An approach to the diagnosis of congenital heart disease

AK APPROACH TO TTIE: I)IAG~OSlS OF

CONGENITAL HEART I)IREASK”

‘hoMAS ,f. DRY. ?rI.Is.

ROPIIESTER. ~IINN.

T HE attitude toward congenital heart tliseasr is chanphg. 11 is becoming more generally recognkd 1 hat iti a poodle number 111’

c*ases the correct approach will lead to a cwrrwt anatomical diagnosis c*linically. Because of the prominence 01’ thtb physical signs, cwngenital ~ardinc anomalies seldom escape tletrctio~l for loll?, but too oftell a11 erroucous prognostic significance is attachetl I0 these signs. Frequciit.lc rnorrgh to demand attention, an iudivitlual with a wnpeuital (:ardial* anomaly dies at an advanced ape from ~~HIISW perhaps unrelateti t II thca murmur for which his activities hnti been restricted since c+hiltl- hood. Then there is the other sitle of the> picture, reprrsentetl by 1 hr slldden death of an individual who hat1 been in apparentlg robust Ikralth, as a result of paracloxical embolism. or akii. t,y the tlrvrlo~~-- rttrnt of subacute bacterial entlocarditis in an illtlivitlr~al whose bkltspiti pulmonic valve had hit,herto Ilot given riw to a. siliyle sign or symptk~m. Quite a. proportion of congenital (~ar(lia(~ tlefwts are, of (.ourst~, of s;u~h 3 1lilt~llW as to be either entirely iii~oin~~atibl(~ wit11 life or peimit !tr11! :I Aort. and crippled existence.

It therefore becomes increasingly inttwstiug. a11(1 in virw of the witit* clifferrnc~es iii prognosis with regard to w rious cwtrgenital lesions. wrj important to differentiate them, not oii1y f~wrri one airother, but i~l~ct from acdquired cardiac disease. What. 1-hen. is lhr ~rpproal~ll to tilt,

c*liiiicdal rec~ognition of these entities I Their ~liliic~al rwognitiorl ~lil IwIlds on : (1) an understanding of t hr outogenesis of eau11 of tbtw anomalies. (3) an understandin p of the physiolopi~al alterations ill1 pcwcl on the cardiovascular system by their ~~CSPIIW~ arttl (3) tllv I’o~‘- wet interpret,ation of groups of fintlinps whkh form ill rnally (‘iis, if s\.ii(lronie ~haractrristic~, or at least- t~xtwmf~ly silpgwt ivr. of ;I iw!‘-

tic*iilni* anomalous arrangwlrnt.

136 ‘I’11IS AMERIC’AN IIEART JOIJIINAI,

ing mammalian heart because it assumes functional activity at a very early stage of gestat,ion. As in its phylogenrti(: history, it starts as a simple tnbelike structure with the salue subdivisions as the adult fish heart (Fig. 1, 0,). Expressed in the simplest form its development from then on consists essentially in : (1) sepia1 formations dividing the auricle, the ventricle, the bulbus cordis, and the common aorta 01 truncus arteriosus each into two sections (Fig. 1, ZJ) ; (2) torsion of the cardiac tube; (3) development of the bulbus cordis ; (4) the incorporation of the sinus venosus into the right auricle (Fig. 1, b) ; (5) the evolution of the aortic arches, some being obliterated, others becoming the permanent aortic arch, pulmonary artery and their branches, and (6) closure of fetal channels after birth.

Ventral aorta Truncus urt eriosus

A

Sinus venosus

a Fig. la-Fish type of heart, which is similar to the heart in the fourth-week human

embryo ; b, septal formation: The sinus venosus is incorporated in the right aurich?. the bulbus cordis becomes part of the right ventricle (mainly) and of the left ventricle, and n clockwise rotation OWUI’S in the bulboventricular part of the cardiac tube.

