02586. To convert the value for triglycerides to
millimoles per liter, multiply by 0.01129. To convert the val-
ues for bilirubin to micromoles per liter, multiply by 17.1.
murmur was heard at the apex; a possible early dia-
stolic sound was reported by one examiner. The ab-
domen was normal. There was trace pedal edema.
The posterior tibial pulses were +, and the popliteal
pulses were trace; the dorsalis pedis and femoral
pulses were ++ bilaterally. Rheumatoid deformities
were most prominent in the hands, without evi-
dence of active synovitis.
Laboratory tests were performed (Tables 1 and
2). An electrocardiogram showed atrial flutter with
a predominant 4:1 response and a ventricular rate
of 74 beats per minute; there were diffuse ST-seg-
ment and T-wave abnormalities. Chest radiographs
revealed bilateral air-space disease that suggested
the presence of pulmonary vascular congestion;
there were also tiny bilateral pleural effusions. The
cardiothoracic ratio was at the upper limit of the
normal range.
A transthoracic cardiac ultrasonographic study

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 case records of the massachusetts general hospital
Table 3. Results of Pulmonary-Function Studies
on Admission.*
Percent of
Predicted
Variable Value Value
FEV1 (liters) 2.80 80
Forced vital capacity (liters) 3.33 75
FEV1:forced vital capacity 0.84 106
Peak expiratory flow rate (liters/sec) 5.98 70
Peak expiratory flow rate at 75% vital 0.81 42
capacity (liters/sec)
Calculated maximum breathing capacity 98 80
(liters/min)
Single-breath carbon monoxide diffus- 26.7 107
ing capacity (ml/min/mm Hg)
Carbon monoxide diffusing constant 4.9 116
(ml/min/mm Hg)
* FEV1 denotes forced expiratory volume in one second.
showed that the size of the left ventricle was nor-
mal and that systolic function was normal, without
segmental wall-motion abnormalities. The estimat-
ed ejection fraction was 64 percent. The left ven-
tricular wall thickness was 11 mm. There was trace
mitral regurgitation with slight left atrial enlarge-
ment. A Doppler spectral tracing of transmitral flow
and pulmonary venous inflow showed elevated left
atrial pressure and a rapid increase in initial diastol-
ic pressure. The mitral E-wave deceleration time
was 135 msec, the isovolumic relaxation time was
80 msec, and the pulmonary venous diastolic in-
flow velocity was 100 cm per second. There was no
phasic variation in the transmitral flow velocity
with breathing. The aortic valve was anatomically
and functionally normal; the size and function of
the right ventricle were also normal. The estimated
right ventricular systolic pressure was 35 mm Hg
when the right atrial pressure was assumed to be
10 mm Hg. There was no pericardial effusion. The
results of pulmonary-function studies are reported
in Table 3.
A diagnostic procedure was performed.
differential diagnosis
Dr. Peter M. Yurchak: May we review the radiographs
of the chest?
Dr. Godtfred Holmvang (Cardiology): The postero-
anterior and lateral radiographs of the chest ob-
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tained on admission suggested the presence of
mild-to-moderate congestive heart failure. There
was slight blunting of the costophrenic angles, a
finding consistent with the presence of small pleu-
ral effusions bilaterally. There was slight enlarge-
ment of the cardiothoracic ratio (the ratio of the size
of the heart to the size of the chest cavity), with pul-
monary vascular redistribution toward the upper
lobes, and mild interstitial edema. No pericardial
calcifications were identified.
Dr. Yurchak: What we recognize clinically as heart
failure (elevated filling pressures and consequent
pulmonary vascular congestion or peripheral ede-
ma) may be due either to systolic dysfunction of the
left ventricle (observed as a left ventricular ejection
fraction of less than 50 percent) or to diastolic dys-
function of the left ventricle (observed as abnormal
resistance to left ventricular filling during dias-
tole),1,2 which results in elevation of the filling pres-
sure, much as systolic dysfunction does. Diastolic
dysfunction has been estimated to be the cause of
clinical heart failure in 40 to 50 percent of patients,
but any patient may have both systolic and diastolic
dysfunction. Diastolic dysfunction can be classified
according to factors intrinsic to the left ventricular
myocardium, such as hypertrophy, infiltration with
substances such as amyloid, or ischemia, which
stiffens the myocardium. It may also be due to fac-
tors extrinsic to the myocardium, such as mitral
stenosis or constrictive pericarditis.
The definitive diagnosis of diastolic dysfunction
traditionally came from invasive catheterization of
the left side of the heart, with measurement of vol-
ume, pressure, and flow. Pulsed-wave Doppler ech-
ocardiography now offers a noninvasive approach.
This technique enables us to evaluate ventricular
relaxation and chamber compliance, which have
been defined as the two principal determinants of
left ventricular filling. Flow across the mitral valve
accelerates early in diastole, as the ventricular pres-
sure falls below the left atrial pressure. The velocity
then decreases as the elastic limits of the ventricle
are reached and atrial systole at the end of diastole
reaccelerates mitral flow. The deceleration time is
an index of left ventricular relaxation.
May we review the echocardiographic findings?
Dr. David Playford (Cardiac Ultrasonography):
The parasternal long-axis view showed that the left
