right ventricular stenosis - heart.bmj.com · ventricular hypertrophy. the diagnosis was failure...

RIGHT VENTRICULAR STENOSIS(BERNHEIM'S SYNDROME)

BY

TERENCE EAST AND CURTIS BAIN

From the Cardiological Departments of King's College Hospital and Harrogate General Hospital

Received December 2, 1948

Since this clinical state was first described byBernheim in 1910, very little has appeared in theEnglish language or in journals easily accessible inthis country; or at all in recent years. The recentpaper on the subject by Russell and Zohman (1945)gives references many of which we cannot check.A good deal was written in 1930 and 1931, and therewere seven papers associated with the name ofMazzei and five with that of Martini. We recordthese cases to draw attention to a pathological statethat appears to explain satisfactorily certain rathercurious clinical phenomena.The essential feature of the syndrome is what

appears to be a clinical paradox. There are con-spicuous features of apparent failure of the right sideof the heart in a patient with a lesion affecting theleft side. The explanation for this was offered byBernheim (1910), who pointed out that the septumof the ventricles bulged into the cavity of the rightventricle, and so prevented it filling. Podestia (1936)has called it dextroventricular stenosis. The pro-gress of the disorder has been divided into twostages by Mazzei (1931). In the first the infundi-bulum becomes dilated and so allows the flow ofblood to be maintained despite the interference withthe filling of the ventricle. We have satisfied our-selves by means of casts taken of the cavity of theupper part of the right ventricle in two cases thatthis is so. In the second phase this adjustmentbecomes inadequate and the signs of hepatic andjugular engorgement are seen. The pulmonary cir-culation remains unaffected until near the end, whena final congestion of the lungs may appear.

CASE REPORTSThe clinical and post-mortem findings of our five

cases now follow and will be discussed and comparedwith others reported.

Case 1. A labourer, aged 32, was admitted to

hospital in January 1945, complaining of swelling ofthe legs and feet and of fatigue, but had no shortnessof breath. As a child he had attended hospital onaccount of his heart, and had not been allowed toplay games at school. Since leaving school, how-ever, he had been well and had lived an unrestrictedlife.The patient was a fat, well-built man. There was

no cyanosis. The veins in the neck were notobviously engorged, but the liver was enlarged aboutone and a half inches below the edge of the ribs.The backs of the legs and the buttocks were swollen.His aspect generally was somewhat pale.The cardiac dullness extended three-quarters of an

inch to the right of the sternum. The apex beat wasforcible and situated five and a half inches to the leftofthemidline in the sixth leftinterspace. Avery loudharsh systolic murmur was best heard three inchesfrom the midline in the fifth left interspace. Thismurmur was accompanied by a thrill. The murmurwas conducted to the mitral and pulmonary areas andto the left axilla, but not particularly upwards. Theheart sounds at the apex were quite loud, whilethose at the base were faint; the pulmonary secondsound was louder than the aortic. The pulse wasregular, of poor volume, and not anacrotic, with ablood pressure of 100/80. Screening of the heartshowed that the right auricle was obviously en-gorged, the left ventricle was not conspicuouslyenlarged, and the pulmonary vessels were somewhatprominent. The aorta was normal (Fig. 1).Barium in the cesophagus showed slight engorge-

ment of the left auricle. The cardiogram showed noaxis deviation; the rhythm was normal but theeffect of digitalis was apparent in R-T negativity inall three leads (Fig. 2). The diagnosis appeared tohave lain between pulmonary stenosis, aorticstenosis, and patent interventricular septum. Thesite of the murmur, the predominance of rightventricular failure, the absence of an anacrotic pulse

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EAST AND BAIN

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FIG. 1.-Case 1. Some engorgement of pulmonary veins but lungs translucent.Right auricle full: left ventricle enlarged.

and the freedom from dyspnoea, also the equivocalcardiogram, made one decide upon the last, par-ticularly in view of the presence of the lesion inchildhood.At first, treatment for the congestive heart failure

was successful. Mercurial diuretics were givenfreely and he was able to go to a convalescent home.After a month or two he returned with furtherdevelopment of failure. In spite of treatment theanasarca gradually returned and steadily increased.He was never orthopnoeic and could lie fairly flat inbed. A pulmonary infarct occurred, and he slowlydeteriorated and died.