Septal Pornlatio?ls.-This process is the physiological response on the part of the cardiac tube to the evolution of a lung-respiratory system so that the venous and arterial systems eventually become completely separatecl from one another. Any of these septal formations may be incomplete, resulting in any one of a variety of well-known defects (Table I). The car biloculare in which no septa have developed is the replica of the fish hea,rt. The amphibian form is represented by the car triloculare biatriatum in which the illterventricular septum is absent, Small interventricular septal defects, such as the maladie de Roger, resemble the adult form of the heart of some of the higher reptiles.

138 THE AMERICAN HEART JOURNAL

to form a large aortic trunk. In either ease this dextroposed aorta, instead of bearing the normal relationship to the left ventricle, overrides the int,erventricular septum (which is usually incomplete) and the right ventricle (Fig. 2). In other words, the great vessels (the aorta and pulmonary artery) are transposed, and this transposition may be present in varying degrees depending on the degree of torsion that has occurred. Sometimes there is a small niche in the right ventricle which represents the obliterated right aorta. It is extremely likely that other developmental defects will accompany such a gross deviation from the normal, such as imperfect septal formations and incomplete evolution of t,he bulbus cordis.

Here, then, one sees the genesis of one of the important and inter- esting anomalies representing arrest at the reptilian stage, namely, the tetralogy of Fallot. This consists of dextroposition of the aorta, with an interventricular septal defect, pulmonary stenosis, and an hyper-

Aorta

Fig. 2.-The tetralogy of Ballot. showing a large aorta which is dextroposed and overrides the interventricular septum. The latter is incomplete. The pulmonary artery is stenosed and the right ventricle is hypertrophied. The left auricle is not indicated in this diagram.

trophied right ventricle. cusp anomalies are frequently associated with the tetralogy, especially in the form of bicuspid leaflets which are, interestingly enough, the normal for the reptilian species.

l’he Development of the Bulbus Cor&s.-Essentially this consists of the incorporation of the major portion of the bulbus into the right ventricle, to form the COIILIS arteriosus, and a smaller portion into the left ventricle. If this process is incomplete, the corresponding ventricle will be constricted or stenosed in that region. Thus in the case of the left ventricle there will be a stenotic band below the aortic valve, that is, a subaortic stenosis. Its counterpart in the right ventricle consists of a subpulmonic or infundibular stenosis.

In the genesis of some of the stenotic congenital lesions, fetal in- flammatory processes probably play a part.

I)lallsihle rsplanatiol~ has ~WII ,zi\.rll 1Jiwl ii’ for illI> wast~ll tilt> Ic.>t’i

fourth awh becomes stenosctl. the11 OII~J (11’ tn-c, trrluinatiolls wslllth.

name1.v. coarctation, or the right fourth :I,WII ~lli~>~ wnlain p:ttent. i’crl.111~

ing the aortic arch.l In tbr latter insta~lt~cl tile l~at.rnt-p of thtt right arc.11 is salutary ; it usually- runs over t hr right hron~+hus ant1 lji~hil~(l the trachea and esophagus to join tlltl tlcw*entling ;torta. The lc+t >ll’cll is here represented by the left snh(*l;tvi;rll ill~trl~~, t fw st.t~nosetl fflll rf I: arch and a diverticulum which woul~~ h;r LY* fom(~l that part clt’ t !!,I

aortic arch between the point whew tllca rln14lis tmtalli ,joins it ;in~l

f-he descending aorta if the left. awfb IlatI lw~~ Ilormallp p;ttrlti g Pi-,

3). (:oarctatiun of the aorta is frtyllwtl~- asswiatrtl wit.11 ;ll~t~nr>~sm+ of the circle of Willis.“+ 3 Permanellt patent>- of the ductus a,rte~rioslls

!hotalli) should he considered together with allornalies of’ the ;itrrtlt. ;rrc~hrs: as the former is derived embryolnpicali~- from the latter. ‘1‘1~~~

140 THE AMERICAN HEART .JOLlRNAJ,

opening up of the pulmonary circnlatiorl after birth usually leads to gradual closure of the ductns. Should conditions remain such tha.t pressure in the pulmonic circuit and the aortic arch remains the same as before birth, the duct will remain patent. Patency of the ductus is frequently associated with other anomalies of the aortic arches.

