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Isolated Congenital Mitral StenosisReport of Two Cases with Mitral Valvotomy in One
By J. L. BiRtAUO, M..R.C.P., S. N. JAVETT, M.D., D.C.H., D. I. ADLER, 1.R.C.S.,AND I. KESSEL, M.R.C.1'., D.C.H.
Of the 8 cases of isolated congenital mitral stenosis reported in the literature the authors add 2 easespersonally observed. The postmortem findings in one of these patients is (lescribed; in the other,improvement was noted following surgical intervention. The literature is reviewed aind the ditag-nostic criteria, including angioeardiographic findings, are described.
ISOLATED congenital mitral stenosis is anextremely rare condition. Only 8 cases
have been reported in the literature, whereas 37cases are recorded in association with othercardiac anomalies, such as patent ductusarteriosus, aortic stenosis, coarctation of theaorta, and aortic valve anomaly.'
This paper describes 2 female infants, 4months and 3 months old, respectively, withisolated congenital mitral stenosis. The diag-nosis was proved in one at autopsy; the secondcase was diagnosed clinically. The latter is aliveand moderately well 16 months after mitralvalvotomy.The first case of isolated congenital mitral
stenosis was recorded by Summons in 1906.2In 1953, Bower and associates3 reported thefirst clinically proved case of isolated congenitalmitral stenosis. The lesion was suspected aftercardiac catheterization and confirmed by angio-cardiography and operation.The over-all prognosis is extremely poor;
4 cases died in the first year of life, 3 in thesecond, and 1 in the third year of life.
Since the advent of surgery for mitralstenosis, 3 patients with congenital mitralstenosis have been operated upon, 2 with iso-lated congenital mitral stenosis and 1 with alarge patent ductus arteriosus. The first 2patients both died postoperatively, one 30hours3 and the other 6 weeks later.4 The thirdpatient was alive 7 months after the operation.
CASE REPORTSCase 1A girl, J. J., aged 3 months was the product of a
full-tcrm normal pregnancy and labor At birth
From the Johannesburg and Transvaal MemorialHospitals, Johannesburg, South Africa.
the weight was 6 lb. The mother noted gruntingrespiration soon after the child was born, and thissymptom persisted until her first admission to hos-pital in severe congestive cardiac failure at the ageof 3 months. Physical examination revealed a poorlynourished infant with marked dyspnea and sub-costal retraction. Slight cyanosis was present; therewas no clubbing. The blood pressure was 110/65,pulse 160, and respiratory rate 50 pci' minute. Thefemoral pulses were easily palpable. The liver wasenlarged 5 cm. below the right costal margin, non-tender, and nonpulsatile. Jugular venous plessurewas elevated to the angle of the jaw. The heart wasenlarged and an apical systolic thrill and a right ven-tricular heave were noted. The anteroposterior di-ameter of the chest w-as increased. The first heartsound was loud and the second sound was accentu-ated. A rough grade 3 apical sy-stolic murmur waspresent. It radiated to the base, but poorly to theaxilla and back. No diastolic murmurs were noted.The breath sounds were normal. There was no pe-ripheral edema or ascites.
Roentgenograms revealed cardiomegaly (cardio-thoracic ratio 83 per cent) and marked increase inpulmonary vasculature. In the left anterior obliquefilm, the left main bronchus was displaced upwardsby an enlarged left atrium. Enlargement of rightventricle and right atrium was also (lemonstrated(fig. 1). The electrocardiograph showed marked rightventricular hypertrophyfwith tall P waves in leadsII and III (fig. 2). A diagnosis of congenital heartdisease with pulmonary plethora was made. Thefeatures were not considered to be characteristic ofa septal defect or patent ductus arteriosus. The pa-tient responded well to digitalis therapy, with dis-appearance of the cyanosis, and was discharged un-diagnosed.
Clinical Course. She remained fairly well on main-tenance digitalis therapy until 1 month later, whenshe became dyspneic and cyanotic and was read-mitted to hospital. The physical findings showed nochange. Despite continuous oxygen and mercurialtherapy she had several sy-ncopal attacks and died48 hours later.
