Extrapulmonic Stenosis of the Pulmonary VeinsBY JAY BERNSTEIN, M.D., ANTHONY C. NOLKE, M.D., AND JOSEPH 0. REED, M.D.

PULMONARY venous stenosis is a rarecondition. A case combining unilateral

stenosis and atresia was included by Ferenezand Dammann' in a series of congenital ab-normalities associated with pulmonary venousobstruction. The abnormality occurred in achild who developed severe recurrent hemop-tysis at 11/2 years of age and thereafter suf-fered from progressive dyspnea and orthop-nea. The patient exhibited right heart failurewith pulmonary arterial hypertension. Deathoccurred at the age of 21/2 years. Post-mortem examination disclosed atresia of thevein from the lower lobe and stenosis of thevein from the left upper lobe; the right pul-monary veins were normal. Arteriolar sclero-sis was restricted to the left lung.

Bilateral obstruction was reported by Reye2in the case of an 8-year-old girl, who wasthought to have had congenital heart diseaseand who terminally developed right heartfailure. She had stenosis of the veins fromthe left upper and lower and the right lowerlobes. The vein from the right upper lobewas atretic.The only comparable cases encountered in

a review of the literature were those reportedby Aust,3 Romberg,3 Posselt,4 and Hart5 as" primary" pulmonary arteriosclerosis. Inthese 4 cases in young adults, pulmonaryarteriosclerosis was associated with diminu-tion in caliber of the pulmonary veins andhypoplasia of the left side of the heart. BothPosselt and Hart thought that the venousabnormality was congenital, and Posselt at-tributed it to a form of fetal endocarditis. Theonset of the disease in adult life would leadus to suspect, however, that the hypoplasia ofthe left ventricle and aorta and possibly theapparent constriction of the pulmonary veins

From the Children 's Hospital of Michigan andWayne State University College of Medicine, Detroit,Mich.

891

were only relative to marked hypertrophy anddilatation of the right ventricle and dilatationof the pulmonary artery.

In the case reported below, marked con-striction of all the pulmonary veins appearedto be the primary factor in the developmentof severe pulmonary arterial hypertension.

CASE REPORTThe patient was a 6-year-old Negro boy ad-

mitted to Children's Hospital of Michigan becauseof recurrent hemoptysis.During the first 4 years of life the child had

occasional respiratory infections. At 4 years ofage a chest roentgenogram revealed cardiac en-largement and an electrocardiogram right ven-tricular hypertrophy. Later the child had repeatedepisodes of hemoptysis, which became progres-sively more severe and for which he was hospital-ized. Angiocardiographic studies showed dilata-tion of the pulmonary artery and its majorbranches but no evidence of cardiovascular mal-formation (fig. 1). Bronchoscopic examination wasinitially negative, but on subsequent examinationvery hyperemic, "granulomatous" tissue was seenpartially occluding the right upper lobe bronchus.A thoracotomy was undertaken and abnormallyvigorous pulsations were present in the azygosand intercostal veins. A faint thrill, which couldbe obliterated by occluding the pulmonary artery,was present in the right upper lobe. This lobewas firmer than the others and was resected. Path-ologic examination of the specimen revealed ex-tensive arterial and venous thrombosis in varyingstages of organization.At 6 years of age, when he was readmitted be-

cause of increasing dyspnea, fatigue, and fever, hewas slightly cyanotic with tachypnea and mod-erate dyspnea. Venous distention was present inthe neck. Rales were heard and breath soundswere decreased in the left upper chest. The bloodpressure was 100/40 mm. Hg and the pulse rate144 per minute. A rumbling systolic and a softdiastolic murmur were heard at the apex. Thepulmonary second sound was booming in charac-ter. A continuous hum was heard to the right ofthe sternum in the second intercostal space. Theliver was felt 5 to 6 cm. below the costal marginin the right midelavicular line. It was smooth,firm, and quite tender. Laboratory data includeda hemoglobin of 9.4 Gm. per 100 ml. and a red

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8 2ERNSTEIN, NOLKE, REED)

FIG. 1. A. Posteroaanterior film, just prior to onsetof illness, showinig a relamtively niorlal helart size ithimioriiial pulmonary vaseularity and clear lungs. B'.