Autopsy. There was gross anasarca, profuseascites, and a moderate hydrothorax on both sides.There was no pulmonary cedema and the lungs werenot grossly engorged: their dryness was remarked

on at the time. The heart was very large-720 g.The left ventricle showed gross hypertrophy, theseptum being very thick and bulging extensivelyinto the right ventricle. This was considerablydilated, particularly in the infundibulum. Theaortic valves were stenosed as a result of congenitalfusion and subsequent calcification. The appear-ance was that of a bicuspid valve. Calcificationwas extensive, and in the depths of the anteriorcusp there seemed to be traces of a small raphe.The interventricular septum was not patent. Thecoronary sinus was greatly dilated, perhaps by thehigh pressure in the right auricle. There was grosspassive engorgement of the liver.

Comments. The diagnosis was missed in thiscase because of the site of the murmur and theabsence of confirmatory signs of aortic stenosis.

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RIGHT VENTRICULAR STENOSIS

The freedom from embarrassment of the pulmonarycirculation, the absence of left axis deviation in theelectrocardiogram, and the conspicuous predomin-ance from the first-of the results of right side failuremade the diagnosis in favour of a patent inter-ventricular septum (Maladie de Roger); for pul-monary stenosis did not appear to be in any wayindicated.

Reflection on the findings at autopsy suggestedthat the clinical manifestations indicated Bemheim'ssyndrome. The stenosis of the aortic valves shouldhave sooner or later led to failure of the left ven-

be to interpret obvious physical signs, and on reflec-tion it is difficult to see what might have led one tosuppose that aortic stenosis was really the cause ofthe murmur and thrill. Failure of the right ventriclewould have been expected to develop early had theventricular septum been patent.

Case 2. A woman, aged 62, became more andmore out of breath on exertion. This symptom wasfirst noted on hills and long walks, and later onclimbing stairs. For the last six months she hadbeen breathless on any slight activity. During the

FIG. 2. FIG. 3. FIG. 4.

FIG. 2.-Case 1. Standard three leads, showing bigeminy and negativeT waves, but no left axis deviation.

FIG. 3.-Case 2. Standard three leads, showing left axis deviation.FIG. 4.-Case 4. Standard three leads, showing left axis deviation.

tricle, but right ventricular failure was predominantfrom the first. On Bernheim's theory the encroach-ment on the cavity of the right ventricle would havebeen responsible for the early state of the failure ofthe right side. The absence of engorgement andcedema of the lungs post-mortem was very striking.The absence of left axis deviation agrees with somecases regarded as examples of Bernheim's syndrome,but it seems likely that unipolar limb leads wouldhave shown that the heart was vertical, and conse-quently the axis deviation due to left ventricularhypertrophy was lacking.The incorrect diagnosis shows how hard it may

winter before coming into hospital she had beenconfined to bed for two months; there had beenseveral attacks of bronchitis. She was now ratherbreathless at rest. There was slight swelling of theankles, but the liver and the external jugular veinswere not engorged. The heart rate was 100, withthe rhythm regular. The pulse showed alternationand the wave was slightly anacrotic. The bloodpressure was 220-210/145. There was thickening ofthe brachial and retinal arteries. The apex beat wasweak and diffuse, extending five inches to the leftof the midline, in the fifth intercostal space. In themitral area a: presystolic gallop rhythm was audible.

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148EAST AND BAIN

At the base, in the aortic area a rough systolicmurmur could be heard, extending into the' arteriesof the neck. No thrill was palpable. The aorticsecond sound was faint; at the bases of the lungswere fine scattered crepitations; the skiagramshowed that the pulmonary veins were engorged.The cardiogram (Fig. 3) showed evidence of leftventricular hypertrophy. The diagnosis was failureof the left ventricle due to hypertension and slightaortic stenosis. Failure of the right ventricle was

to 22 from 30 a minute. On the evening of thethird day she died suddenly.