Autopsy Findings. The heart was grossly enlarged(fig. 3). There was marked right ventricular hyper-
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BRAUDO, JAVE4TT, ADLER, AND KESSEL
FIG. 1. Case 1. Teleroentgenogram shows gross car-
diomegaly with increased pulmonary vasculature.
VR... b
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marked right atrial and right ventricular hyper-trophy with probable left atrial hypertrophy in V1.
U~~~~~~~~~~~~~~~~~~~~~~~~~~~~~FIG. 3. Case 1. Cardiomegaly, marked thickening
of the right ventricular musculature, and gross dilata-tion of the main pulmonary artery.
trophy, the wall measuring 1 cm. in diameter. Theright atrium was dilated but not hypertrophied.The left atrium was also greatly enlarged (fig. 4). Themitral valve was severely stenosed (fig. 5) and thetricuspid valve incompetent. The atrial and ven-tricular septa were intact, and there was no patentductus arteriosus or coarctation of the aorta. Thepulmonary artery was dilated, and the lungs wereslightly edematous. There was no macroscopic pul-monary arterial disease. The enlarged liver exhibitedthe nutmeg pattern of severe congestive failure. Mi-croscopic sections of the heart demonstrated gen-eralized fibroelastosis of the left atrial endocardium.There was no evidence of rheumatic inflammation ineither myocardium or endocardium. Stains for col-lagen were negative. The lung was not sectioned.Case 2A female infant, B. P., was first seen at 3 weeks
of age on September 7, 1954. The pregnancy andlabor were normal and the birth weight was 6 lb. 14oz. The complaints were difficulty with feeding,vomiting, failure to thrive, and excessive sweating.Physical examination revealed a dyspneic infantwith profuse sweating and pronounced subeostal re-traction. The face and extremities were cyanosed.The blood pressure was 80/50, pulse 180, and respi-ratory rate 80 per minute. Femoral pulses were pal-pable. Jugular venous pressure was elevated to theangle of the jaw. The liver was enlarged 4 cm. belowthe right costal margin. Peripheral edema and asci-tes were not evident. The heart was enlarged clini-cally. There were no thrills; a vigorous systolicthrust and diastolic shock were palpable in thesecond and third left intercostal spaces. The firstheart sound was loud. The pulmonic second soundwas booming. At the apex a blowing systolic mur-mur, grade I to II, was heard. No diastolic murmurs
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ISOLATED CONGENITAL MITRAL STENOSIS
FIGS. 4 and 5. Left. Case 1. The very large left atrium is demonstrated. Right. Case 1. Demonstratesthe stenosed mitral valve and marked thickening of the left atrial endocardium.
were audible. After the heart rate had been slowedby digitalis the first heart sound was noted to besplit as was the pulmonic second. A fourth heartsound became audible. The cyanosis disappearedand was replaced by pallor.
Roentgenograms showed cardiomegaly (cardio-thoracic ratio (63 per cent) with right ventricu-lar and right atrial enlargement, double cardiacdensity, and pulmonary plethora. Isolated left atrialenlargement was noted in the right anterior obliquefilm. The electrocardiogram showed marked rightventricular hypertrophy with tall P waves in lead IIand V1 (fig. 6). Phonocardiography showed a sys-tolic murmur, a presystolic gallop, and a fourthheart sound.
Cardiac catheterization was performed at 7 weeksof age under general anesthesia. The pressure find-ings are recorded in table 1. Unfortunately, all theblood samples were hemolyzed, except that from theaxillary artery. Despite numerous attempts, thecatheter did not enter the descending aorta. Evenunder rectal pentothal anesthesia the axillary arterysample showed a nearly normal oxygen content,which excluded a large right-to-left shunt. Themarked increase in right ventricular pressure oversystemic arterial pressure indicated an intact ven-tricular septum. The elevated pulmonary capillarypressure was compatible with an obstruction at themitral valve. A tentative diagnosis of congenital iso-lated mitral stenosis was made.