ventricle was neither dilated nor hypertrophied
and that systolic function was normal. The left atri-
um was slightly dilated. The mitral and aortic
valves opened normally, and there was trace mitral
www.nejm.org january 16, 2003 245
 The new england journal
regurgitation. There was abrupt cessation of dia-
stolic relaxation, a finding known as diastolic
“checking.”
The short-axis views showed that the movement
of the septum was abnormal. During normal iso-
volumic relaxation, the tricuspid valve opens first,
followed by the mitral valve. Right ventricular fill-
ing, followed by equalization with left ventricular
filling, then occurs. In early systole, or isovolumic
contraction, the mitral valve closes first, and then
the tricuspid valve closes. This order of events caus-
es a slight shudder, or bounce, of the interventric-
ular septum, which is not visible under normal
conditions. In this patient, the septal bounce was
clearly visible and was a sign of ventricular inter-
dependence.
The pulsed Doppler study showed that the atrial-
filling wave had been abolished by atrial fibrillation.
There was a high E-wave maximal velocity (160 cm
per second) and a short deceleration time (135
msec). With respiration, the mitral and tricuspid in-
flow velocities varied by approximately 25 percent,
which may be considered the upper limit of nor-
mal. The isovolumic relaxation time, or the time
between the end of aortic outflow and the begin-
ning of mitral inflow, was normal. Systolic pulmo-
nary venous flow was absent, and tall diastolic
waves (100 cm per second) with rapid deceleration
were present. This set of findings is consistent with
an elevation in left atrial pressure and the presence
of constriction. The inferior vena cava and the he-
patic veins were dilated, a sign of increased right
atrial pressure.
In summary, the echocardiogram showed nor-
mal ventricular systolic function and no evidence
of valvular disease or pericardial effusion. There
was abnormal diastolic function with ventricular
interdependence. These signs are suggestive, but
not diagnostic, of pericardial constriction.
Dr. Yurchak: I shall consider pericarditis and rheu-
matoid arthritis. Charcot3 reported finding peri-
carditis at autopsy in four patients with rheuma-
toid arthritis. Pericardial involvement can be found
in 30 to 50 percent of patients with rheumatoid ar-
thritis in whom autopsy is performed; clinical acute
pericarditis is less common. In a series of 17 pa-
tients with acute pericarditis complicating rheuma-
toid arthritis, the disease tended to be aggressive,
progressing to pericardiectomy or to death; the
mortality rate was 15 percent.4 Isolated constrictive
pericarditis (pericarditis that has not progressed
from an acute episode) has also been well docu-
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of medicine
mented. This patient’s history does not suggest that
he had an episode of acute pericarditis.
Constrictive pericarditis is typically manifested
by dyspnea and systemic venous congestion in the
form of ascites and peripheral edema. Venous pres-
sure is usually elevated, and certain characteristics
of the pressure and pulse form — namely, Fried-
reich’s sign (diastolic collapse of distended neck
veins) and Kussmaul’s sign (paradoxical elevation
of the mean venous pressure on inspiration) — have
been described. This paradoxical elevation must be
distinguished from pulsus paradoxus, which re-
flects the effect of constriction on the systemic ar-
terial pressure and is reported in about a third of
patients with constrictive pericarditis. The abrupt
tensing of the rigid pericardium in early diastole
can produce a “pericardial knock,” a low-frequency
sound that is heard 80 to 100 msec after the second
sound and that is usually audible over the precordi-
um. Atrial fibrillation is common in constrictive
pericarditis, and this patient presented with atrial
flutter that shifted to fibrillation.
In the past decade, there have been four reports
of echocardiographic studies of left ventricular
diastolic function in a total of 138 patients with
rheumatoid arthritis.5-8 Diastolic dysfunction was
present in a higher percentage of the patients with
rheumatoid arthritis than of the age-matched con-
trols.6-8 Two studies in which systolic function and
diastolic function were examined showed no alter-
ation in the former.5,6 In the current case, these ob-
servations could justify a diagnosis of diastolic dys-
function due simply to myocardial involvement by
rheumatoid arthritis. However, abrupt diastolic
checking in early or mid-diastole, increased venous
pressure (a finding that cannot be explained by left-
sided diastolic dysfunction), and increased caval
size on the echocardiogram (a finding that sug-
gests chronic elevation of the right atrial pressure)
indicate a definitive diagnosis of pericarditis. On the
basis of these findings, I think that constrictive peri-
carditis is the best diagnosis in this case.
The most definitive diagnostic technique in cas-
es such as this one is cardiac magnetic resonance
imaging (MRI), as demonstrated by Masui et al.9
The pericardium is easily visualized by MRI and is
normally less than 4 mm in thickness. A thickness
of 4 mm or more is very strong evidence of con-
strictive pericarditis. If the MRI findings are defini-
tive, the traditional reason for performing invasive
cardiac catheterization — to show equalization of
filling pressures on both sides of the heart — is less
january 16, 2003
 case records of the massachusetts general hospital

