ANOMALOUS ORIGIN OF THE LEFT CORONARY ARTERY FROM THE PULMONARY ARTERY (BLAND-WHITE-GARLAND SYNDROME)

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CASE REPORTS

498

ANOMALOUS

ORIGIN

OF

THE

LEFT

CORONARY

ARTERY

FROM

THE

PULMONARY

ARTERY

(BLAND-WHITE-GARLAND

SYNDROME)

Report

of

Four

Cases

By BENJAMIN

M.

GASUL,

M.D.,

AND ERNST LOEFFLER, M.D.

Chicago, ill.

F

OUR cases of anomalous origin of the left coronary artery from the pulmonary artery have been studied by the authors between the years 1938 and 1946. This anomaly was

considered to be a pathologic curiosity until Bland, White and Garland’ reported a case

in 1933 ; they were the first to suggest the possibilities of a clinical diagnosis. In 1938, one of the authors (B. M. G.) of the study presented here made a clinical diagnosis of this anomaly. A study of these four cases, as well as of the cases published in the

litera-ture up to date, offers some suggestions as to the pathogenesis and possible treatment of this malformation.

.

FIG. 1. (Case 1) Roentgenogram showing increase of transverse diameter of heart.

Case 1. A baby, aged 5#{189}mos., was referred because of failure to gain wt., occasional loose stools, crying spells during and after feedings following which the baby became pale and perspired

pro-From the Hektoen Institute for Medical Research and the Childrens Division and Department of Pathology of the Cook County Hospital, and the Department of Pediatrics of the University of Illinois College of Medicine, Chicago, III.

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Lead 1 Lead 2 Lead 3 Lead No. 1. Between Right and Left Arms.

Lead No. 2. Between Right Arm and Left Leg.

Lead No. 3. Between Left Arm and Left Leg.

FIG. 2. (Case 2) Electrocardiogram.

fusely, and development of “colicky’ attacks during the previous 2 mos. Past history was negative otherwise.

Physical examination revealed a poorly developed baby whose weight was 3.5 kg., and length, 53 cm. Heart was enlarged with the greatest diameter on the roentgenogram in the A-P view 8.5 cm., and of the chest, 12 cm. (Fig. 1) . Pulse was regular, 120 to 130/mm. There was no murmur or

cyanosis.

Patient was hospitalized and tests for glycogenesis and glycogenolysis were performed. Repeated urine examinations for acetone were always negative. Two fasting blood sugar determinations were

1 19 and 100 mg./100 cc., and a blood sugar tolerance test started at 1 19 mg. went up to 160 and down again to 110 within 3 hrs.

Electrocardiogram showed normal axis deviation, tachycardia, ST, and ST2 depressed, T1 and T2 inverted (Fig. 2).The cardiologist reported this to be a case of coronary thrombosis.

Repeated fluoroscopic and roentgenographic examination revealed that the hypertrophy involved

the L. ventricle and the last roentgenogram showed an aneurysmal dilatation of the L. ventricle (Figs. 3 and 4).

The episodes of dyspnea, pallor and excessive perspiration continued and the infant died during 1 of the attacks at the age of 13 mos. An autopsy could not be obtained.

Case 2. (See Figs. 5 and 6.) This patient, aged 3 mos., had been delivered by cesarian section.

FIG. 3. (Case 1) Roentgenogram now showing what was probably aneurysmal dilatation of L. ventricle.

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FIG. 5. (Case 2) Arrow points to origin of L. coronary artery from pulmonary artery. Birth wt. was 4.1 kg. He had ‘colicky” pains which had developed during the previous week, es-pecially during feedings. Mother stated that the respirations had become rapid, a slight cough had developed during the morning of her visit and temperature had always been normal.

Physical examination revealed a well developed baby, weighing 5.8 kg. Temperature was 37.4#{176}C., pulse 130 to 140/mm. and respirations 50/mm. The marked dullness over the cardiac area extended to the 5th ICS to the anterior axillary line. There was no cyanosis, no cardiac murmur and no clubbing of the fingers or toes. Blood counts and urine were normal.

Because of the history and findings, a provisional clinical diagnosis was made of an anomalous left branch of the coronary artery arising from the pulmonary artery instead of the aorta. No ECG was made. Patient died the same day.