Angiocardiograiii demlonst rating imarked dilatation of

tIme miflin pulmonary artery and the hilar I)ranclles.Other filams ini study show ed Ilorilmal peripiciral vatscti-

larity.

blood( cell e((uIlt of 3,080,000 per mimiii. A roent-genogramii of the chest revealed furtimer enllarge-Inent of the heart (11.3/18.8 cm.), rather markedproinimlence of the pulmonary artery seginent along,the left sternal border, vascular congestion of bothlungs, and parenelhyiial infiltration of the leftupper lobe. An eleetrocardiogram revealed a

marked increase in time right vemitricular hyper-trophy pattern and nonspeeific umyoc.ardia.l chamiges.

The patient was pllaced in oxyvemn and treatedwith digitalis anmd antibiotics. His temperaturestabilized betweemi 99 ammiid 100 F. orally, his heart

rlate fell to 86 to 92 per minute, and the liver wasl1( longer palpa)Ibl(e. He was more comfortable,Ivut his cough was occasiolly productive of con-si(lerable amounts of briglht0l(1 blood. Approxi-mnatelv 1 month. after admission hie suddenly\ de-veloped marked left alnterior chest painl, rapidlrising temiiperature, profuse dyiapioresis, cyalalsis,.ai1d tachypnea. The patient died four hours afttethe onset of these symptoms.

lAt postmiiorteiii examination the heart was

greatly enlarged aCind weighled 2S0 G']iln. (nior.iaalweight approxiiimately 95 Gmi.). The rihlit atriumi1.anld ventricle were grealy dilated an(ld hypertr o

phied. The pulimmonary artery was wide anid pre-sented atheromima tons plafques on its intinial suiffa((.There was dilatatioi of thie left side of the hea itin association with. sliglht ventricular hypertrophv,aiid a iiaoderatelv severe de-ree of endoeardialsclerosis was l)iesent in the left atrium. There wasnO evidnce, grossxly or. microscopically, of m11uralth roiimbosis to a ccount for the endocardial thick-(lmiingo. The 3 reimiaining piliiioimarii'v veins were(steiiotie at their respective junctions with the leftatrium. Onl the left, the 2 veiiis entere(l sepa-Ima-tely', tand the lumen mif each was only 1 to 2 lain.ill dialleter (ftig. 2B) . The atrial endocardiuna round the veimous orifices was greatly thickened,anid there was iimarked imtimial sclerosis of tile veins.On the right, the '(^iii from the uipper lobe hadbeen ligated ws-hen the lobe was reiiioved, and thevein fromt the lower lobe was both stenotie and1artiallv occluded by an organizing thronibusfig. 21). The thiromabus appearel to hlave re-

stilted fronl the ligation(of nd marked prolifera-tive reIatiomi aroumnd tile stumipm1) of the upper vein.i\[i(croscopic examiiinatioil of the heart rrevealed, inalditioii to mlvoemi rdial lhv-pertrol)lphy, a very slighitvenltricular infiltrate of 11mononuclear cells, ilnsuf-ficient to warramIt the dianglosis of nivocarditis.There were, however, plroilenllt intimilal fibrosisand nioderate medial hypertrophv of the branchelsof both coronary arteries. There was no obviousrelationship betweemi the changes ill the coronaryarteries and those iii the left atrium, unless bothwere the result (f (a cOilllisio iilfla.iiimiitol plr)ocess.The ventri(ula r enldocar(liuill, on tile otheer hand,ws only mlliiliiii.lvN thickeiled.

Tile lulllinonlaiy changes were striking, cllad lmlostpronlinemlt aimlonlo themwiwere innlllumerable arterialthronibi in all stages of orgailization and recanali-zation. Tile large arteries coImtaiileld grossly vis-ible, usuially wllite thromlbi, whillh partially oc-

(luded the luimina; the lumina (listal to the throllibiwere frequently dilated. Tlme thriombi extendedinto the smallest vessels (fig. 3A ) .cand were .asso-ciated with focal necrosis ami(d irTegular areas ofheiorrlhage .ald( o(rgaizingi pii(euiiioniitis. The de-gree of eonimective tissue plroliferation exceeded

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EXTRAPULA()NIC PULMONARY STENOSIS