compelling than it would be otherwise. On the oth-

er hand, given the diagnosis of constriction and the
mandate for relieving it by pericardiectomy, a car-
diac surgeon would be most interested in the status
of the coronary anatomy. If arteriography revealed
coronary disease, coronary-artery bypass surgery,
in addition to pericardiectomy, would be required.
In summary, with echocardiographic evidence of
abnormalities consistent with the presence of peri-
cardial constriction and features that indicate more
than simple intrinsic diastolic dysfunction, my di-
agnosis is pericardial constriction due to rheuma-
toid arthritis. Figure 1. Simultaneous Left (Yellow) and Right (Green)
Ventricular Pressure Tracings Showing the Square-
Root Sign.
clinical diagnosis
Most of the diastolic filling occurs early and is followed
Constrictive pericarditis due to rheumatoid ar- by a plateau (arrow). This finding indicates the presence
thritis. of constriction. (Image courtesy of Dr. Igor Palacios and
Dr. Dugene Pomerantsev, Cardiology Division, Massa-
chusetts General Hospital.)
dr. peter m. yurchak’s
diagnosis
Constrictive pericarditis due to rheumatoid ar-
thritis.

pathological discussion
RV
Dr. Eugene J. Mark (Pathology): Dr. Rubenstein,
would you present the results of the cardiac-cath- LV
RA LVOT
eterization studies?
Dr. Mark H. Rubenstein (Cardiology): The patient
underwent right- and left-sided cardiac catheteriza-
tion. The mean right atrial pressure was 17 mm Hg
LA
with a rapid Y descent, a finding consistent with rap-
id early filling of the right ventricle. The patient’s
atrial fibrillation prevented assessment of the
X descent. The right ventricular pressure was 39/17
mm Hg, and the tracing had a diastolic “dip-and-
plateau” configuration, also referred to as the
“square root” sign (Fig. 1). The mean pulmonary-
capillary wedge pressure was 20 mm Hg. The left
ventricular pressure tracing also showed the dip- Figure 2. Axial MRI Scan at the Level of the Left Ventricu-
and-plateau configuration and was nearly superim- lar Outflow Tract.
posable on the right ventricular tracing, with less There is pericardial thickening, visible as a dark layer be-
than 5 mm Hg separating the ventricular pressures tween the bright layers of epicardial and pericardial fat
in diastole. When fluid was administered, the differ- (arrow and small white bar [which represents 4 mm]).
ence between the ventricular pressures in diastole The thickening is most prominent over the anterior atrio-
ventricular groove and extends into the basal portion of
did not increase. These findings are consistent with the anterior free wall of the right ventricle. The left atrium
the presence of constriction. Finally, coronary angi- is dilated. There are bilateral pleural effusions. RV de-
ography revealed minimal coronary artery disease. notes right ventricle, RA right atrium, LVOT left ventricu-
Dr. Mark: Dr. Holmvang, would you describe the lar outflow tract, LV left ventricle, and LA left atrium.
cardiac MRI scan?

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 The new england journal of medicine

Dr. Holmvang: The patient was in atrial fibrilla-

tion during the study, which resulted in some loss
of detail on the image. The pericardial layer was
visualized, in multiple images from several views,
as a contour of low signal intensity in profile be-