Postmortem Examination (Dr. Ernst Loefiler) .-Pericardial sac contained 5 cc. of clear fluid. Heart weighed 180 gm., much enlarged, apex rounded, formed by the L. ventricle exclusively; longi-tudinal diameter measured 7.5 cm., the transverse 9 cm. Palpation revealed that the anterior apical

portion of the L. ventricle was thin. Epicardium was smooth, glistening and greyish-red. L. ventricle

was extensively dilated, endocardium diffusely thickened, glistening and greyish-white ; myocardium was firm, measuring 9 mm. near the base and 1 mm. near the apex. The cut surface revealed 2 distinct layers. The outer layer was brownish-red, the inner layer light greyish-white. Mitral ostium measured 4 cm. R. ventricle was only slightly dilated, measuring 3 mm. in thickness. Aortic ostium measured 2.5 cm. There was only a right coronary artery present, which originated behind the right cusp. Pulmonary ostium measured 3 cm. ; a coronary artery originated behind the left cusp and divided in a large descending and a short circumflex branch ; the descending branch curved downward on the anterior surface of the heart near the septum in the usual place of a normal left coronary artery ; the 2nd short branch supplied the upper portion of the L. ventricle.

Measurements were: MO 4 cm., AO 2.5 cm., P0 3 cm., Tr. 0.6 cm., L. ventricle 9 mm., R.

ventricle 3 mm.

Lungs were congested and somewhat edematous. Spleen weighed 16 gm. and was congested. Liver

weighed 190 gm. and was congested. Kidneys weighed 50 gm. and showed congestion.

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almost completely replaced by dense hyalized fibers, between which only groups of vaculated muscle cells were found. Endocardium was diffusely thickened throughout. Generally the fibrotic changes were near the endocardial rather than the pericardial surface.

Lungs: Alveolar walls were thickened, alveolar capillaries dilated. Many alveoli contained heart failure cells, often accumulated in small groups. Some were filled with red blood cells and fibrin, some contained white blood cells; many were filled with pink-staining fluid. Diagnosis: chronic congestion ; foci of bronchopneumonia ; edema.

Anatomic Diagnosis: Left coronary artery originating from pulmonary artery; extreme dilatation and hypertrophy of L. ventricle of heart; fibrosis of myocardium of L. ventricle; diffuse thickening of endocardium; relative incompetence of mitral valve; congestion of lungs, liver, spleen and kidneys.

FIG. 6. (Case 2) Photograph of L. ventricle showing dilatation and hypertrophy of L. ventricle and thickening of endocardium.

Case 3. A female Negro infant, aged 7 mos., was admitted with a history of having had pneumonia 2 mos. previously, from which she recovered in 3 wks. Three days before admission, the baby de-veloped a cough, again associated with fever.

Physical examination revealed no cyanosis and no murmurs. Dullness was noted over the L. lower lobe. A diagnosis of bronchopneumonia was made and the baby died on the same day before any studies could be made.

Postmortem Examination (Dr. Ernst Loeffler) -Abdominal cavity contained 10 cc. of amber clear fluid. Thymus was small, weighing about 5 gm. Pericardial sac contained 5 cc. of clear fluid.

Heart weighed 110 gm. Longitudinal diameter was 8 cm. It was much enlarged, 8:6.5:4.5 cm.,

compressing the L. lower lobe ; the apex rounded, reaching the L. thoracic wall. Epicardium was

smooth and glistening. Coronary arteries showed on the surface the usual distribution. The entire

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hypertrophic. Left coronary artery originated from pulmonary artery, somewhat above left cusp. Right coronary originated in the usual place.

Measurements were: L. ventricle 9 mm., R. ventricle 7 mm., MO 5.5 cm., P0 3.2 cm., AO 3 cm., TO 6.5 cm.

Right lung weighed 110 gm. All lobes were edematous and the right lower lobe contained dense, prominent, greyish-red foci of bronchopneumonia. Left lung weighed 55 gm. Lower lobe was almost completely atelectatic due to compression by the heart ; both lobes were edematous.

Microscopic Examination: Heart: Sections of the L. ventricle revealed the muscle fibers hyper-trophic with areas of fibrosis in between, increasing in size and number towards the apex. Mvo-cardium, however, was not completely replaced by fibrous tissue in the apex. Endocardium was diffusely and markedly thickened.

Anatomic Diagnosis : Left coronary artery originating from pulmonary artery ; eccentric hyper-trophy of both ventricles of heart (1 10 gm.) ; diffuse thickening of endocardium of L. ventricle and

auricle ; bronchopneumonia of R. lower lobe ; partial atelectasis of L. lower lobe ; edema of lungs; congestion of liver, spleen and kidneys.