Autopsy. There was gross cedema and venouscongestion. The liver was "nutmeg," weighing1615 g. The spleen showed severe chronic conges-tion. The heart weighed 600 g. The left ventriclewas enormously hypertrophied, the wall being about30 mm. thick (Fig. 5). The septum, which was20 mm. thick, bulged into the cavity of the rightventricle. The aortic valve was stenosed, the cusps

FIG. 5.-Case 2. Transverse section of ventricles looking towardsthe base. The thickened septum bulges into the right ventricle.

developing. Under treatment she improved andkept fairly well on leaving hospital until six monthslater, when there was a further attack of bronchitis.This time there was rapid development of oedemaand venous congestion. The liver was three inchesbelow the ribs, and there was anasarca to the waist.The jugular veins were prominent half way up theneck. She was rather blue, but not orthopnceic, andcould lie fairly flat. A few crepitations were heardin the lungs; the pulmonary second sound was loud.After three days in hospital the respiratory rate fell

being fused and calcified. A slight ridge below thefree margin suggested a rheumatic infection in thepast. The lungs, in contrast to the liver, were freefrom engorgement, and showed hardly any cedema;the right weighed 550 g. (normal 500 g.), and theleft 380 g. (normal 420 g.). Microscopical sectionshowed some engorgement and scattered heartfailure cells only. There was but a trace!of fluid inthe left pleural sac. There was nothing to explainthe sudden death except the aortic stenosis.

Comments. This patient, developed gradual

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failure of the left ventricle about two years beforeher death. (Edema of the ankles did not appearuntil the last six months. The final failure appearsto have been precipitated by an attack of bronchitisand was marked by severe venous congestion, whichincreased rapidly in the last three weeks. Althoughshe was breathless on admission to hospital, thiswas soon relieved. The important point is the free-dom of the lungs from cedema and engorgementpost-mortem. It would appear likely that the bulg-ing of the septum into the right ventricle preventedthe lungs from being overfilled, although the aorticstenosis and hypertension affecting the left ventriclewould have made this a likely finding. It is truethat it is common to find failure of the right ventriclefollowing that of the left in such cases as these, andthis has always been regarded as a true " backpressures" phenomenon. In this instance it wouldseem more probable that the cause was different;otherwise the lung would have shown the usualintense engorgement associated with a failing leftventricle. The course of the illness suggests thatin the earlier phases the lungs may have beeninvolved but that the development of the stenosisof the right ventricle relieved them.

Case 3. A woman, aged 63, had complained ofdyspnoea, gradually increasing in intensity, for theprevious four years. During the last six monthsshe had had acute attacks of breathlessness at nightand had often been orthopnceic. In the last monththe legs had become oedematous, and since then shehad been confined to bed. Auricular fibrillationwas present, with a heart rate of 70, for she had beentaking Guy's pill twice a day for two years. Theheart was greatly enlarged to the left, with a heavingapex beat. A rough systolic murmur was heard atthe apex. The pulmonary second sound was

abnormally loud. Crepitations were heard at thebases of both lungs. (Edema was present halfwayup the thighs, and there was a small sacral pad.Ascites was present, and the liver was enlarged twoinches below the ribs. The cervical veins were

engorged.A cardiogram showed auricular fibrillation. The

limb leads indicated right axis deviation, but thepr=cordial leads confirmed the clinical evidence ofleft ventricular hypertrophy.

It was supposed that she had previously had highblood pressure and was now in the later stages ofcongestive failure with auricular fibrillation. Sherefused to. come into hospital and deterioratedsteadily at home; but after a month she had to beadmitted. There was now massive cedema of thelegs and abdominal wall, and even the hands were

somewhat swollen. There were no signs in the

lungs and the breathing was easy; she was able tolie quite flat without discomfort.The cardiogram now showed advanced right axis

deviation, with a vertical heart, but the chest leadsstill indicated hypertrophy of the left ventricle

FIG. 6.-Case 3. Standard leads show right axis devia.tion. Unipolar limb leads show a vertical heart.Unipolar chest leads show hypertrophy of the leftventricle.

(Fig. 6). She slowly got worse, and she died amonth later.The clinical diagnosis of Bernheim's syndrome

was suggested on the finding of gross congestivefailure in a case of predominantly left-sided disease

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150EAST AND BAIN

together with freedom from embarrassment of thepulmonary circulation. The findings at autopsyconfirmed this diagnosis.

Autopsy. (Edema was present in the lower partsof the body. There was no free fluid present in thepleural sacs; the lungs were well aerated throughoutand free from cedema. Venous congestion was notconspicuous. The weight of the right lung was420 g. (normal 500 g.), and of the left lung 390 g.(normal 425 g.).

