Mumps of the Heart Clinical and Pathologic Features
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Mumps of the Heart
Clinical and Pathologic Features
By WILLIAM C. ROBERTS, M.D., AND SAMUEL M. Fox III, M.D.
THIS REPORT concerns a patient who cytes, 10 atypical lymphocytes, 2 monocytes
died of severe congestive cardiac failure and 1 per cent eosinophils. By February 20. 1959.
8 months after the onset of a clinical illness he had developed severe headache, stiffness of
the neck and bilateral testicular tenderness. At
indistinguishable from mumps, characterized this time he was admitted to a local hospital
by submaxillary gland enlargement, orchitis, where, in addition, he developed abdominal pain
pancreatitis, meningitis, and myocarditis. associated with an elevated serum amylase (533
During the past 2 decades, several papers have Somogyi units). Frequent ventricular premature
appeared describing electrocardiographic contractions also were noted, and he was told that
his heart was enlarged. A presumptive diagnosis
changes in many patients with mumps,1-5 and of mumps was made and he was treated with
clinical signs and symptoms of myocarditis as prednisolone. The white blood-cell count was
well as electrocardiographic changes in a few 10,000/mm.3 and the erythrocyte sedimentation
patients with mumps.0-8 A patient dying of rate was 20 mm. in 1 hour. Twenty-five per cent
mumps myocarditis was recorded in 1932 by
atypical lymphocytes were observed in the periph-
eral blood smear on February 25. By the end
Manca,9 who described the autopsy findings in of 2 weeks his symptoms had subsided, but the
a 21-year-old soldier who died 14 days follow- tachycardia, cardiomegaly, and ventricular pre-
ing the onset of his illness, which occurred mature contractions persisted, and on June 8,
during a severe epidemic of mumps in the 1959, he was admitted to the Clinical Center.
barracks. Manca's paper appears to be the His health before this illness had always been
good. There had been no previous history of
first to describe pathologic alterations in the mumps or known exposure to mumps, and there
heart of a patient dying from a viral myocar- was no history of acute rheumatic fever or
ditis.10 Recently, Krakower and Roberg" re- scarlet fever. The parents were healthy.
ported a 4-year-old girl, who died of heart On examination, he was well-developed and
failure 55 days after the onset of an acute appeared well-nourished. The blood pressure was
105/70 mm. Hg. The salivary glands were not
illness that may have been mumps. The palpable. Prominent v waves, which increased on
present communication describes the clinical inspiration, were noted in the superficial jugular
and pathologic findings in another patient veins. The heart was very large. The pulmonic-
valve closure was palpable, but the apical first
dying from probable mumps myocarditis. sounds were weak. A grade-II/VI "grunting"
Report of a Patient systolic murmur, which was accentuated on
inspiration and practically nonapparent on ex-
A. M. (no. 02-49-32), a 17-year-old school piration, was audible along the lower left sternal
boy, died October 10, 1959, after an 8-month border. A different grade-II/VI blowing systolic
illness. He had been in good health until Feb- murmur was heard at the apex and in the left
ruary 16, 1959, when he noted pain in the left axilla. The liver was palpable and tender. The
side of his neck. The following day the entire testes were soft.
left side of his neck was swollen, and tender The hematocrit value, white blood-cell count
"lymph nodes" were palpated at the angle of the and differential, sedimentation rate, blood urea
left jaw. Two days later he developed fever (104 nitrogen, serum electrolytes, proteins, calcium, al-
F.), and the peripheral blood showed 40 poly- kaline phosphatase, and transaminase were nor-
morphonuclear neutrophils, 47 mature lympho- mal. The serum total bilirubin was 2.0 mg./100
ml. Lumbar puncture disclosed normal pressures:
From the Laboratory of Pathology, Clinic of Sur- the spinal fluid was clear, but microscopically two
gery, and the Cardiology Branch, National Heart red cells and 17 white cells, all lymphocytes,
Institute, National Institutes of Health, Bethesda, were seen per mm.3 Spinal fluid sugar was 77
Maryland. mg./100 ml. and protein 25 mg./100 ml. Chest
342 Circulation, Volume XXXII, September 196.5
Downloaded from http://circ.ahajournals.org/ by guest on August 4, 2015MUMPS OF TI-IE HEART 343
condlitio)n, which progressivel dleterioratecl. He
(lie(l in severe riglht- an(d left-sided heart failure
oii October 10, 1959.