Case 4. A Negro female infant, 3 mos. of age, was admitted with the chief complaint of difficulty in breathing noted soon after birth which had become much more pronounced during the past wk.

There was no fever, cough or cyanosis at any time. Birth wt. was 3.6 kg. On examination, the baby

weighed 4.9 kg. ; ht. was 52 cm. Temperature 37.4#{176}C. (R), pulse 120/mm. and respirations 90/mm.

There was no cyanosis or clubbing of fingers or toes. There was dullness in the L. chest anteriorly extending to the anterior axillary line in the 5th ICS. There were no murmurs.

Roentgenogram of chest showed a diffuse enlargement of the heart and ECG showed a tachy-cardia, low amplitude QRS complex, inversion of the T waves in all leads.

Postmortem Examination-Right pleural cavity contained about 3 cc. of clear straw colored fluid.

L. cavity about 4 cc. of the same fluid. Pericardial cavity contained about 4 cc. of clear, straw colored fluid. Pericardial surface was smooth and shiny.

Heart measured 6 cm. from apex to base, 5 cm. at its widest portion and 3 cm. in thickness. It

appeared to be enlarged. Apex was formed mainly by the L. ventricle. Epicardium was smooth and glistening. There was little fat present. Myocardium was firm. All cardiac chambers were dilated.

Myocardium was reddish-brown in color. Right auricle was dilated and measured 3x2.5 cm. R.

ventricle was dilated and measured 5x3 cm. The wall measured 3 mm. in thickness. Valves were thin and delicate. Trabeculae were moderately prominent. Endocardium was smooth. Left auricle was

dilated and measured 3x3 cm. L. ventricle was markedly dilated and measured 5 cm. from apex to

base and 7 cm. transversely. Wall was 8 mm. thick. The trabeculae comae were flattened with marked cupping present at the apex. Papillary muscles were not hypertrophied and were 4 mm. in width.

At the apex and the chordae tendinae marked arteriosclerotic changes were present and appeared yellow-grey in color. Chordae tendinae showed a slight tendency to fusion at the distal aspect. Endo. cardium showed a considerable degree of thickening. On section the myocardium was a deep reddish tan.

Mitral valve measured 3 cm., tricuspid valve 5 cm., aortic valve 2 cm. and pulmonary valve 2.5 cm.

Interventricular septum and interauricular septum were intact. The ductus arteriosus was patent and

admifted a fine probe. Right coronary artery arose from just above the R. cusp of the aortic artery. Left coronary artery arose from the L. pulmonic cusp and about 1 cm. from its origin divided into the L. circumflex artery and the L. descending coronary artery.

Microscopic Examination.-Sections of the L. ventricle revealed hypertrophy of muscle fibers with

foci of fibrosis in between. This replacement fibrosis increased toward the apex, where a considerable amount of muscle fibers disappeared ; there was, however, no complete fibrosis of the entire wall. Sections through the papillary muscle showed multiple areas of calcification, especially near the apex.

Entire endocardium was diffusely thickened. Sections of the R. ventricle showed no fibrosis.

Anatomic Diagnosis: Left coronary artery originating from pulmonary artery ; extreme dilatation and hypertrophy of L. ventricle of heart ; fibrosis of myocardium of L. ventricle ; diffuse thickening

of endocardium ; bronchopneumonia of R. upper and L. lower lobes of lung.

COMMENT

Twenty-two cases122 of an anomalous origin of the left coronary artery from the

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ANOMALOUS ORIGIN OF THE

CORONARY

ARTERY

cases in this study make a total of 26 cases. Five of these cases lived to adulthood. None of these five adults had symptoms referable to their anomaly and in all five cases autopsy revcaled definite collateral circulation between the two coronary arteries. Of the remaining

2 1 cases, all except two died between three and six months of age. Two lived to 1 3 months. Bland, White and Garland’ found eight other cases reported in the literature, six of which occurred in infants under one year of age. None of the cases had had ECG and the clinical condition was not suspected. Their case was the only one in which an electro-cardiographic study was made and they suggested that ‘‘in future cases of uncomplicated cardiac hypertrophy in infancy, the finding of a similar electrocardiogram in the absence

TABLE I

REPORTED CASES UP TO DATE

Authors Yr. Reported Age Mos. Age Yrs.