Clos~c of Petctl Chn,~lrlcls.-This refers to the elosnre of the dnctus arteriosns and the foramen ovale.

Classifimf io>r.--Associated with each of these processes, anomalous de- velopments may nc(~ur and congenital cardiac lesions conveniently clas- sify themselves under the correspoiidiil, (r s~:bdivjsions shown in Table I. Such a classification is self-rxplallator- aud easily remembered. Tliewecl in this light, the corresponding physiological disturbance caused by each anomalous condition is readily understood and the symptoms and physical findings are more readily explained. There is, therefore, no particu- lar advantage in dividing them into clinical groups.

(‘KRTAIS FAWS B1JD E’INDINOS TVIII~‘11 SIIO7lI.D ISAD ONE TO SUSPECT THE

Krlrits Not ELcploi/r(lOlc 011 the 1jtr.si.s 01 the Corlvctttkttral Acqzci~ccl. 1,‘(11- z~zcln~ Lcsiorrs.-These have usually bee11 Ilotetl ill illfancy and arp rather constant over a period of years. The point of maximal intensity should be noted as well as the direction in which the murmurs are propagated.

Thyills.-These are frequently present over the areas of maximal intensity of the bruits, and both bruits and thrills become more readily elicited cdlinically after exercise.

Evidc,ttcc, of Ticnozrs-il~tclial #llqcnt, With flt,,e D’se,rrl Xawifcs2ation.s:

Cyc~ttosis. Pol!~c’ytltemia, Ned GYG3bed Pinglprs encl. Toes.-The group of

cdases i~r which the venous-arterial shunt is transitory, depending 011

temporarily induced increased pressnrc 011 the veilous side, frequent1.v ]ia~t a llist,ol*J. of episodes of dyspnea 01’ (~)7tliosis. A rather uniqnp fra.tnre rrlati\e to the cya.nosis of c*oltgeitital heart disease is t.he a.b- sctl(ae of rdema whell t,lle cyanosis is c1uit.r pl’olloullcrtl.

i 1 ttjf l:ttrf~,srfcrZ Heart Contour itt the Rourrtlletlf,llt’frttr, 87rrh us fl Promi-

I~(JH~ Ptthrottrmy Artcry.-Points readily overlooked a,re : lack of promi- ltence of the aortic knob ; shadows to the right of the sternum running up toward the right sternoclavicular joint, as is seen in persistent right aortic ar~ll. and erosion of ribs, which may in itself be diagnostic of coarctatiou of the aorta. These features are often bet,ter elicited by Auoroscop~.

Uypc~f~wsioIr.--111 a >-OLlll, (1 individual hypertension should lead one to examine the strength of the pulsation in the abdominal aorta and femoral arteries and to look for other evidence t.0 exclude or confirm the presence of coarc:t.at,ion of the aorta.

Cort,grttitnZ ,l~~o~~/~Zies.-C”ol~~el~ital anomalies in any part of the body slioultl lead 01le to examine (*ilJV?fLllly for cardiac anomalies. In Ab-

TABL

E 11

A RE

COED

OF

FO

URTH

LE

ADS

IN

CASE

S OF

CO

NGEN

ITAL

HE

ART

I~SE

ASE

CASE

1 2 3 4 5 6 7 8 0 10

11

12

13

14

15

16

17 ‘R

AGE

YR.

___-

22

8

-- 45

1

__- 32

__ 41

__- 27

ri 10

__

_-

61

zr I_. 23

_I

. 25

52

__- 24

c_

- 20

__. 10

27

__. 10

~‘LI

KTCA

T~

DIAG

NOSI

S /

ASIS

DE

VIAT

IOK

Auric

ular

se

ptal

de

fect

an

d M

arke

d R.

V.

I’.”

m

itral

st

enos

is

Pate

nt

duct

us

arte

riosu

s an

d B.

V.

P.

(d

espi

te

th;

paie

nt

int.e

rven

tricu

lar

pres

eme

of

a su

p3

sept

um

impo

sed

hype

rten-

1

sion)

Au

ricul

ar

sept

al

defe

ct

analM

arke

d R.

V.

P.