FIG. 2. Stenosis of the pulmonary eillns .at their junction wvith the left atrium: A. Rightlowerci ini admits oildy fine needle; oeclusion of upper vein and advIentitial fibrosis second(larto surgical ligaltioni. 73. Localized constriction in left uippr eia a(llittiag bllack thread.

that uisulally seeii inpulilama cv itaretioii, but thereactioni was conspicuousl and. It ws appa-eat iiiieroscopia.llvxr that some of the throinbosedVessels were veilis ( 3C. 3e) and ill a few areasthere weren(ecosis antid iniflaiiiiiiatorv\ cell infiltra-tim)ii of arterial walls (hfig. 31)). Extreme1l (lillatelrojiithial vessels, a pproximna tinig varices, a1)l)iicre(1

to rep)r(seint ollateral iilatioii, 81d(1 the bron-(hail a rteries laid thickened walls (fig. 3E, l).Noe(xtral(iiliiOliii SOurcle ot emibl)i~li w'as touiiid,, :indthe inflamimaatory arterial changes are regar-dedis hypertensive. Intiliaal Wclerois was l)resenlt illthea(rter'iles a 11(1n eie(lleme to be (leilltigood iieas-urc to the recaaliizatiii ()t tllr()bi ( tg. 3.1).A1Iedial1 livpertlropllv of tine Simall vessels existed1)()tll tog)etlher with and apart from the intiiiialfib)rosi;s (lih. 3B).

Il suIilllal v, there was extrapulmollic stellosist the pouliolililal Veilns, ill asslialtioIl with pulniii-narv a sclerosis alnd pulmiionari arteriala i(1 venous throibshrkis. A marked de-ree of corl)puliiiinale was p(resenit and(l was associated withhvpem(lte lia-ie pulnoizlllar alitoiliti-.

1scusstIo.I)ISCUISSION

Strutictural alterations in the pulmonaryv-ascular system are eominionlv associated withand(l attribllted to sufficiently- prolonged and(se'velre obstruction to the flow of blood fronithe lugs thoughl the left side of the heart.ross (lilatati(oI alnd sclosis4 a 11(1l licO

s(ol)ic alter ation"'3 of the plulinonar- artericshave logl) ein rc(cog) iiizc(d( as an aecompani-menit of acqiliid(l mitral and as early

aslX )'?7 Atosc(coxvitz'siiil7(1 out hypertciisioii of the lesser circulation as the factor'common1 to (ases of piulmonar- arteriosclerosisa.ssoc.iated with both ol)struc.tiv e lesions iieither the heart or lungs and vascular slniitsin either the heart or great vessels. Congenitalmitral stenosis,' cor triatriatum with stenosisof either the (conini1lon0 Pulmonary veilmi or

illtral)ullioiaiv veins; constrictive enldo(ar -

dial sclerosis,'0 tuniLors of the left attrimiia,'and extrillsic) pressure (o the lpulmlmonaryvciiism have all ilecel related to the develop-meat of pulmlioniary arterial and arteriolarSclerosis.

Ini the case of acquire(l mitral stetiosis sOnicevidenc( e has been offered that the extemlt ofthe vascular changes in the lungs correlateswith the severity of the obstrllction at themitral valve13 and the dulraitioln4 and de-gree v', 16 of pulhuonary hypertension, and thatsevere hypertension may lead to vascularnleerosis in the lun1gs11 S13 17-20 Other evidence,both ciniiopathologic and experimental,"'has been adduced to show that increased rc-s istance an(1 pressure are due to reversiblev'as(@cular spa1sm, and that aniatomic changesill the pulmonary vessels are largely the resultof thromboemnbolicphiehnomena, eveni im asso-

ciation with ol)str'uctioii of the palimonaryvenllous flow.

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BERNSTEIN, NOLKE, REED

w-t~ nw-4. _;

FIG. 3. A. Intimal fibrosis in arterioles and small pulmonary arteries. Verhoeff elastinstain. B. Medial hypertrophy or muscularization of arterioles. Verhoeff elastin stain. C.Organizing arterial (left) and venous (right) thrombosis; intervening area of chronic inflam-mation and fibrosis. Hematoxylin and eosin stain. D. Acute arteritis with inflammatory cellinfiltrate in wall. Heiniatoxyliin and eosin stain. E. Dilated, thick-walled vessels in bronchialmucosa. Hemiatoxylin and eosin stain. F. VcnOus varices il bronchial wall. Mallory anilineblue stain.