Section of the lungs showed no evidence ofchronicvenous congestion. On the whole congestivechanges were mild. An early bronchopneumoniawas developing in the right lower lobe, and herethere appeared cedema in the alveoli and congestionof capillaries.

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myocardium showed a generalized increase infibrous tissue which was evenly scattered betweenthe muscle fibres. These fibres themselves showedno degeneration but were definitely hypertrophied.The liver was enlarged (1480 g.) and showed evidenceof venous congestion. The kidneys were slightlycontracted and granular. There was much freefluid present in the abdomen.

Comments. The conspicuous finding was hyper-trophy of the myocardium of the left ventricle, withgreat increase in thickness of the interventricularseptum, which encroached upon the cavity of theright ventricle. The conspicuous venous engorge-ment of the portal system was in striking contrastwith the absence of engorgement in the pulmonarycirculation.

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FIG. 7.-Case 3. Transverse section of the ventricles, looking towardsthe base. The thickened septum bulges into the right ventricle.

The heart was greatly enlarged, weighing 810 g.The most striking feature was the concentric hyper-trophy of the muscle of the left ventricle. The wallof the right ventricle was also hypertrophied, andthe thickness of the interventricular septum wasmuch increased. The thickness of the right ven-tricle about halfway up was 4 to 5 mm., and that ofthe left ventricle about the same level was 20 mm.The septum was 20 to 24 mm. in thickness through-out. The cavity of the right ventricle was en-croached upon by the bulge of the thickened inter-ventricular septum into it (Fig. 7). There was noapparent dilatation of this chamber. The internalcapacity was therefore very considerably diminished.The right auricle was dilated. All valves werenormal. There were also numerous areas of athero-matous degeneration in the coronary arteries. The

On these findings the clinical diagnosis of Bern-heim's syndrome would appear to be confirmed.

Case 4. A woman, aged 54, first came underobservation in 1932 when she attended hospital fora mild toxic goitre. This was removed and shemade a good recovery.

In 1938, when she was 47, she again attendedhospital. She had had several severe paroxysms ofauricular fibrillation. There had been a swelling ofthe ankles and pain over the front of the chest. Thesigns in the heart now showed aortic stenosis.

In 1945, when she was 54, she was again admittedto hospital. During the past seven years she hadhad attacks of fibrillation from time to time, and inthe last year or two she had had a good deal of painunder the sternum on walking. Breathlessness had

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not been a conspicuous symptom; there never hadbeen any orthopncea. There was a good deal ofswelling of the ankles and a considerable pad in thesacral area. The veins in the neck were considerablyengorged and filled from below up to about four.inches above the level of the right auricle when shewas sitting nearly upright. The liver was a good dealenlarged. The apex beat reached the sixth spacefive inches from the midline. There was a typicalmurmur of aortic stenosis. The aortic secondsound was not audible. Auricular fibrillation cameand went. There was, however, no satisfactoryimprovement in the signs of congestive heartfailure; digitalis and diuretics were ineffective:gradually the oedema became more general and hercondition deteriorated. She was never.'in any waybreathless and she gradually sank and died. Theelectrocardiogram had shown auricular fibrillation,with left axis deviation.

It was noticeable that this patient, who hadevidently had aortic stenosis for a good many years,never complained of shortness of breath. The finalphase of heart failure lasted two months and wasmarked by symptoms of failure of the right ventricle,whereas one would have expected a phase of leftventricular failure.

Autopsy. There was generalized anasarca; afew ounces of fluid were present in each pleural sacbut the lungs were remarkably dry, but little en-gorged and quite free from aedema. The rightweighed 510 g. (normal 500 g.) and the left 390 g.(normal 425 g.). The heart weighed 540 g.' Therewas much engorgement of the right auricle and ofthe great veins. The right ventricle was full; theleft ventricle was greatly hypertrophied; and theseptum was very thick and bulged prominently intothe cavity of the right ventricle. The tricuspid ringwas slightly enlarged. The aortic valves were fused,so that a small slit-like opening only was left. Thevalves were heavily calcified and a ridge of nodularcalcium deposit seemed to mark a raphe where thecommissure of the two anterior cusps might havebeen. These were probably congenital bicuspidaortic valves which had become calcified. Thestenosis had presumably developed progressively inthe course of the last fourteen years.

