Vertebral Grand LarcenyBy MARVIN L. DAVES, M.D., AND ALBERT TREGER, M.D.

THE "subelavian steal" is a clinical syn-drome that has been described only re-

cently.1-10 Patients so afflicted are usually eld-erly, with an atherosclerotic plaque blockingthe left subclavian artery between the aorticarch and the origin of the left vertebral artery.The left vertebral artery carries blood in retro-grade fashion, siphoning part of the brain'ssupply from the circle of Willis to fulfill thedemands of the left arm. With the stimulus ofexercise of the left arm, these patients maybecome syncopal. This syndrome focuses at-tention on the vertebral arterial confluence asa collateral pathway in patients with periph-eral vascular disease.An infant in whom retrograde flow of the

left vertebral artery supplied blood to the leftarm, the trunk, and the lower extremities, andto some extent the lungs, made us aware of thepossible importance of this pathway in pa-tients with congenital obstructive lesions ofthe aortic arch.

Case ReportF.G., CGH no. 189642. was the product of an

uneventful gestation and delivery and appeared tobe a normal 5 lb., 81/2 oz. infant at birth. At the ageof 1 month, vomiting and cyanosis were firstnoted. He was treated at another hospital forpneumonia and congestive failure. When he failedto respond, he was transferred to this hospital atage 3 months.The remarkable physical findings were absent

femoral and left brachial pulses with a boundingright brachial pulse. The liver was down twofingerbreadths below the costal margin and thespleen was down one fingerbreadth. Palpation ofthe precordium revealed a lift and thrust of rightventricle and a faint systolic thrill along the leftsternal border, felt best at the fourth right inter-costal space. Auscultation revealed a loud, split,second heart sound, the second component being

From the Departments of Radiology and Medicine(Division of Cardiology), University of Colorado Med-ical Center, Denver, Colorado.

Supported by General Research Support Grants 21and 91, Institutional grants from the U. S. PublicHealth Service.

Circulation, Volume XXIX, June 1964

louder than the first. A third heart sound washeard at the apex. There was a grade-IV/VI harshpansystolic murmur heard all over the precordiumbut loudest at the third and fourth intercostalspaces. The infant's color was described as normal,dusky, or cyanotic by various observers andseemed to fluctuate with the degree of respiratorydistress. (Clinically and radiographically, varyingdegrees of pneumonia and atelectasis were presentthroughout the hospital course.) No difference incolor was evident in comparing the upper andlower body.

Plain films of the chest revealed moderate gen-eralized cardiomegaly and increased pulmonaryvascularity, in addition to the pulmonary changesalready mentioned. Reneated electrocardiogramsshowed sinus tachycardia, probable left atrial en-largement, biventricular enlargement, and rightaxis deviation. An electroencephalogram was notdone. Cardiac catheterization demonstrated posi-tive hydrogen curves in the pulmonary artery andright ventricle and a negative curve in the rightatrium. Pulmonary artery pressure was 60 to 82/45 mm. Hg and femoral artery pressure was 70 to75/50 mm. Hg. Oxygen saturation in volumes percent was as follows: mid right atrium 3.85, out-flow of right ventricle 7.11, pulmonary artery 9.39,femoral artery 11.03. Pulmonary flow measuredfive times systemic flow and pulmonary resistanceat rest was 340 dynes sec. cm.-5 M2. Left-to-rightshunts at the level of the right ventricle and pul-monary artery confirmed the clinical impression ofventricular septal defect and patent ductus arterio-sus, and a retrograde right brachial arteriogramwas performed to outline the clinically apparentaortic coarctation (fig. 1). Evident from this studywas the fact that circulation reached the descend-ing aorta via an ascending route to the basilarartery and circle of Willis through the right verte-bral and right (and perhaps left) carotid arteriesand thence by retrograde flow down the left ver-tebral artery to the left subelavian artery. The ori-gin of the latter was unusually low on the aorta.There was bidirectional flow in the left subclavianartery: toward the arm distal to the vertebral ori-gin and toward the aorta proximal thereto. Someof the contrast medium that reached the aorta inthis way shunted left to right through the patentductus arteriosus, demonstrating the pulmonaryartery. Apparently the coarctation completely ob-structed the aorta proximal to the origin of the leftsubelavian artery.