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The alterations in arterioles and smallarteries are generally compounded of medialhypertrophy and intimal fibrosis or prolifera-tion. The former may reasonably be attributedto increased vascular tension, and althoughthe problem of persistence of fetal vascularstructure need not concern us here there seemsto be ample evidence for muscularization ofarterioles and medial hypertrophy in responseto obstruction of the pulmonary venousfloW.15' 23, 24 Intimal fibrosis in the smallervessels has also been regarded as a conse-quence of pulmonary hypertension.15' 24 In thecase reported herein, the intimal thickeningis irregular and seems to have arisen at leastin part from thrombosis and recanalizationof the smaller vessels. The presence of suchwidespread thrombosis is regarded as a directcomplication of hypertension and vascularsclerosis, possibly mediated by an arteritis,rather than as an embolic phenomenon.The development of arteritis in this case

must be regarded as the consequence of hy-pertension. Inflammatory lesions occurred in-dependently of thrombi, although they mayhave preceded them. In several areas thereappeared to be a healing or healed arteritis,but "fibrinoid" necrosis of the very smallvessels was not seen.The venous thrombi present an unusual

complication that is not easily explained.Previously described instances of pulmonaryvenous thrombosis in association with pul-monary thrombophlebitis25 and primary vas-cular sclerosis,26 or as an anatomic finding ininfants dying unexpectedly27 offer little to theunderstanding of this case. In the case re-ported by Schonlebe28 of a 4-month-oldchild with endocardial sclerosis and pulmo-nary venous thrombosis there were alsotransposition of the great vessels, pulmonicstenosis, and an interventricular septaldefect. It is possible that the venous thrombo-sis in our case may have been enhanced bystasis due to obstruction at both ends-arterialthrombosis and venous stenosis-but there isno direct evidence to support this view. Thealternate supposition that venous thrombosisled to phlebosclerosis and constriction doesnot make the case any more plausible or less

unique. In the case of a young child who de-veloped diffuse interstitial fibrosis of thelungs during infancy, reported by Diamond29as a case of Hamman-Rich syndrome, therewere extreme constriction of the pulmonaryartery and vein and severe arteriolar sclerosisin one lung. Complete constriction of the pul-monary vein was present at its junction withthe left atrium, and because of the inflamma-tory process in the lungs and the hilar adven-titial tissue the abnormality of the vesselswas attributed to inflammation and scarringrather than to a congenital malformation.More than a slight degree of pulmonary in-flammation was not seen in our case andsignificant scarring in the hilar structureswas limited to the stump of the right upperlobe vein.More satisfactory is the view that the

venous stenosis, uncommon as it might be, wasthe primary factor in the development of pul-monary hypertension and vascular disease.The 2 cases cited above" 2 combined stenosisand atresia, indicating that the abnormalitywas a congenital malformation. Despite theage of the patient and the relatively late onsetof symptoms in our case, the abnormalitymight still be regarded as congenital. Theclinical course suggests that it may have beenprogressive, and possibly it bore some rela-tionship to the endocardial sclerosis of theleft atrium and to the intimal changes inthe branches of the coronary arteries. How-ever, as commonly as we see involvement ofthe left atrial endocardium in both primaryand secondary endocardial sclerosis we havenot seen it associated with pulmonary venousstenosis in either reported30 or observed cases.Indirect evidence in support of venous ob-struction was the early development of ex-tensive collateral circulation. Hemoptysis, theinitial complaint, appears to have been dueto bleeding from bronchial mucosal varices, acondition similar to that seen in acquiredmitral stenosis.3' At the time of the pulmo-nary resection there were abnormally dilated,pulsating azygos veins. Arterial and venousthrombosis was seen in the resected portionof lung, but the initial cause of venous ob-struction could not be determined.

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BERNSTEIN, NOLKE, REED

SUMMARYA case is reported of a 6-year-old boy who

had developed pulmonary hypertension be-cause of obstruction to the pulmonary venousflow by severe stenosis of the pulmonary veinsat their junction with the left atrium. Thedevelopment of collateral circulation throughthe bronchial vessels led to early, severehemoptysis. The course was complicated bythe development of pulmonary arterial andvenous thrombi and hypertensive arteritis.

ACKNOWLEDGMENTThe authors are indebted to Mr. Charles L.