Angiocardiography was carried out at 3 monthsof age. Under general anesthesia 12 ml. of 70 per centDiodrast was injected into the superior vena cavathrough a polythene catheter (figs. 7 and 8). Thefirst film taken 3 seconds after the injection outlinedthe right atrium, right ventricle, and pulmonary
artery. The subsequent films showed the dye return-ing from the lungs into a large left atrium and func-tioning left ventricle (fig. 7). The last film, (2 min-utes after the injection), showed the left ventriclepractically free from dyie with the left atrium stillfull of contrast medium (fig. 8). The above featuresindicated a tight mitral stenosis.
In view of the presence of congestive cardiac fail-ure at 3 weeks of age and ultimate poor prognosis,mitral val-otomy was performed on November 16,1954. The patient was 3 months of age at this stageand weighed 7 lb. At thoracotomy the left lung ap-peared normal, but there was gross cardiac enlarge-ment. The pulmonary artery felt exceptionally tense,but the aorta was small and of low tension. The leftatrium, anterior to the pulmonary veins, was mark-edly enlarged. Through a left atrial incision the sur-geon felt the mitral orifice to be rounded with nei-ther irregularity, commissure, nor palpable regurgi-tation. The tip of the finger was pushed through thenarrowed orifice with immediate, audible, splittingto admit the finger almost to the first knuckle. Noregurgitation had ensued and it was estimated thatthe orifice, originally of a diameter of less thanhi2 em., was opened to about 2 cm. The pulmonaryartery pressure was then markedly reduced, theaortic pressure felt increased, and no systolic thrillwas felt at the back of the atrium. The child's con-dition appeared excellent at the end of the piroce-dure.
Clinical Course. The profuse sweating disappearedsoon after the operation and she steadily gainedweight, reaching 16 lb. 2 oz. at 16 months of age.Three bouts of congestive cardiac failure occurredfrom January to August 1955, each associated withan acute bacterial infection. Digitalis, Diamox, and
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BRAUDO, JAVETT, ADLER, AND KESSEL
Mg1,1
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TABLE 1-Results of Cardiac Catheterization in Case 2
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VFIG. 6. Case 2. Electrocardiogram showing right
ventricular hypertrophv anti tall P waves in leadsII, III, and V,.
Mcr cur ial therapy was finally stopped in August1955, and thc patient has since been well. recentbacterial infection did not result in congestive fail-
ure. At the time of writing she has plroglessed nor-
mall-, and can walk and say a few words. The physi-cal findings have altered. Thee is no evidlence ofcongestive cardiac failure. The sy stolic thrust anddiastolic shock in the pulmonary area are much lessplrominent and the l)ulmonary secondl sound, al-though loud, is no longer booming. The apical svs-
tolic murimur has increased in intensity to grade III.
There are no diastolic murmurs and the fourth heartsoundl is no longer audible. The x-ray findings of theheart are unchanged. The electrocarldiogram stillshows marked right ventricular hypertrophy., butthe P waves have decreased in height and the leftventricular R wave in V6 is more plrominent. Theoperation has undoubtedly prolonged her life.
DIscussIoN-
The maini features of all the cases of isolated
Site
Left pulmonary artery..Main pulmonary artery.Pulmonary capillary....Mid right ventricle.....Mid right atrium.......Axillary artery........