Early in the fourth month the patent ductus ar-teriosus was ligated. No vestige of aorta was noted

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9DAN7I\S, TJIV(;VLi

Figuire 1

Infawtile utr^tcl)rtil ---giand laiceuiy." Rig/it bratilial ar-

tlry inbjectionl. Top. The rig/t. subcl/avianiland rig/t ycr-

te>bral arteries are filled an1d a little contiast -?niet1inoi is

ctid/tnt in the rig,lit commont car.otid artery. Earlti col-

lateral fillitng is present. Centce. Contrast material lins

immediately prioxirnal to the dluctus. Banding ofthe maimi ptulmonai-v aiteoyv failed to dlecrease p1-es-sure distal to the I)an(l. W7hile the band wvas beingadutistedl, cadiac rii.iest entsel ati the patient(lied, despite attemipts at I esxisu-itatioii. At autopsythe lilated pateit diue.tiis ai tci io.s .1n1 ventrioilar septail dlefect were conefirmed. Th bandedptilmil-oiiaiV airteriywas lar-ge. \ nornmal ascenldiligaorta gave origiii to inni-omionaite ancd left common1carotid 'vessels buit \as totally al)senit fi rm thispoin-t to the rather lost letel off (oigini of the lefts1ubelavianll iI-tei-v.

Diseussion1in essence, this ease represented a precdictal

or infantile coarctation. Comiplicating factorswere the ventricular spetal defect and agene-sis of the aortic isthmtus. Two uniuisuial featiureswere the low\ piilmonary resistaince that per-mitted left-to-right flox through,l] the diuctilsdespite the preduictal position of the aorticobstruction and maintenance of systemic cir-ctilation (all bitt the right arm and the head)via retro)grade left vertebral arterial flow.

Roberts et al."' bave suimimiarized 55 re-ported cases of coimiplete interruption of theaortic ar-eh. In. at leatst 32 of these, the obstrue-tionl xx as proximal to the origin of the left stilu-clavian artery. All siich1 cases bave a patentduictus arteriosus and constituite a form of pre-dtuetal or infantile coaretation of the aorta. Thelarge series of reported cases of prediuctal co-arctations that ste were able to find uisuially failto mention the positioni of the left suibclavianartery. In view of the anatomy encoulntered inRoberts' series, it seems likely that a significantnumber of patients wilth prediuctal coaretationwould have a congenital collateral pathway tothe descending aortaxvia the vertebral arterialconflluec(c.Edwards et al.12 oricginally hxpothebsized that

the compatibilitv of isthimuis obstruction witlnormail fetal eircillationxvs. the necessitv for

g,one upj i/it rightlt itt )11arl 1. (olottn the left, a7n1dfills the pnroxina left1 s1ob1 tio ark ip. Collateroalts-scis from on(t? tloiyroe rtiwal trunk to i/h other a(lt seene ros.sitn, i/c midlinfe antila rih/ collateral netu ork veert/ie rigt, ulpjt lob)e from tiit' t/iiroeei ic atId costo-eerciali triizks is ut iiiniii to fill a ilar-1)iogllbrlloial ai-terl. Bottom. Five-eighths second lnfr, the 1)bronieh1 ialco/llaftratl i/it t/est(tin oaOrtai. tzii tl/ Y7loiiairq (or-tenr, are wecll dernonsttt ed. Jh potent dItietus arterio-sts Cinlbieb set in tde simultari ous lateral projection.

(n1' 'li/i;o I 'oh,ime \X\I, it I904

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VERTEBRAL GRAND LARCENY

development in utero of collateral circulationto the descending aorta in patients with post-ductal coarctation constituted a reason for thegraver prognosis of the isthmus defect. It isobvious that in evaluation of this hypothesis,the position of the left subelavian artery rela-tive to the obstruction must henceforth beconsidered.North et al.2 have indicated five collateral