Da

tent

, du

ctus

ar

terio

sus

I Pa

tent

du

ctus

ar

terio

sus

with

’R,.

V.

P.

mitr

al

and

aorti

c en

do-

card

itis

Pate

nt

duct

us

arte

riosu

s I&

. v.

P.

Pate

nt

duct

us

arte

riosu

s R.

V.P.

Ve

ntric

ular

se

ptal

de

fect

No

pr

epon

dera

nce

Pate

nt

duct

us

arte

riosu

s -R

.V.P

. Ve

ntric

ular

se

ntal

de

fect

-I

No

DreD

OndW

XKc

L I

I

Pate

nt

duct

us

arte

riosu

s No

pr

epon

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nce

Vent

ricul

ar

sept

al

defe

ct

INo

prep

onde

ranc

e Au

ricul

ar

sepi

a1

defe

ct

with

lR.

V:P.

m

itral

st

enos

is Pa

tent

du

ctus

ar

terio

sus

Vent

ricul

ar

sept

al

defe

ct

with

R.

V.

P.

pa

tent

du

ctus

ar

t.erio

sus

Pate

nt

duct

us

arte

riosu

s wi

th

R.

V.

P.

vent

ricula

r se

ptal

de

fect

Pa

tent

du

ctus

ar

terio

sus

No

prep

onde

ranc

e Ve

ntric

ular

se

ptal

de

fect

an

d M

arke

d-R.

V.

P.

pr

obab

le pa

tulo

us

fora

men

ov

ale

ZX

i

!I

I -I. -1.

- -

____

FOUR

TH

LEAI

) ( W

OLFE

RTH)

C’pr

ight

T-

wave

Ab

sent

R-

wave

CARD

IAC

SYh6

PTO

blS

CO&I

LfEN

T

Early

de

com

pens

atio

n Ex

agge

rate

d P,

an

d P,

wa

ves

with

cy

anos

is an

d clu

bbin

g Di

phas

ic T-

wave

Ab

sent

Q-

wave

1)

ecom

pens

atio

n Ex

agge

rate

d P,

an

d P,

; di-

ph

asic

T,

and

T,;

delay

ed

A-V

cond

uctio

n

I Up

right

T-

wave

Ea

rly

deco

mpe

nsat

ion

Exag

gera

ted

Pa

and

P,

/ I

Uprig

ht

T-wa

ve

with

Ea

rly

deco

mpe

nsat

ion

Auric

ular

fib

rilla

tion

eleva

ted

R-T

seg-

m

ent

Diph

asic

T-wa

ve

/Abs

ent

Norm

al 1 A

bsen

t No

rmal

_I

_--i

Abse

nt

Norm

al I A

bsen

t No

rmal

/Abs

ent

____

__

Norm

al Ab

sent

No

rmal

Abse

nt

Isoe

lect

ric

T.na

ve

Deco

mpe

nsat

ion

Auric

ular

fib

rilla

tion

Norm

al Ab

sent

EI

uge

inver

ted

Poor

ca

rdia

c re

serv

e In

verte

d T,

an

d T,

; in

com

plet

e T-

wave

bu

ndle-

bran

ch

bloc

k ;

auric

- ula

r fib

rilla

tion

Slig

ht

depr

essio

n of

Dy

spne

a on

ex

ertio

n R-

T se

gmen

t No

rmal

Abse

nt

Deep

ly inv

erte

d T-

Dy

spne

a on

ex

ertio

n,

Exag

gera

ted

P,.

Inco

mpl

ete

wave

. i (

M

’ ’

notch

- Cy

anos

is an

d elu

b-

bund

le-br

anch

bl

ock.

In

- in

g of

QR

S wi

th

bing

pr

esen

t ve

rted

T2

and

T,.

dim

inish

ed

Q an

d ex

agge

rate

d s-

wave

1

I _-

-

o point of maximal lntenaltg of bruit dmaln dlrectlon in rhlch propagated I-location of thrill, if present q Onnxslcal characteristica of bruit

144 THE AMERIVAN HEART JO~IRNAIJ

“This murmur is uncomplicated by other murmurs; it begins with systole and is prolonged to such an extent that it entirely covers the uatural tic-tat of the normal heart sounds. ” The heart’s shape is usually normal, as is the electrocardiogram. Occasionally, however, there is evidence of interference with the conduct,ive system. Symptoms are absent, but subacute bacterial endocarditis is a frequent complicat,ion.