Blood pressure(mm. Hg)
100/48 (64 mean)100/4420 mm. systolic98/85 mm. (mean)68/54
B loodoxygen
saturationper cent
89
congenital mitral stenosis reported in theliterature together with our 2 cases are detailedin table 2. Symptoms frequently commenceat birth but may be delayed until 2 years ofage. Failure to thrive and dyspnea were notedsoon after birth in our 2 patients and are com-mon to most of the described cases. Congestivecardiac failure with cardiomegaly, apicalsystolic murmur, and accentuated pulmonicsecond sound are the most common physicalsigns. I'ersistent cyanosis is not a feature.Temporary cyanosis was present oni admissionin both our cases but disappeared after digi-talization. X-ray examination reveals cardio-megaly, pulmonary plethora, left and usuallyright atrial enlargement together with rightventricular hypertrophy. The electrocardio-gram shows marked right ventricular hyper-trophy together with either left or right orcombined atrial hypertrophy. Angiocardi-ography is diagnostic. The enlarged leftatrium retains the dye for an abnormally longtime because of the obstruction offered by thestenosed mitral valve. In our case 2 the con-trast medium was still demonstrable in theleft atrium 2 minutes after its injection into theaxillary vein, yet the left ventricle was com-pletely devoid of dye. Intracardiac or extra-cardiac shunts are not present. Cardiaccatheter findings comprise elevated pulmonaryartery and pulmonary capillary pressures.
Clinical diagnosis is suggested by the abovesymptoms and signs. Other forms of acyanoticcongenital heart disease may present similarfindings. Patent ductus arteriosus, ventricularseptal defect, including the Eisenmenger com-plex, and atrial septal defect are easily differ-entiated by cardiac catheterization. Thepresence of isolated left atrial enlargementexcludes primary pulmou ary hypertension. In
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ISOLATED CONGENITAL MITRAL STENOSIS
FIGS. 7 and 8. Left. Case 2. Angiocardiogram 20 seconds after injection shows the dye returningfrom the lungs into a large left atrium and definite left ventricle. Right. Case 2. Film taken 2 minutesafter injection shows the left ventricle practically free from the dye with the left atrium still full ofcontrast medium.
TABLE 2.-The Salient Symptoms, Signs, and Investigations in Ten Cases of Isolated Congenital Mitral Stenosis
Angio-Symptoms Signs X-ray ECG cardio-
gram
No., age and Onstosymptoms U BIo .no.
ri 22 0. Cd >0.8jX W tJ<
24onths) -|I
1.~~~~~~~~~~~~~~~~~~~~~~Z
4 months2 Birth --+I_ _|+- - ++._l_ _]._|.|
24onhs 10 + + +--_+ + ++-|- - - L
34months46 Birt |+--- |+ |+|+|+|~|
30molnt~hs |Brt24 L-|++- |-+ - -|-1/5-12+5/90++ +
l3ontks5 8it + |++ - - - - + ~|~118/0 |+|+|+|+|+| L
mOnth cs3 s
8.~~~~~~~~~~~~~~~~~~~~~~~~C ao4
19months2 Birth + + -1/512.
3 weekhs Birth +- 8 /5 + ++ +*4u. css
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BRAUDO, JAVETT, ADLER, AND KESSEL
TABLE 3.-Catheterization and Operative Data
Cardiac catheterization
Abs. t
Abs.
Abs.
* Our 2 cases.
t Absent.
Abs.
Abs.
Abs.
Pulmonaryartery
pressure(mm. Hg)
67
50/18
100/48
Elevated pulmonarycapillary pressure
(mm. Hg)
25/13
20 mrm. (syst.)
Mitral valvotomy
Age atoperation(months)
9
4
3
Size of valve
0.5 cm.
1.0 cm.
0.5 cm.
Result
Died 36 hourspostop.
Died 6 weekspostop.
Alive 16 monthspostop.
FIGS. 9 and 10. Left. Case 2. Section of the left lingula under low power showing cellular infiltrateand thickened media of the pulmonary arterioles. Right. Case 2. High power showing thickened mediaand prominent internal and external elastic laminae of the pulmonary arterioles. There is no evidenceof endarteritis.
our case 2, the diagnostic possibility of con-
genital mitral stenosis was suggested by thecatheter findings of severe pulmonary hyper-tension and raised pulmonary capillary pres-sure in the absence of intracardiac or ex-
tracardiac shunts. Angiocardiography was
considered mandatory and revealed the pre-sence of severe mitral stenosis.