tween the bright epicardial and pericardial layers of
fat (Fig. 2). Regional pericardial thickening was
observed, particularly over the atrioventricular
groove anteriorly and posteriorly as well as over the
basal portion of the ventricles, mostly in the ret-
rosternal region. In these areas, the thickness typi-
cally ranged from 2 to 4 mm; in one area, the maxi-
mal thickness was 6 mm. In other areas, including Figure 3. Pericardial-Resection Specimen (Hematoxylin
the midventricular and apical regions and over the and Eosin, ¬80).
anterolateral wall, the appearance of the pericardi- There is thickening of the pericardium with dense fibro-
um was essentially within normal limits. sis, calcification, and focal inflammation.
Dr. Mark: Dr. Hourigan, what were your impres-
sions as you cared for this patient?
Dr. Lisa Hourigan (Cardiology): After the cardiac
catheterization, our primary diagnosis was constric-
tive pericarditis related to the patient’s history of
rheumatoid disease. We also wondered whether the
hypertensive heart disease from his long-standing
history of hypertension contributed to his diastol-
ic dysfunction. The transverse echocardiogram
showed that the thickness of the left ventricular wall
was only 11 mm, which argues against an impor-
tant contribution from the history of hypertension.
Dr. Alan D. Hilgenberg (Surgery): We performed a
pericardiectomy through a median sternotomy. The
pericardium was thickened and rigid and had a nod-
ular consistency. In some areas, the pericardium
was densely adherent to the epicardium. The peri- Figure 4. Pericardium at Higher Magnification (Hema-
cardial excision extended from one phrenic nerve to toxylin and Eosin, ¬125).
the other anteriorly and included all of the diaphrag- There is a rheumatoid nodule with central fibrinoid ne-
matic surface. At the start of the operation, the cen- crosis, surrounded by palisading histiocytes.
tral venous pressure was 26 mm Hg, and at the con-
clusion of the procedure it was 8 mm Hg.
Dr. Vikram Deshpande (Pathology): The pericardial
specimen was thickened to about 3 mm and was Rheumatoid pericarditis was first described by
densely fibrotic, with focal calcification. Foci of in- Charcot in 1881.3 He stated, “Pericarditis probably
flammation composed predominantly of plasma occurs frequently in chronic rheumatism, for in nine
cells were identified (Fig. 3). Multiple rheumatoid autopsies which I performed in 1863, I met with it
nodules were seen within the pericardium (Fig. 4). four times.” Pericarditis is the most common car-
Most of the nodules were characterized by three diac manifestation of rheumatoid arthritis.
zones: a central zone of fibrinoid necrosis sur- The pericarditis may be fibrinous or may devel-
rounded by a zone of spindle-shaped macrophages op into fibrous pericarditis, as in this case. Although
arranged in a palisaded fashion and then by an outer pericarditis is not clinically evident in most cases of
layer of lymphocytes. Other nodules had very exten- rheumatoid arthritis, a series of cases studied at au-
sive areas of fibrinoid necrosis. The presence of topsy showed that the proportion associated with
rheumatoid nodules with fibrosis and chronic in- pericarditis is as high as 16 to 36 percent.10 Con-
flammation is diagnostic of rheumatoid pericarditis. strictive pericarditis tends to be more common in