pathways to the left subelavian artery fromright brachiocephalic vessels including thevertebral confluence. In our enthusiasm for"vertebral grand larceny" we should not failto emphasize that all these pathways may playa part in our patient's collateral circulation.The angiogram demonstrates the vertebral-vertebral communication and a network of in-tercommunications between branches of thethyrocervical trunks. In addition, the area ofthe right upper chest demonstrates a rich net-work of vessels from the right subelavian ar-tery reaching the descending aorta via a largebronchial artery. Paradoxically, the congenitalcollateral pathway that one would expect tobe well developed is not seen in our patient-or at least not on the angiogram-namely, theinternal mammary, superior epigastric, inferiorepigastric, and external iliac circuit. At anyrate, the sum of these collateral pathways wasable to maintain a pressure in the descendingaorta in excess of the elevated pulmonary ar-tery pressure. This situation is not unusual inpatients with preductal coarctation. The ab-sence of arterial pulsation in the lower bodyreflects the lack of a systolic thrust and doesnot necessarily indicate a low mean pressure.The importance of a reasonably normal meandescending aortic pressure is the possibility ofa left-to-right shunt through the ductus despiteits postcoarctation position. Therefore, in the-orizing on the etiology of pulmonary hyper-tension and pulmonary arterial changes in pa-tients with preductal as opposed to postductalcoarctation, it is not reasonable to assume aright-to-left shunt through the ductus. Thepressures during life in .the descending aortaand the pulmonary artery and the exact natureof the collateral pathways should be estab-lished. A detailed discussion of this facet is

Circulation, Volume XXIX, June 1964

beyond the scope of this paper but constitutesa continuing subject of investigation in thisinstitution.

SummaryA case is presented of atresia of the aortic

arch between the left common carotid arteryproximally and the left subelavian artery anda patent ductus arteriosus distally. Collateralcirculation including a pathway via the verte-bral arteries maintained an adequate meanpressure in the descending aorta to produce aleft-to-right shunt in the patent ductus, de-spite an elevated pulmonary arterial pressure.

References1. REIVICH, M., HOLLING, H. E., ROBERTS, B., AND

TOOLE, J. F.: Reversal of blood flow through thevertebral artery and its effect on cerebral circu-lation. New England J. Med. 265: 878, 1961.

2. NORTH, R. R., FIELDS, W. S., DE BAKEY, M. E.,AND CRAWFORD, E. S.: Brachial-basilar insuffi-ciency syndrome. Neurology 12: 810, 1962.

3. SIMON, M., RABINOV, K., AND HORENSTEIN, S.:Proximal subelavian artery occlusion and re-

versed vertebral blood flow to the arm. Clin.Radiol. 13: 201, 1962.

4. MANNICK, J. A., SUTER, G. G., AND HUME, D. M.:The "subelavian steal" syndrome: A furtherdocumentation. J.A.M.A. 182: 254, 1962.

5. WILLIAMS, C. L., SCOTT, S. M., AND TAKARO, T.:Subclavian steal. Circulation 28: 14, 1963.

6. SPROUL, G.: Basilar artery insufficiency secondaryto obstruction of left subelavian artery. Circula-tion 28: 259, 1963.

7. BOSNIAK, M. A.: A collateral pathway through thevertebral arteries associated with obstruction ofthe innominate and proximal subclavian arter-

ies. Radiology 81: 89, 1983.8. STEINBERG, I., AND HALPERN, M.: Roentgen mani-

festations of the subelavian steal syndrome. Am.J. Roentgenol. 90: 528, 1983.

9. FISCHER, M. J., AND MATTEY, W. E.: The sub-clavian steal syndrome. Am. J. Roentgenol. 90:

532, 1963.10. AsHBY, R. N., KARRAS, B. G., AND CANNON, A. H.:

Clinical and roentgenographic aspects of the

subelavian steal syndrome. Am. J. Roentgenol.90: 535, 1963.

11. ROBERTS, W. C., MosRow, A. G., AND BRAUN-WALD, E.: Complete interruption of the aorticarch. Circulation 26: 39, 1962.

12. EDWARDS, J. E., DOUGLAS, J. M., BURCHELL, H. B.,AND CHRISTENSEN, N. A.: Pathology of the in-trapulmonary arteries and arterioles in coarcta-tion of the aorta associated with patent ductusarteriosus. Am. Heart J. 38: 205, 1949.

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MARVIN L. DAVES and ALBERT TREGERVertebral Grand Larceny

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1964 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Circulation doi: 10.1161/01.CIR.29.6.911

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