Comments. In this case it is notable that thepulmonary circulation escaped engorgement rightup to the end. One might conclude that this was anexample of Bernheim's syndrome in which a ter-minal "failure" of the right side of the heartoccurred, without any indications of failure of theleft ventricle. The presence of aortic stenosis wouldhave led one to expect symptoms of left ventricularfailure, but in this case again it would appear thatengorgement upon the cavity of the right ventricle

by the bulging septum precipitated the failure of theright side and protected the lungs.

Case 5. A clerk, aged 58, a tall, thin man, wassent to hospital with severe epistaxis. He wasfound to have a blood pressure of 220/130, someenlargement of the left ventricle, the apex beat beingof a powerful, thrusting character in the sixth inter-costal space, four and a half inches from the midline.The peripheral arteries were thick, and the ischoemic,narrow retinal arterioles compressed the veins.There was a trace of albumin in the urine. Therewas no hepatic or jugular engorgement.A month later he returned with cedema halfway

up the shins, and distended jugular veins, whosefullness increased on compression of the abdomen.The heart rate was 80, the beat regular. A galloprhythm was audible and with this was associated aduplication of the apex beat, which was easily seenand felt. The aortic second sound was loud, but thepulmonary second sound was not. The cardiogramshowed left axis deviation with a negative T I (Fig. 4).He had complained of no dyspnoea at all.

In connection with the last of these indications ofembarrassment of the pulmonary circulation it wasnoted that there were no crepitations at the basesof the lungs, the skiagram (Fig. 8) showed no grosspulmonary engorgement.

After three weeks' treatment all signs of failurehad cleared up and the gallop rhythm had dis-appeared. A few months later he died suddenly athome.Comment. In this patient signs of congestive

failure appeared in the systemic circulation, withoutthe symptoms and pulmonary signs indicating priorfailure of the left ventricle. The skiagram was clear;the circulation time (decholin) of only 28 secondswas but little prolonged.For these reasons it seems correct to class this as

an early case of Bernheim's syndrome. Althoughthere was ready response to treatment at first, deathoccurred a few months later.

TYPES OF LESIONThe underlying lesion in all these cases was either

hypertension or aortic stenosis. These cause con-centric hypertrophy of the left ventricle. Perusal ofBernheim's original series suggests that most of hispatients were hypertensive, but no readings of theblood pressures were made. The same causes werepresent in Russell's series and those of Mazzei(1931), also in the series of 9 reported by Casaffourthand Superviola (1936). Aortic stenosis was presentin Olmer's patient (1933) and in that described byGlushien and Geer (1943). For some reason the

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152EAST AND BAIN

FIG. 8.-Case 5. No indication of pulmonary engorgement.

gross dilatation of the left ventricle caused by freeaortic incompetence does not lead to right ven-tricular stenosis. Possibly the explanation is thatthe septum does not become sufficiently thick.

Appearances in the skiagram. It has been claimedthat distension of the right auricle is a feature(Glushein and Geer, 1943). Two of our. casessuggested this, but in Case 5, admittedly in an earlystage (Fig. 8), it is not present. The important pointis the absence of engorgement of the fields of thelungs, although there may be slight overfilling of thepulmonary veins. We agree with other observersthat the important triad is large left ventricle, clearlung fields, and full right auricle.

Hypertrophy of left ventricle.

POST-MORTEM FINDINGSThe encroachment of the septum upon the cavity

of the right ventricle is very obvious when theventricles are cut across at right angles to the longaxis of the heart, midway between the apex and thebase. This finding is likely to be missed when theventricles are opened by V-shaped cuts, one downthe outer border and the other upwards to thepulmonary artery (or aorta), as is usually done.The transverse cut should really be made first of allin any post-mortem examination of the heart; thisprocedure might prevent the septal bulging frombeing overlooked, as we fancy it easily may be ifthe other procedure is followed.

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Photographs of the transversely divided ven-tricles are apt to be unsatisfactory, as by the timethe heart has been opened the relative positions ofthe walls of the ventricles is lost: and plugging withcotton wool and fixing in formalin easily spoils thetrue shape. We attempted to make a cast, in twocases, of the upper part of the right ventricle andinfundibulum. It is almost impossible to get agood photograph of this, but we were satisfied thatthis part, the outflow tract, remains tubular in form,leading up to the pulmonary artery, thus giving anoutlet relieving the constriction below, as suggestedby Russell and Zohman (1945) and earlier byMazzei (1931).