At aiutopsy (A59-202), the lheairt was lhyper-
tr(phlie(l (weight, 550 Gm-i.), all chambers xvere
lilated, anid tdie mn-vocar(linin was soft. Recenit
Mild orgalli/ing throm-ibi wer'e piresenit ini the apex
of eachi venitr icle anicl in the righlt atrium. Tlhe
tricuspid and mitral vaCixvidar leaflets an(dIchordac
xvere niormiial, buLt their rings xvere (liliatedl. The
semilunlar valves xvere nor-mal. The enidocardium
of the left atrium anid venitr-icle xvas mildly
thickenedl. The coronary arteries were normal in
oIrigini and (listril)ution an(l xvere fr ee from luminal
lisease.
Mlicroscopicallv, sectionls of the hleart disclosed
diffuse inter-stitial mnvocardial fibrosis, smlall focal
areas of mv ocardial lyIvsis, ad, rarely, a fexv
inonucleair cells in the initerstitial fibrouis tisstIe
anid in the focal areas of myoicardial necrosis
Figure 1 (fig. 3). MIost myocardial fibers xver-e lhyper-
Pos.seoantIerioi- roentgenogarani of chest. trophied, but a fev were atroplhic. No Aselhoff
1)odies vere seeni. Stainis of the mvocardlium for
roentgenogr-am (fig. 1) showed generalizedI car- fat (oil-red1 0), glvcogen (periodic acid-Schiff,
dio:megaly. Electrocardiogram (fig. 2) slhowed and PAS-diastase) , amyloid, and iron were nega-
sinulls tacliyeardia, freqluent iniultifocal ven-tricular tive. The parotid, submaxillary, thyl roid, para-
premature contractions, and probadle atriallhyper- tlhyrioid, and adrenad glands xvere inorm-a-al. The
tr-ophly. Sem- um- imntinmips cormplemnent-fixation titer seminiiferouis tubtules of the testes were sever elx
xvai 1:256. atr-oplhied. Section-s of the liver r-evealed ovei-
Shlortly after admissioni, the patient developeol wlvelminig centrolobtilar conlgestioin a(1
niIiecrosis.
overt conigestive c.IaIrdiac failure, whlichl responided The pancreas also shoxxwed the lesion of clhroniic
only termporarily to digitalis and dIiurletic tlheLpy. passive congestion. The leptomeniniges xvere
Tlhe cardiac index measured onll July 21 xvas focdlly tlhiekened and contained smnall foci of
1.8 L., im 1.I/>'2, and tlhe arteriovenous oxyvgen mononuiclear cells. Thlere xvas iitense generalized
dilffereiic was 8.8 vol. per cenlt. Predmuisolonie, subpial and sutbepenidx mzild gliosis, extend(inig inito
160 ni mg. daily, was then admiinistered for 1 the brain parenelvhma, wlhich fr eqtuenitly shoxved
wecek, but tlere xiv.as no apparent chliange in hiis chaniges of edlemiia.
Figure 2
:l.cc'troearjdio r'a ni.
( Urcullio, V1olue X',\ [1i, S plc;btr 1965
Downloaded from http://circ.ahajournals.org/ by guest on August 4, 2015344 ROBERTS, FOX
Figure 3
Photo7nicrographs of heart. Left. Lar£ge areas of replacement and initerstitial fibrosis are present.
Right. Close-npi? of myocardium showing hypertrophied atid atrophied fibers and loose inter-
stitial fibrons stromita. Masson connectivec-tissue stain (left) and hbneatoxyllinz anicd cosinl staini
(riglht); origina(il magnification X35 (left), x235 (right).
Discussion are similar to those of the patient reported by
The diagnosis of mumps in the present pa- Krakower and Roberg.11
tient appears justified. The clinical picture was According to Saphir and Cohen'2 the his-
compatible, the mumps complement-fixation tologic appearance of the heart in the present
test was elevated, and the testicular atrophy, patient and in the patients reported by Manca
myocardial fibrosis and necrosis, and central- ancd Krakower anCd Roberg is consistenit with
nervous-system changes wvere consistent with a viral origin. In viral myocarditis degenera-
previous acute orchitis, myocarditis, and men- tion and actual necrosis of isolated or grouLips
ingoencephalitis, respectively. The necropsy of myocardial fibers invariably occur, whereas
cardiac findings in the patient described dif- in isolated or Fiecdler's inyocarditis (presuimed-
fered from those in the patient stuidied by ly nonviral) the interstitial tissuie of the myo-
Manca, but understaindably so, in view of eardium is priincipally involved and involve-
the far longer course in the present patient. ment of muisele fibers is rare. 1 2Saphir and
The heart of Manca's patient, who lived only Cohen believed that necrosis of individual
14 days, was neither dilated nor hyper- myocardial fibers, a prominent histologic fea-
trophied. Histologically, his patient had a ture in the patient herein described, is stuffi-
fibrinous and leuikocytic exudate in the inter- ciently characteristic of viral myocarditis that
it may be used as a differential diagnostic
stitial tissue of the myocardiuim and the myo-
cardial fibers showed various degenerative
feature betweeni isolated and viral myocarditis.