Zinser for the photographs and photomicrographs.

SUMMARIO IN INTERLINGUAEs reportate le easo de un puero de 6 annos

de etate qui habeva disveloppate hypertensionpulmonar in consequentia de obstruction delfluxo pulmono-venose per sever grados destenosis del venas pulmonlar al sito de lorjunction con le atrio sinistre. Le disveloppa-mento de un circulation collateral via le vasos

bronchial resultava tosto in sever hemoptysis.Le curso clinic del easo esseva complicate per

le disveloppamento de thrombos pulmono-arterial e -venose e arteritis hypertensive.

REFERENCES1. FERENCE, C., AND DAMMANN, F. J., JR.: Sig-

nificance of the pulmonary vascular bed incongenital heart disease. V. Lesions of theleft side of the heart causing obstruction ofthe pulmonary venous return. Circulation16: 1046, 1957.

2. REYE, R. D. K.: Congenital stenosis of thepulmonary veins in their extrapulmonarycourse. M. J. Australia 1: 801, 1951.

3. AUST, C.: Muinchen med. Wchnschr., 1892;ROMBERG, E.: Deutsches Arch. klin. Med.,1891. Cited by Posselt.'

4. POSSELT, A.: Die klinische Diagnose der pul-monal Arteriensklerose. Volkmann's Samm-lung klinischer VortrAge. Leipzig, 1908, pp.361-474.

5. HART, C.: Ueber die isolierte Sklerose derPulmonalarterie. Klin. Wchnschr. 53: 304,1916.

6. PARKER, F., JR., AND WEISS, S.: The natureand significance of the structural changesin the lungs in mitral stenosis. Am. J. Path.12: 573, 1936.

7. MOSCHCOWITZ, E.: Hypertension of the pulino-

nary circulation. Am. J. M. Sc. 174: 388,1927.

8. EDWARDS, J. E., DUSHANE, J. W., ALCOTT,D. L., AND BURCHELL, H. B.: Thoracic ve-nous anomalies: IV. Stenosis of the com-mon pulmonary vein (cor triatriatum)(case 4.). Arch. Path. 51: 446, 1951.

9. BECU, L. M., TAUXE, W. N., DUSHANE, J. W.,AND EDWARDS, J. E.: Anomalous connec-tion of pulmonary veins with normal pul-monary venous drainage. Arch. Path. 59:463, 1955.

10. EDWARDS, J. E.: Differential diagnosis of mi-tral stenosis: A clinicopathologic review ofsimulating conditions. Lab. Invest. 3: 89,1954.

11. BLOCK, W. J., PARKER, R. L., AND EDWARDS,J. E.: Cardiac Clinics, CXXXIX. "Myx-oma" of the left atrium clinically simu-lating mitral stenosis: Report of case andpathologic studies. Proc. Staff Meet., MayoClin. 27: 361, 1952.

12. EDWARDS, J. E., AND BURCHELL, H. B.: Multi-lobar pulmonary venous obstruction withpulmonary hypertension: "Protective" arte-rial lesions in involved lobes. Arch. Int.Med. 87: 372, 1951.

13. SPAIN, D.: Necrotizing and healing pulmonaryarteritis with advanced mitral stenosis. Arch.Path. 62: 489, 1956.

14. CLOWES, G. H. A., JR., HACKEL, D. B., MUEL-LER, R. P., AND GILLESPIE, D. G.: Relation-ship of pulmonary function and pathologicchanges in mitral stenosis. Arch. Surg. 67:244, 1953.

15. HEATH, D., AND WHITAKER, W.: The pulmo-nary vessels in mitral stenosis. J. Path. &Bact. 70: 291, 1955.

16. DENST, J., EDWARDS, A., NEUBERGER, K. T.,AND BLOUNT, S. G.: Biopsies of the lungand atrial appendages in mitral stenosis:Correlation of data from cardiac catheteri-zation with pulmonary vascular lesions. Am.Heart J. 48: 506, 1954.

17. BRAUNSTEIN, H.: Periarteritis nodosa limitedto the pulmonary circulation. Am. J. Path.31: 837, 1955.

18. HICKS, J. D.: Acute arterial necrosis in thelungs. J. Path. & Bact. 65: 333, 1953.

19. SYMMERS, W. ST.C.: Necrotizing pulmonaryarteriopathy associated with pulmonary hy-pertension. J. Clin. Path. 5: 36, 1952.