The pathologic changes in the mitral valveare uniform. It is usually thickened, hard,nodular, and white with a pearly semitrans-lucent appearance. It may be semicarti-laginous in consistency. The chordae tendineaeare thickened, shortened, and fused. The valveaperture is extremely small even during life:the diameters in the 3 operated cases were 0.5
Right-to-lft Left-to-rightshunt shunt
No.
1.2.3.4.5.6.7.8.9.*
10.*
Age atdeath
(month)
19244
36169122524
Alive
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ISOLATED CONGENITAL MITRAL STENOSIS
cm. in 2 and 1 cm. in 1. The endocardium ofthe left atrium and right ventricle frequentlyshows thickening due to fibroelastosis. Thecapillaries in the lung are usually distendedand the alveoli may contain heart-failure cellscharacteristically seen in cases of severe ac-quired mitral stenosis. Medial hypertrophy ofthe pulmonary arterioles has been described in7 cases of congenital mitral stenosis. Threecases exhibited persistence of the fetal stateof the arterioles. No single instance of intimalthickening of the pulmonary vessels has beenrecorded.' The biopsy of the left lingula re-moved at operation in our case 2 showed similarfindings (figs. 9 and 10). However, we areunable to account for the striking cellularinfiltrate of the peribronchiolar connectivetissue, respiratory bronchioles, and alveolarducts.
In view of the poor prognosis-8 out of 9children dying before the age of 2 years thequestion of surgery warrants consideration. Inrheumatic heart disease one is dealing withacquired pathology imposed upon a normalvalve, whereas in congenital mitral stenosis thevalve structure is congenitally distorted. Insome cases of acquired mitral stenosis val-votomy results in restoration of normal func-tion by the separation of the fused segments ofthe valve cusps, the valves themselves beingotherwise relatively normal; on the other hand,congenital mitral stenosis is the result of adevelopmental malformation of the entirevalve and commissurotomy will do no morethan enlarge the stenosed aperture withoutrestoring valve function. Hence the stenosismust be partly replaced by incompetence, andboth structure and function remain abnormal.The operation is indicated only in the presenceof a functioning left ventricle. Since her opera-tioln, our patient has had 3 bouts of congestivecardiac failure associated with bacterial infec-tion. Between these bouts she was in mildfailure and required maintenance digitalis andmercurial or Diamox therapy. For the past 6months all treatment has been discontinuedand she has remained well. We feel thatvalvotomy has definitely prolonged her life.
SUMMARY
Two cases of isolated congenital mitralstenosis are described, both of which presentedwith congestive cardiac failure before the ageof 3 months. The physical examination wasinconclusive. The diagnostic possibility ofcongenital mitral stenosis was suggested bythe catheter findings of severe pulmonaryhypertension and raised pulmonary capillarypressure in the absence of intracardiac orextracardiac shunts. Angiocardiography wasdiagnostic. The left atrium in 1 case remainingfull of contrast medium after the left ventriclehad emptied.One patient was subjected to surgery at
the age of 3 months. She is alive 16 monthsafter mitral valvotomy.
ACKNOWLEDGMENT
The authors would like to thank D)r. I. Wcbsterand D)r. W. J. Pcpler of the South African Instituteof _Mcdical Rcsearch for the pathologic findings inthe 2 cases. Thev arc also indebtcd to l)is. B. VanLingen, .1. Kayc, and other mcmbhcrs of the Car(liacClinic of the Johanncsburg Hospital for their assist-ancc in the cardiac (atheterization an(d angiocar(li-ography of our second case. Mr. A. AM. Shcwitz was
reslponsil)le fore thc excellent phIiotogratphls.
SUMMA.R10 IN INTEREINGi TA
Es describite duo casos de isolate conigeniitestenosis mitral. Amibes esseva presentate con
congestive disfallimento cardiac ante le etatede 3 menses. Le examine physic esseva indecise.Le possibilitate de congenite stenosis mitralesseva suggerite per le constatation cathetericde sever hypertension pulmonary e de elevatepressiones pulmono-capillari in le absentia dederivationes intra- o extracardiac. Le diagnoseesseva establite definitivenmente per medio deangiocardiographia. In un caso le atrio sinistreremaneva plen de substantia de contrastopost que le ventriculo sinlistre esseva vacuate.Un del patientes esseva subjicite a un opera-
tion chirurgic al etate de 3 menses. Illa vive 16menses post valvotomia mitral.