THE LUNGSThe dryness of the lungs at autopsy, free from

engorgement and cedema, as shown by their normalweight, is very striking. In all four cases this was anotable feature. This agrees, of course, with therelatively rapid circulation rate. Other observershave noted (e.g. Bernheim in five of his ten cases)infarcts in the lungs: whether these are due toemboli or thromboses is not clear.Cooke and White (1941) point out that in tri-

cuspid stenosis there is conspicuous jugular engorge-ment with freedom from pulmonary congestion, sothat the patient may be able to lie flat and evenwalk about with but little distress. Constriction ofthe pericardial sac presents the same apparentparadox, as Glushien and Geer (1943) have noted.The syndrome of Bemheim, by reason of the rightventricular stenosis, presents a third example ofthis curious combination of signs; it amounts, infact, as Fishberg has stated (1940), to "a virtualtricuspid stenosis."

OTHER FINDINGSThe circulation rate. In two of our patients

(Cases 1 and 5) in which the observation was madethe circulation rate was not grossly slowed, the armto tongue time in both being 28 seconds. This isquite unlike the result one would expect in ordinarycongestive failure, when it should be well over40 seconds. Similar observations were made byRussell and Zohman (1945). As slowing chieflyoccurs in the pulmonary circulation, the resultsindicate the relative freedom of the lungs fromembarrassment.

The cardiogram. It will be noted that three ofthe curves in these cases of left ventricular hyper-trophy show the expected left axis deviation in thethree standard limb leads. In one this feature isabsent and in another there is actually right axis

deviation. There has been a good deal of commenton this absence of the curve of left axis deviation,and it has been suggested that the bulging of theseptum of the ventricles to the right may be the causeof these curves by affecting the electrical axis(Russell, Zohman, 1945). It seems to us that theexplanation is to be found in the unipolar limbleads, which show that the heart is actually verti-cally placed in the chest, and so the presence of thehypertrophy of the left ventricle cannot cause leftaxis deviation. This is not an uncommon findingin certain cases of left ventricular hypertrophy;quite apart from the presence of septal displacementto the right. We have recently noted three patientswith aortic stenosis, two congenital in youths, andthe third of the fibrocalcareous acquired type in anelderly man, who showed no left axis deviation, butwith unipolar limb leads showing the heart to bevertical.We therefore conclude that there are no cardio-

graphic changes peculiar to Bernheim's syndrome.Further investigation. It seems likely that two

lines of investigation in such cases as these will befruitful. It would be interesting to know whatpressures may be revealed in the pulmonary arteryby intracardiac catheterization. Angiocardiographyshould show the peculiar shape of the cavity of theright ventricle.

TREATMENTIn these cases the question of venesection may

arise. It would seem inadvisable to bleed in thesecircumstances, as a raised venous pressure is nodoubt beneficial. Anything that reduces the venouspressure might do harm; and this perhaps appliesto such drugs as digitalis and cardophylin.

SUMMARYRight ventricular stenosis (Bernheim's syndrome)

may be found in patients with hypertension or aorticstenosis.The symptoms suggesting failure of the right

ventricle come on early, and may be transient atfirst. The pulmonary circulation remains free fromembarrassment, and the patient is free from orthop-noea, even to the end.The clinical diagnosis is confirmed at autopsy by

the state of the lungs and transverse section of theventricles.

There are no cardiographic changes peculiar tothe condition.

Our thanks are due to Professor Magnus for Fig. 5,and Dr. J. V. Wilson for Fig. 7.

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REFERENCESCasaffourth, C. F. S., and Suberviola, J. (1936). Prensa Mazzei, E. S. (1931). Rev. de Mid., 48, 493.

med. Arg., 23, 193. Olmer, J., Buisson Paillas, J., and Bernard, R. (1933).Cooke, W. T., and White, P. D. (1941). Brit. Heart J., Marseille-mid., 2, 615.

3, 147. Podesti, F. E. (1936). Cuore e Circolaz., 20, 290.Fishberg, A. M. (1940). Heart Failure. Philadelphia, Russell, H. I., and Zohman, B. L. (1945). Amer. Heart

Lee and Febiger. J., 30, 427.Glushien, A. S., and Geer, J. A. (1943-44). Med. Bull.

Vet. Admin., 20, 277.



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