20. WEITZMAN, D., AND HUSAIN, 0. A. N.: Pul-monary haemosiderosis in mitral stenosis:Report of a case with pulmonary arteriolarnecrosis. Brit. J. Tuberc. 46: 231, 1952.

21. THOMAS, W. A., LEE, K. T., RABINS, E. R.,AND O'NEAL, R. M.: Mitral stenosis and

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pulmonary arteriosclerosis. Arch. Path. 62:257, 1956.

22. JAQUES, W. E., AND HYMAN, A. L.: Experi-mental supravalvular mitral stenosis in thedog. Arch. Path. 64: 67, 1957.

23. HENRY, E. W.: The small pulmonary vesselsin mitral stenosis. Brit. Heart J. 14: 406,1952.

24. LARRABEE, W. F., PARKER, R. L., AND ED-WARDS, J. E.: Pathology of intrapulmonaryarteries and arterioles in mitral stenosis.Proc. Staff Meet., Mayo Clin. 24: 316, 1949.

25. SPAIN, D. M., AND MOSES, J. B.: Thrombosisand embolism of the pulmonary vessels with.special reference to pulmonary vein throm-bosis. Am. J. M. Se. 212: 707, 1946.

26. EPPINGER, H., AND WAGNER, R.: Zur Patholo.gie der Lunge. Wien. Arch. f. inn. Med. 1:83, 1920.

27. EMERY, J. L.: Pulmonary thrombosis and itsassociation with unexpected death in child-hood. Arch. Dis. Child. 28: 187, 1953.

28. SCHONLEBE, H.: Cber Gefisswandschiidigun-gen des Lungenkreislaufes bei fetaler undfriihkindlicher Endokarditis. Virchow's Arch.path. Anat. 304: 527, 1939.

29. DIAMOND, I.: The Hamman-Rich syndromein childhood: Report of a case with unilat-eral pulmonary arterial and venous stenosisand atriovenous occlusion. Pediatrics 22:279, 1958.

30. CRAIG, J. M.: Congenital endocardial sclero-sis. Internat. A. M. Museums Bull. 30: 15,1949.

31. FERGUSON, F. C., KOBLAIK, R. E., AND DEI-TRICK., J. F.: Varices of the bronchial veinsas a source of hemoptysis in mitral stenosis.Am. Heart J. 28: 445, 1944.

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Thomas, C. B., and Murphy, E. A.: Further Studies on Cholesterol Levels in the JohnsHopkins Medical Students: The Effect of Stress at Examinations. J. Chron. Dis 8:661(Dec.), 1958.In a study of the effects of stress on serum cholesterol levels, the serum cholesterol,

total circulating eosinophils, body weight, blood pressure, and heart rate were meas-ured at 3 different periods that were associated with varying degrees of stress. Thefirst set of data was collected 3 weeks after starting the first year course in ana-tomy, the second set at the time of the final examination period in anatomy whichwas felt to be the period of maximal stress, and the final set of data was col-lected at a varying interval after the anatomy examination period at the convenienceof the subject. Subjects were 52 male first-year medical students. The highest meancholesterol value was found to occur at the time of the anatomy examination. It was225.7 mg./100 ml. It was significantly greater than the value of 204.7 mg./100 ml.found at the examination made at random with presumably little stress. The meancholesterol level of 224.4 mg./100 ml. found 3 weeks after starting medical school wasnot significantly lower than the value at the time of the anatomy examination. Themean eosinophil count at the time anatomy examination was 97 par cm.3 while at thetime of the third or random examination the mean was 129 per cm.,3 which was thoughtto be a significant difference. The measurements of pulse rate and systolic and diastolicblood pressures showed a significant difference only in the measurement of the diastolicblood pressure, which was highest at the time of the anatomy examination, nexthighest at the time of the initial examination, and lowest at the time of the randomexamination. Variations in body weight were effectively excluded as a cause forvariation in cholesterol levels.

MAXWELL

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JAY BERNSTEIN, ANTHONY C. NOLKE and JOSEPH O. REEDExtrapulmonic Stenosis of the Pulmonary Veins

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1959 American Heart Association, Inc. All rights reserved.

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