Intwawicuhr 8cptal Dcfcct (Widely Patent Pommsn~ Ovale).- Mechanism. The shunt again is arteriovenous until conditions arise which cause a reversal of pressures. Cyanosis is t,hus a frequent termiual event.

The syudrome. Until such events as just described occur, there are generally uo signs or symptoms, no cardiac enlargement or abnormal contour features, and the condition may thus remain unsuspected and undiagnosed. A patent foramen ovale should be suspected when (1) t,here is a history of cyanotic spells or ruidue cyanosis during pulmonary illfections, alul (2) wheu syst,olic or presystolic bruits, with or

Fig. a.-Lutembacber’s disease (patulous foramen ovale with mitral stenosis).

without thrills, are audible over the upper portion of the sternum and are not otherwise explainable. Wheu symptoms do occur, there is usually evidence of right veutricular hypertrophy with enlargement of the pulmonary artery and also of the right auricle. The roentgenologic am1 electrocardiographic findings will then be in keeping with such events.

Comment. Among congenital heart lesions, a widely patent foramen ovale is the only one which at times terminates in auricular fibrillation. Paradoxical embolism may occur, but subacute bacterial endocarditis is a rare complicat~iou.

Ldcnchmd~c~‘s Disease (Mitral Htcwosis ad I?dwawicdtrr H&al Defect).-Mechanism. Something of a vicious circle is created by the fact that an easier egress exists through the interauricular septal defect for the blood in the left auricle than through the stenosed mitral orifice (Fig. 5). This means that blood already agrated reaches the right side of the heart, to be sent to the lungs again. While this is no special disadvantage at first, the right ventricle soon hypertrophies,


C’omment. Right heart. failure eventually results. S’~sbaorfic Rtenosis.-1\Iechanism. The mechanism is the same as in

acquired aortic stenosis. The syndrome. The syndrome consists of: (1) a harsh systolic bruit

at the base transmitted to the vessels in the neck, (2) an accompanying thrill, (3) forceful action of the left ventricle in contrast to a weak radial pulse, (4) absence of symptoms, and (5) evidence of left ventricular strain roentgenolopically as well as electrocardiographically (Fig. 7).

o point of maximal lntenelty of bruit *m&n direction in which propagated zlocatlon oi thrill, if present q Omuslcal characteristic8 of bruit

Fig. 7.-Subaortic stenosis. The left ventricle is hypertmphied and the electrocardiogram shows left axis deviation.

Comment. The prognosis is good. Pulmonary Ste?losis.-Mechanism. 1. With a closed interventricular

septum, the right ventricle naturally hypertrophies markedly. De- pending on the degree of the defect, cyanosis almost inevitably super- venes, although the individual may reach adult life before it becomes noticeable. Once it begins, it is likely to be progressive, with increas- ing clubbing and polycythemia. 2. With an interventricular sept,al defect (which is far more common)j the load is taken off the right

148 THE AMERICAN IIEART .JOUHNAI,

1’1~ Tctdogy of PoZlot.-nlecllallisl~~. As the right ventricle empties itself, the smaller portion of venous blood enters t,he much narrowed pulmonary artery, whereas the major portioll enters the large aorta which usually directly overrides tile defect in the interventricular septum (Fig. 2). The venous blood which does get acrated returns to the left auricle and so to the left ventricle. With contraction of the latter, this aikat.ed blood joins tjhc stream of venous blood from the right ventricle in the aorta. It is apparent, tllen, that with the conl-

o point of maximal intensity of bruit ---main direction in which propagated

2?2,2ocation of thr111, if present q Omusical characteristics of bruit

Rig. Y.-The tetraloyy of Fallot: Note the bo(~t-~ll:rlmI heart. the right axin deviation in the electrocardiogram, with a positive T-nave in the fourth lead (Wol- ferth) The shading of the lips indicates c;l-anosis.

bined effects of the venous-arterial shunt and the much restricted pulmonary circulation, cyanosis will be prominellt. The peribronchial vessels help, to a greater or lesser degrecl, to cany,- blood for ai$ation to the lungs, and the efficiency of this alternate route does a good dea1 toward establishing the prognosis in the individual case.