Abrikosoff 1911 5

Heitzmann 1917 3

Kiyokawa 1923 4

Carrington and Krumbhaar 1924 10

Scholte 1930 24

Stevenson 3

Abbott 64

Bland, White and Garland 1933 3

Kockel 1934 38

Sanes and Kenny 1934 3

Bartsch and Smekal 1934 3

Linck 1936 8

Chown and Schwalm 1936 5

R#{252}bberdt 1937 27

Barnard 1938 44

Dietrich 1939 53

Soloff 1942 44

Ruddock and Stehly 1943 30

Proescher and Baumann 1944 13

Eidlow and Mackenzie 1946 4

Lyon, Johansmann and Dodd 1946 6

Lyon, Johansmann and Dodd 1946 3

Gasul 1938 13

Gasul and Loeffler 1946 3

of abnormal axis deviation, or toxemia, may indicate an inadequate and anomalous coronary supply to the heart.”

The infants reported were apparently healthy at birth and developed normally until two or three months of age when they began to have ‘‘colicky’ ‘ pains, usually occurring

during or soon after feedings, associated with a rapid pulse, rapid respirations, pallor and profuse perspirations. They all showed an enlarged heart and, in those cases where

an electrocardiogram had been taken, inversion of the T waves in the leads was noted,

but there was no axis deviation. Low amplitude of the QRS complexes was usually noted.

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case in an infant

#{189}

mos. of age, on whom no clinical diagnosis had been made, but whose autopsy revealed the same characteristic pathologic picture.

Ruddock and Stehly’8 reported a case of an adult aged 30 yrs. who died suddenly. Autopsy revealed the origin of the left coronary artery from the pulmonary artery and the left coronary communicated with the terminal branch of the right circumflex artery over the basal portion of the central surface of the left ventricle.

Proescher and Baumann’9 reported a case of an infant, aged 1 3 mos., in whom the

diagnosis was made at autopsy. Eidlow and Mackenzie20 reported a case of an anomalous origin of the left coronary artery from the pulmonary artery diagnosed clinically and confirmed by autopsy. The infant died at the age of 4 mos. Lyon, Johansmann and

Dodd2l reported two additional cases, one infant dying at the age of 6 mos. and the other

at the age of 3 mos.

The fact that the four cases presented here were seen in a comparatively short time points to the possibility that the condition is not as unusual as a review of the literature would lead one to believe. Some of these cases have probably been called idiopathic cardiac hypertrophy ; others might have been labeled as “thymic deaths.” It is felt that as a result of familiarity with this entity more cases will be recognized.

The entity has well defined pathologic features. All the cases show hypertrophy and dilatation of the left ventricle and myocardial degeneration which in some cases goes on to complete fibrous tissue replacement in the regions supplied by the left coronary artery. The explanations that have been offered for the marked enlargement of the left ventricle and for the degenerative changes in the myocardium are two-fold: first is the fact that the left coronary brings nonoxygenated (venous) blood to the left ventricle and, second, the low pressure existing in the pulmonary artery as compared to the aorta. These viewpoints are obviously correct. However, it would seem that the myocardial damage is too severe and progressive to be explained by venous blood and low pressure only. The attacks simulating angina pectoris suggest an additional factor. The fact that no myo-cardial damage whatsoever is found if the right coronary originates from the pulmonary artery and the fact that extensive anastomosis can prevent myocardial damage point to an additional factor. Low pressure and venous blood will lead to impairment of the func-tional capacity of the left ventricle. The dilated heart performs more mechanical work and the oxygen consumption goes up. Dilatation is the basis on which hypertrophy arises, even though the absolute work of the heart is not augmented. There is a relative increase in the sense that the actual work performed approaches more closely the maximum of the heart’s capability. The dilatation and subsequent hypertrophy will lead to a temporary and

permanent compression of parts of the left coronary artery which has a lower pressure

than a normal left coronary artery. As in any case of dilatation, the parts near the ventric-ular apex are dilated first and most. It is the compression of the coronary artery starting near the apex and in time progressing towards the base which is responsible for the extensive fibrosis of the myocardium. The more replacement of myocardium by granula-tion tissue and later fibrous tissue, the more pronounced will be the bulging of the left ventricle and the more extensive and complete will be the occlusion of the left coronary artery which again, in a vicious circle, will lead to additional myocardial damage. This would seem to be the explanation for severe fibrosis simulating the picture of coronary occlusion in adults.