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BRAUDO, JAVETT, ADLER, AND KESSEL
REFERENCES1 FERENCZ, C., JOHNSON, A. L., AND WIGLESWORTH,
F. W.: Congenital mitral stenosis. Circulation 9:161, 1954.
2 SUMMONS, W. H.: Congenital heart malformations.Case 14. Intercolon. M. J. Australasia. 11: 65,1906.
3 BOWER, B. D., GERRARD, J. W., D'ABREAU, A. L.,AND PARSONS, C. G.: Two cases of congenitalmitral stenosis treated by valvotomy. Arch. Dis.Child. 28: 91, 1953.
4 MAXWELL, G. M., AND YOUNG, W. P.: Isolatedmitral stenosis in an infant of three months:
Report of a case treated surgically. Am. HeartJ. 48: 787, 1954.
DAY, H. B.: A case of mitral stenosis fatal at 2years of age. Lancet 1: 1144, 1932.
6 CRAIG, J. M.: Congenital endocardial sclerosis.Bull. Internat. Am. Museums 30: 15, 1949.
EMERY, J. L., AND ILLINGSWORTH, R. S.: Congeni-tal mitral stenosis. Arch. Dis. Child. 26: 304,1951.
8 BLUMBERG, R. W., AND LYON, R. A.: Endocardialsclerosis, cases 17, 20, 23, and 25. Am. J. Dis.Child. 84: 291, 1952.
pt
Dubois, E. L., and Martel, S.: Discoid Lupus Erythematosus: An Analysis of Its Systemic Mani-festations. Ann. Int. Med. 44: 482 (Mar.), 1956.Chronic discoid lupus erythematosus has been regarded as primarily a skin disease with rare
systemic manifestations. In order to determine the truth of this statement the authors studied aseries of 41 patients with chronic discoid lupus erythematosus. The patients were divided into 2groups: the localized discoid form, with skin lesions above the chin, and the generalized discoidform with cutaneous involvement on the face and elsewhere. Sixteen of the 26 patients (62 percent) of the localized discoid group had evidence at some time in the course of their illness of ar-thritis, fever, Raynaud's phenomenon, pleurisy, or other systemic changes by history and physicalexamination alone. Fourteen of the 15 cases of generalized discoid disease had such changes. If,in addition, laboratory abnormalities such as leukopenia, elevated sedimentation rate, hyper-globulinemia, or abnormal flocculation tests were considered, then 24 of the 26 with localizeddiscoid disease and all 15 of the generalized discoid group showed such changes. Therefore, therewas evidence of systemic involvement in 96 per cent of this group of patients with chronic dis-coid lupus. Three different modes of onset of discoid lupus were found. Thirty-three patients (72per cent) had cutaneous changes initially, followed, in 45 per cent of this group, by rheumatoid-like arthritis. Seven patients had rheumatoid arthritis prior to the appearance of discoid lesions.The classification of lupus erythematosus is an arbitrary one. There are many transitions be-tween the types. In this report it is shown that discoid lupus, from its inception, is a systemicdisorder that is a variant of the more malignant acute disseminated form. The "benign"-appearingcutaneous lesion may be a herald of advanced systemic manifestations which may be present atthe same time or at a later date, when the skin changes have healed. Therefore, all patients withdiscoid lupus erythematosus should have a thorough general medical survey. The form of therapyinstituted depends entirely upon the extent of the disease.
WENDKOS
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J. L. BRAUDO, S. N. JAVETT, D. I. ADLER and I. KESSELValvotomy in One
Isolated Congenital Mitral Stenosis: Report of Two Cases with Mitral
Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1957 American Heart Association, Inc. All rights reserved.
75231is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TXCirculation
doi: 10.1161/01.CIR.15.3.3581957;15:358-365Circulation.
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