The syndrome. The syndrome is as follows: (1). Cyanosis tends to begin early in life and often becomes extreme, (2) bruits may be

150 THE AMERICAS HEART JOURNAL

interspaces (Gerhardt’s ribbon dullness), (3) a prominent, conus shadow, and (I) right axis deviation ill the electrocardiogram (Fig. 10).

C~onimeiit. This is a t)-picdal example of a congetlital lesion ii) which symptoms are absent in marked contrast to the prominent physical findings. The frquellt tlevelopment of subacute bacterial endocarditis renders the prognosis gnartled, even though no serious mechanical dif- ficulties are likely to develop.

C!otrrdrrtiorl of tlw ;lo~ttr.-Jlecliat~isiii. The obstrnctioii to the aorta is usually just beyond the origin of the left subclarian artery, that

Fig. Il.-Roentgenologic appearance of coarctation of the aorta: Note the absence of the aortic knob and the erosion of many of the ribs. The left ventricle is hypertrophied.

is, at or near the junction of the ligamentum arteriosum and the aorta. The ligamenturn arteriosum is the occluded ductus arteriosus, and it often remains patent when anomalies of the aortic arches are present.. Interference with circulation beyond the point of obstruction depends (1) on the degree of coarctation, and (2) on the degree of collateral circulation which can be built up. The latter element, affecting mainly the intercostal arteries and the jnternal mammary artery and its branches, gives rise to characteristic clinical and roentgenologic findings in the form of pulsatin, 0’ vessels and erosion of tlie undersurface


Cotqmital dlzoldies Which dre. Rare Bat i,tt Wlvich the Diagnosis May Be Suspected.-Anomalies of the coronary artery. McGinn and Whites described the ease of an infant who manifested attacks of distress on effort, such as when nursing, while the electrocardiogram showed T-wave changes of the coronary type. The heart was hypertrophied. At necropsy a single coronary artery was founcl arising from the pulmonary artery. The effects of anoxemia in this case were illialOgOUS to those in coronary occlusion.

Car triloculare biatriatum. On the basis of another anomaly the same authors laid down the dictum that when in the roentgenogram a “water-bottle” shaped heart resembling a pericardial effusion is associated with intraventricular conductive disturbances in the electrocardiogram, a three-chambered heart of the foregoing type should be kept in mind.

THE PROGNOSIS IN CONGEKITAL HEART DISEASE

It is not always easy to prognosticate the future course of congenital heart disease. There is, however, with a few reservations, no reason to deviate from the usual criteria for judging cardiac efficiency. The heart is essentially a muscular pump and its main function is to main- tain adequate circulation under the vary& v conditions incident to the daily life of the individual. With this as a premise, and it is common to all cardiac states, and with the general principle common to the wider fields of diagnostic medicine that an isolated sign rarely has much significance, the degree to which this, its main function, is inter- fered with in the main establishes the prognosis.

The nature and degree of the mechanical disadvantage are the first considerations ; hence, again, the importance of establishing an anatomical diagnosis. In states such as patent foramen ovale, patent ductus arteriosus, maladie de R,oger, and subaortic stenosis, it may be practically negligible and in spite of loud murmurs there may be little if any interference with the patient’s activity. When, however, the degree of altered fuuction is such as to place undue strain on one or more chambers of the heart, hypertrophy, dilatation, and later, loss of cardiac reserve, must inevitably follow. This undue strain is mainly brought about by abnormal shunts of blood through incomplete septa or through stenotic orifices, and finally, through extracardiac factors such as increased pressure within the pulmonary circuit. Evidence of hypertrophy or enlargement of individual chambers or of the heart as a whole then definitely influences the prognosis adversely, aceord- ing to the degree of such enlargement.