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or third months of life. Not one of them died before 21/2

to

3 mos. of age. The following speculation may be offered as an explanation:

During fetal life, the lungs do not function for all practical purposes and the pressure in the lesser circulation is higher than in the systemic circulation so that blood is directed through the ductus arteriosus into the aorta. There is also little or no difference in the oxygen saturation of the blood from the pulmonary artery and that of the aorta, so that at birth the babies are born with a normal heart.

The ductus arteriosus begins to close soon after birth and in the average case it is closed by the end of the second or third month. But since the pressure existing in the lesser circulation is about equal to that of the greater circulation during the first two or three

months of the baby’s life, there is usually no flow of blood in either direction, and even though the ductus arteriosus may be patent anatomically, functionally it closes soon after

birth, because of the equilibrium in the existing pressure relationship between the two

circulations.

It is well known, for example, that the electrocardiogram shows a slight right axis

shift during the first two or three months of the infant’s life. So long as the pressure in

the pulmonary circulation is as high as it is in the greater circulation, so long will the blood flow through the left coronary artery into the left ventricle under at least as much

pressure as the blood that flows through the .right coronary artery to the right ventricle.

The nutrition of the myocardium of the left ventricle will not be as good as that of the right ventricle because it will receive nonoxygenated blood. However, the important point to remember is that even venous blood contains 75% oxygen. Anyone who sees cyanotic

infants and children with congenital malformations of the heart knows that they may live

many years with an arterial oxygen saturation well below 75% and yet none of them show either the pathologic picture or the electrocardiographic findings that are present in this malformation. It is doubtful if it even makes much difference whether or not some oxygenated blood will enter the left coronary artery from the aorta through the patent ductus. The important point is the pressure relationship existing between the greater and

lesser circulation.

But after the second or third month of life, the ductus usually closes, and, what is more important for these cases, the pressure in the aorta becomes definitely higher than in rite pulmonary artery, and it is then that the symptoms and the clinical findings of this inal-formation become evident. It is probably not so much the difference in the oxygen satura-tion as the low pressure in the left coronary artery that gives rise to the clinical and pathologic picture of this malformation, and since this low pressure does not really appear until about the third month, infants do not manifest any symptoms until then.

SUGGESTED TREATMENT

Since this is an apparently uniformly fatal disease, it would seem reasonable to attempt to raise the pressure in the pulmonary artery and at the same time try to supply oxygenated blood to the left branch of the coronary artery by anastomosing the pulmonary artery

to

the aorta. It is suggested that either a Potts-Smith operation to connect the left or right pulmonary artery to the descending aorta be performed, or, even better, if this is techni-cally possible, attempt to anastomose the main pulmonary artery to the ascending aorta. This would then direct oxygenated blood closer to the origin of the coronary artery than if a Potts-Smith operation were performed.

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infants are apparent. A review of the reported cases will show that in some instances a clinical diagnosis had been made several weeks or months before death, however, and it is possible that surgical intervention of the type suggested might have been successful on these patients.

CONCLUSIONS

The anomalous origin of the left coronary artery from the pulmonary artery is a definite pathologic and clinical entity. A review of the literature reveals 22 reported cases. Four additional cases are presented. Additional considerations explaining observa-tions in this syndrome and a suggestion for the possible treatment of this malformation are presented.

REFERENCES

1. Bland, E. F., White, P. D., and Garland,

J.,

Congenital anomalies of coronary arteries: Report

of unusual case associated with cardiac hypertrophy, Am. Heart J. 8:787, 1933.

2. Abrikosoff, A., Aneurysma des linken Herzventrikels mit abnormer abgangsstelle der linken Koronararterie von der Pulmonalis bei einem f#{252}nfmonatlichen Kinde, Arch. f. path. Anat.

203:413, 1911.

3. Heitzmann, 0., Drei Seltene Falle von Herzmissbildung, Arch. f. path. Anat. 223:57, 1917. 4. Kiyokawa, W., Anomalie der linken Kranzarterie des Herzens und ihre Folgen, Arch. f. path.

Anat. 242:14, 1923.

5. Carrington, G. L., and Krumbhaar, E. B., So-called idiopathic cardiac hypertrophy in infancy,

Am. J. Dis. Child. 27:449, 1924.

6. Abbott, Maude E., Congenital Heart Disease, in Osler’s Modern Medicine, ed. 3, edited by T.

McCrae and E. H. Funk, Philadelphia, Lea & Febiger, 1927, vol. 4, chap. 21, p. 612. 7. Stevenson, J. A., cited by Abbott,’ p. 666.