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 case records of the massachusetts general hospital

males and is generally but not always associated
with the presence of subcutaneous rheumatoid nod-
ules and high titers of rheumatoid factor. Rheuma-
toid nodules are actually not commonly found with-
in the pericardium, and the histologic findings may
be nonspecific. The other cardiac manifestations
of rheumatoid heart disease include myocarditis,
valvulitis, and (more rarely) aortitis. The literature
contains rare but well-documented cases of coro-
nary vasculitis. Amyloidosis is unusual, at least on
examination at autopsy. An endomyocardial biopsy
was also performed in this case and did not reveal
evidence of myocarditis, vasculitis, or amyloidosis.
Dr. Mark: Dr. Hilgenberg, would you give us fol-
low-up information about the patient?
Dr. Hilgenberg: Two months after the operation,
the patient was able to walk a mile with no dysp-
nea. He said that his capacity for exercise was bet-
ter than it had been for many years. On examina-
tion, his jugular venous pressure was normal, and
he had atrial fibrillation with a controlled ventricu-
lar response.
anatomical diagnosis
Rheumatoid pericarditis.

references
1. Grossman W. Diastolic dysfunction in
congestive heart failure. N Engl J Med 1991;
325:1557-64.
2. Idem. Defining diastolic dysfunction.
Circulation 2000;101:2020-1.
3. Charcot JM. Clinical lectures on senile
and chronic diseases. Vol. 95. London: New
Sydenham Society, 1881:172-5.
4. Franco AE, Levine HD, Hall AP. Rheu-
matoid pericarditis: report of 17 cases diag-
nosed clinically. Ann Intern Med 1972;77:
837-44.
5. Mustonen J, Laakso M, Hirvonen T, et
al. Abnormalities in left ventricular diastolic
function in male patients with rheumatoid
arthritis without clinically evident cardio-
vascular disease. Eur J Clin Invest 1993;23:
246-53.
6. Montecucco C, Gobbi G, Perlini S, et al.
Impaired diastolic function in active rheu-
matoid arthritis: relationship with disease
duration. Clin Exp Rheumatol 1999;17:407-
12.
7. Corrao S, Salli L, Arnone S, Scaglione R,
Pinto A, Licata G. Echo-Doppler left ventric-
ular filling abnormalities in patients with
rheumatoid arthritis without clinically evi-
dent cardiovascular disease. Eur J Clin Invest
1996;26:293-7.
8. Di Franco M, Paradiso M, Mammarella
A, et al. Diagnostic function abnormalities
in rheumatoid arthritis: evaluation by echo
Doppler transmitral flow and pulmonary
venous flow: relation with duration of dis-
ease. Ann Rheum Dis 2000;59:227-9.
9. Masui T, Finck S, Higgins CB. Constric-
tive pericarditis and cardiomyopathy: evalu-
ation with MR imaging. Radiology 1992;
182:369-73.
10. Cameron J, Oesterle SN, Baldwin JC,
Hancock EW. The etiologic spectrum of
constrictive pericarditis. Am Heart J 1987;
113:354-60.
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