The reservations previously referred to are occasioned by the vul- aerability of the congenitally anomalous heart to rheumatic fever, by the frequency with which subacute bacterial endocarditis becomes en- grafted upon it, and by the sudden death of an individual in appar-

154 THE AMER,ICAN HEART JOURNAL

of interventricular and interauricular septal defects, including Lutem- bather’s disease, subaortic and pulmonary stenosis, the tetralogy of Fallot, patent ductus arteriosus, coarctation of the aorta, persistent right aortic arch, one type of coronary artery anomaly, and the car biatriatum triloculare have been described.

While electrocardiographic evidence is important in the recognition of congenital heart disease, there is no diagnostic picture for any type except congenital dextrocardia with complete situs transversus.

The uncomplicated septal defects, patency of the ductus arteriosus, subaortic stenosis, and persistent right aortic arch may interfere with activity only to a limited extent, but the frequent occurrence of subacute bacterial endocardit,is as a complication renders their prognosis guarded. Occasionally an individual with a gross cardiac defect lives t.0 an advanced age.

REFERICYCES

1. Arkin. A.: Double Aortic Arch With Total Persistence of the Right and Isthmus Stenosis of the Left Arch; New Clinical and X-ray Picture; R,eport of (i Cases in Adults, All. HEART J. 11: 444, 1938.

2. Baker, T. IV,, and Shelden, W. D.: Coarctation of the Aorta With Intermittent Leakage of a Congenital Cerebral Aneurysm, Am. J. M. SC. 191: 626, 1936.

3. Woltman, H. W., and Shelden, W. D. : Neurologie Complications Associated With Congenital Stenosis of the Isthmus of the Aorta. A Case of Cerebral Aneurysm 1Vit.h Rupture and a Case of intermittent Lameness Presumably Related to Stenosis of the Isthmus, Arch. Neurol. & Psychiat. 17: 30:<, 1927.

4. Abbott, Maude E.: Congenital Heart Disease. In: Nelson Loose-Leaf Medicine, New York, Thomas Nelson and Sons, vol. -1, p. 222.

5. Barnes, A. R., and TVhrtten, M. B.: Study of T-wave Negativity in Predominant Ventricular Strain, AX HEART J-. 5: 14, 1929.

6. McGinn, Sylvester, and White, P. D.: Progress in the Recognition of Congenital Heart Disease New England 3. Med. 214: 763, 1936.

7. Edeiken, Joseph, Wolferth, C. C., and Wood, F. C.: The Significance of an Upright or Diphasic T-wave in Lead IV J+hen It Is the Only Definite Ab- normality in the Adult Electrocardiogram, Aht. HEART J. 12: ti6ci, 1936

8. Roger, H.: Reeherchcs cliniques sur la communication cong6nitale des deux coeurs, par inocclusion du septum interventriculaire, Bull. dc 1’Aead. de med. 8: 1074, 1879.

9. Abbott, Maude E.: Congenital Heart Disease. In: Nelson Loose-Leaf Medicine, New York, Thomas Nelson and Sons, vol. 4, &art 1, p. 207.

10. Firket. : Quoted bv White. P. D.: Heart Disease. New York. 1931. The Macmillan Comp&y, p. 4+3.

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11. Lutembacher: Quoted bv White, P. D. : Heart Disease. New York. 1931. The Macmillan Company, p. 47:;. ’

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12. Bonnabel: Quoted by \Vhite, P. D.: Heart Disease, New York, 1931, The Macmillan Company, p. 473.

15. White, P. D., and Sprague, H. B.: The Tetralogy of Pallot. Report of a Case in a Noted Musician, Who Lived to His Sixtieth Year, J. A. M. A. 92: $87, 1929.

14. Erickson, C. \V., and \Villius, F. A.: Cardiac Clinics: Cardiopathy of Un- determined Origin : Enormous Cardiac Enlargement, Recurrent Congestive Failure, Heart Block, and Cerebral Embolism; Clinical and Post-Mortem Findings, Proc. Staff Meet,., Mayo Clin. 11: 248, 193ri.

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An approach to the diagnosis of congenital heart disease