8. Scholte, A. U., Ueber einen Fall von abnormer abgangstelle der linken Karon-arterie aus der Pulmonalarterie, Zentralbl. f. allg. Path. u. path. Anat. 50: 183, 1930.

9. Kockel, H., Eigenartige Kranzschlagadermissbildungen, Beitr. z. path. Anat. 94: 220, 1934. 10. Sanes, S., and Kenny, F. E., Anomalous origin of left coronary artery from pulmonary artery,

Am. J. Dis. Child. 48:113, 1934.

1 1. Bartsch, G. H., and Smekal, T., Ueber den Ursprung eines Kranzgefasses aus der

Lungenschlag-ader, Frankfurt. Ztschr. f. Path. 47:256, 1934.

12. Linck, K., Aneurysmatische Erweiterung der linken Herzkammer infolge Ursprungs, der linken Kranzschlagader aus der Pulmonalis bei einem 8 Monate alten M#{228}dchen, Virchows Arch. f. path. Anat. 297:113, 1936.

13. Chown, B., and Schwalm, F. G., Congenital abnormality of heart, Am. J. Dis. Child. 52:1427, 1936.

14. R#{252}bberdt, H., Abnormer Abdang der linken Kranzarterie aus der Lungenschlagader, Beitr. z.

path. Anat. 98:571, 1937.

15. Barnard, W. G., Aneurysm of left ventricle due to left coronary artery taking origin from pulmonary artery, J. Path. & Bact. 47:311, 1938.

16. Dietrich, W., Ursprung der vorderen Kranzarterie aud der Lungenschlagader mit ungewohn-lichen Ver#{228}nderungen des Herzmuskels und der gefasswande, Arch. f. path. Anat. 303:436,

1939.

17. Soloff, L. A., Anomalous coronary arteries arising from pulmonary artery, Am. Heart J. 24:118, 1942.

18. Ruddock, J. C., and Stehly, C. C., Anomalous origin of left coronary artery from pulmonary artery, U. S. Nay. M. Bull. 41: 175, 1943.

19. Proescher, F., and Baumann, F. W., Abnormal origin of left coronary artery with extensive

cardiac changes, J. Pediat. 25: 344, 1944.

20. Eidlow, S., and Mackenzie, E. R., Anomalous origin of left coronary artery from pulmonary artery, Am. Heart J. 32:243, 1946.

2 1. Lyon, R. A. (Cincinnati) , Johansmann, R. J., and Dodd, K., Anomalous origin of left coronary

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ANOMALOUS ORIGIN OF THE

CORONARY

ARTERY

507

22. Gasul, B. M., and Loeffler, E., Cardiac enlargement in infants simulating cononary disease, Am.

J. Dis. Child. 73:122, 1947.

SPANISH ABSTRACT

Origen

An#{243}malo de

Ia Arteria

Coronaria

Izquierda

de

Ia

Arteria

Pulmonar

(Smndrome

Bland-White-Garland)

Se informa acerca de cuatro casos y una revista de literatura de hipertrofia cardlaca en infantes debida a un origen an#{243}malo de Ia arteria coronaria izquierda de Ia arteria pulmonar. La diagnosis est#{225}basada en el caso de un nacimiento aparentemente normal y de desarrollo normal hasta Ia edad de 2 a 3 meses, cuando venlan dolores c#{243}licos, generalmente durante o luego despu#{233}s de comer, y los ex#{225}menes revelaron un coraz#{243}n ensanchado, pero no cianosis ni murmullos. El ensanchamiento es debido a Ia dilataci#{243}n del ventrIculo izquierdo, lo que se puede ver mejor por medio de un examen fluorosc#{243}pico en la vista oblicua anterior izquierda. En esta vista el conducto de aflujo del ventrIculo izquierda se ye definitivamente ensanchado, y no importa cuanta giraci#{243}n se Ic d#{233}al paciente, es difIcil que el ventrIculo izquierdo aclare Ia espina. En algunos casos, una dilataci#{243}n aneurismal del ventriculo izquierdo tiene lugar, y el EEG muestra complejos QRS de baja amplitud e inversion de las ondas T, pero no una desviaci#{243}n del axis. Este sindrome se puede diferenciar de todas las otras condiciones que causan ensanchamiento cardiaco en la infancia por los criterios presentados.

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1949;4;498

Pediatrics

BENJAMIN M. GASUL and ERNST LOEFFLER

Four Cases

PULMONARY ARTERY (BLAND-WHITE-GARLAND SYNDROME): Report of