The couirse, and the radiographic an d elec-
changes. The patient reported herein had no trocardiographic features of the present patient,
significant cellular infiltration in his heart at howcver, wexre not uinlike those described by
autopsy, but the cellular response would be Levy and Von Glahn'8 in patients with "car-
expected to have disappeared long before 8 diac hypertrophy of uinknown cauLse." It may
months had elapsed. Had the myocardial in- be worth while to perform the muimps comple-
flammatory reaction persisted, a beneficial ment-fixation and sskin tests in all patients with
response to the administration of prednisolone obscure myocarditis or idiopathic myocardial
might havc been expected. The autopsy find- enlargemenit. Certainly, meningoencephalitis
ings in the patient described herein, however, due to mu-mps is seen 'without the associated
(irmulhtion, l'oluine XXXIJ, Seprember 1965
Downloaded from http://circ.ahajournals.org/ by guest on August 4, 2015MUMPS OF THE HEART 345
or antecedent occurrence of parotitis, orchitis, (epidemic parotitis). Arch. Int. Med. 76: 257,
or pancreatitis. It is conceivable that the 1945.
3. ROSENBERG, D. H.: Electrocardiographic changes
mumps virus may involve the heart without in epidemic parotitis (mumps). Proc. Soc. Ex-
attacking other organs. The left ventricular per. Biol. & Med. 58: 9, 1945.
endocardium of the present patient and of the 4. IRVIN, M. Z., BACHARACH, T. H., AND PULLEN,
patient described by Krakower and Roberg R. L.: Mumps myocarditis. Northwest Med.
was mildly thickened, a finding frequently 50: 583, 1951.
5. BENGTSSON, E., AND ORNDAHL, G.: Complications
observed in the hearts of patients with pri- of mumps with special reference to the in-
mary myocardial disease. Recently, Noren et cidence of myocarditis. Acta med. scandinav.
al.14 reported positive skin reactivity to mumps 149: 381, 1945.
virus antigen in patients with endocardial 6. FLEXNOR, G. E., AND PULLEN, R. L.: Mumps
fibroelastosis. This finding would appear to be myocarditis: Review of literature and report
of case. Am. Heart J. 31: 238, 1946.
further evidence that infection with the mumps 7. BLAND, J. H.: Mumps complicated by myocarditis,
virus may play a role in the etiology of some meningoencephalitis and pancreatitis: Review
forms of heart disease. of the literature and report of a case. New
England J. Med. 240: 417, 1949.
Summary 8. HORTON, G. E.: Mumps myocarditis: Case report
with review of the literature. Ann. Int. Med.
The clinical and pathologic findings of a pa- 49: 1228, 1958.
tient who died from diffuse myocardial disease 9. MANCA, C.: Miocardite da parotite epidemica.
8 months after an attack of mumps is pre- Arch. Ital. di Anat. e Istol. Patol. 3: 707,
sented. His illness was complicated by myo- 1932.
carditis, meningoencephalitis, pancreatitis, and 10. WHITE, P. D.: Heart Disease. New York, The
Macmillan Company, 1951, p. 22.
orchitis. A study of past reports discloses 11. KRAKOWER, C. A., AND ROBERG, N. B.: Clinical
that electrocardiographic evidence of myocar- pathologic conference. Am. Heart J. 63: 276,
dial involvement in mumps is common, that 1962.
clinical evidence of myocardial involvement 12. SAPHIR, O., AND COHEN, N. A.: Myocarditis in
is unusual, and that death from myocardial in- infancy. Arch. Path. 64: 446, 1957.
13. LEVY, R. L., AND VON GLAHN, W. C.: Cardiac
volvement is extremely rare. hypertrophy of unknown cause. A study of
the clinical and pathologic features in 10
References adults. Am. Heart J. 28: 714, 1944.
1. WENDKOS, M. H., AND NOLL, J., JR.: Myocarditis 14. NOREN, G. R., ADAMS, P., AND ANDERSON, R. C.:
caused by epidemic parotitis. Am. Heart J. Positive skin reactivity to mumps virus anti-
27: 414, 1944. gen in endocardial fibroelastosis. J. Pediat. 62:
2. ROSENBERG, D. H.: Acute myocarditis in mumps 604, 1963.
V
Circulation, Volume XXXII, September 1965
Downloaded from http://circ.ahajournals.org/ by guest on August 4, 2015Mumps of the Heart: Clinical and Pathologic Features
WILLIAM C. ROBERTS and SAMUEL M. FOX III
Circulation. 1965;32:342-345
doi: 10.1161/01.CIR.32.3.342
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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