Anomalous Origin of the Coronary Arteries

in Two Calves*by R. P. Botts, D.V.M., M.P.H.; L. D. Kintner, D.V.M., M.S.**

ABSTRACTAnomalities of the coronary arteries may

include one or more of the following varia-tions: abnormal number, abnormal course, orabnormal origin. Many of these anomalieshave been described in man.'281 Anomalousorigin of the left coronary artery from thepulmonary artery (A.O.L.C.A.) has been es-timated"9' to occur in one of 300,000 childrenand to represent approximately 0.5% of alltypes of congenital heart disease. In a recentreview'281 of these conditions in man, anoma-lous origin of the right coronary artery fromthe pulmonary artery (A.O.R.C.A.) had beenreported 16 times, A.O.L.C.A. 39 times, andanomalous origin of both coronary arteriesfrom the pulmonary artery (A.O.B.C.A.) 5times.A review of the available literature disclosed

12 reports (3,6,8,10,20,23,24,25,26,27,31 & 32) of anoma-

lies of the coronary arteries in animals. Fourof these reports (10, 20, 31 & 32) described A.O.R.C.A. in cattle. This review failed to discloseany accounts of A.O.B.C.A. in that species.The purpose of this paper is to describe thefindings of two cases of A.O.B.C.A. in cattle.

ObservationsCASE No. 1

The first case occurred in a three weekold male Aberdeen Angus calf which waspresented to the Department of VeterinaryPathology for routine postmortem examina-tion.The history obtained from the owner

was not contributory. The animal was in

*FroIm the Ecology Field and Training Station, HeartDisease Control Program, Public Health Service, U.S.Department of Health, Education and Welfare, Colum-bia, Missouri, and the Department of Physiology andPharmacology, School of Veterinary Medicine, Univer-sity of Missouri (Botts).**Department of Veterinary Pathology, School of Vet-erinary Medicine University of Missouri, Columbia(Kintner). The authors wish to acknowledge the as-sistance given to them by Dr. C. J. Bierschwall, Dr.R. C. McClure and Mr. J. D. Wallach.

fair condition and considered to be smallfor its age (weight approximately 23 Kg.).One liter of serous fluid was observed inthe abdominal cavity. The wall of the smallintestines was congested and blood waspresent in the lumen. The liver as well asthe lungs were congested. All other sys-tems were normal except the cardiovascularsystem.The nomenclature employed in this report

to describe the heart and great vessels isadopted from Preuss.21' External examina-tion of the heart disclosed the following: anenlarged heart, normal atria, and fibrosis ofthe epicardial surface of the apex. Theheart and great vessels were opened in theusual manner. Measurements of the heartand great vessels listed in Table 1 weretaken after the specimen was fixed in 10%formalin. The pulmonary veins and venaecavae were anatomically normal. The ductusarteriosus was closed, and the foramen ovalewas patent which is not unusual for an an-imal of this age. The tricuspid, mitral, pul-monary, and aortic valves were normal. Theendocardium of the left atrium and leftventricle was thickened and opaque.One coronary ostium was noted in the

wall of the pulmonary artery. This ostiumwas located behind the right cusp of thesemilunar valve near its junction withthe left cusp (Fig. 2). It measured 0.8 cm.in diameter and opened directly into a ves-sel 1 cm. in length which was directed tothe right and terminated in a bulbous struc-ture. Two large and one small vessel arosefrom this structure. The smaller vessel con-tinued to the right and descended into theinterventricular septum. The distributionof the two larger vessels corresponded tonormal (2 & 31) right and left coronary ar-teries.The left coronary artery measured 1.0 cm.

in circumference at its widest point. It con-tinued to the left between the aorta and

Vol. 28 -July, 1964 169

TABLE 1: Weight and Measurements of the Heart and Great Vessels

Case No. 1 Case No. 2

Weight of the heart (Pericardial sac removed) 415.0 Gm. 745.0 Gm.Thickness of the right ventricular wall (1 cm. from base). 0.7 cm. 1.1 cm.Thickness of the left ventricular wall (1 cm. from base) 1.5 cm. 1.8 cm.Circumference right A-V orifice ........ ................ 11.5 cm. 14.3 cm.Circumference left A-V orifice ......................... 12.2 cm. 15.9 cm.Pulmonary artery

Circumference (base of semilunar cusps) ............ 7.0 cm. 8.6 cm.Thickness of wall (1 cm. dorsal to semilunar cusps). 0.4 cm. 0.3 cm.

AortaCircumference (base of semilunar cusps) ............ 6.5 cm. 6.8 cm.Thickncss of wall (1 cm. dorsal to semilunar cusps) .. 0.6 cm. 0.5 cm.

Fig. 1. Photograph of the endocardial surface of theright ventricle and pulmonary artery of a 3 month oldcalf (Case 'No. 2) with anomalous origin of both coron-ary arteries. A probe is insertc'd in the ostium locatedin the wall of the pulmonary artery.

Fig. 3. Schematic drawing of the left lateral view ofthe heart of a 3 week old calf, (Case 1) with asnomalousorigin of both coronary arteries.

p.v,

D. S.

t.R.C.

C. R.R.C. '

Fig. 2. Schematic drawing of a cross-section through the Fig. 4. Schematic drawing of the right lateral view ofbase of the heart of a 3 week old calf (Case 1) with the heart of a 3 week old calf, (Case 1) with anomalousanomalous origin of both coronary arteries. origin of both coronary arteries.

Con. J. Comp. Med. Vet. Sci.170

LEGEND FOR FIGURES 2, 3, AND 4AO. - AortaA.V.C. - Anterior Vena CavaC.R.L.C. - Circumflex Ramus of the Lcft CoronaryArteryC.R.R.C. - Circumflex Ramus of the Right CoronaryArteryD.P.R. - Descending Paraconal Ramus of the LeltCoronary ArteryD.S.R. - Descending Subsinous Ramus of the LeftCoronary ArteryL.A. - Left AtriumL.A.V. - Left Atrioventricular OrificeL.C. - Left Coronary ArteryL.V. - Left VentricleP.A. - Pulmonary ArteryP.V. - Pulmonary VeinsP.V.C. - Posterior Vena CavaR.A. - Right AtriumR.A.V. - Right Atrioventricular OrificeR.C. Right Coronary ArteryR.V. - RigSht VentricleS.R. - Septal Ramus

pulmonary artery for 2.5 cm. where it bi-furcated (Fig. 2 & 3) into a circumflexramus and a left descending paraconal ra-mus. The left descending paraconal ra-mus followed the paraconal interventricularsulcus to the apex. The circumflex ramus,as it continued in the coronary sulcus, gaveorigin to several small vessels to the leftventricular wall and terminated in the rightdescending subsinous ramus (Fig. 4).The right coronary artery at its origin

measured 0.8 cm. in circumference. It fol-lowed a cephalad course between the rightatrium and pulmonary artery (Fig. 2 & 3).One branch which supplied part of theconus arteriosus originated from the rightcoronary artery before that artery gainedaccess to the coronary sulcus (Fig. 2 & 3).Many vessels which descended to the rightventricular wall arose from the circumflexramus of the right coronary artery (Fig.4). Terminal branches of this vessel on theright ventricle appeared to anastomose withbranches of the right descending subsinousramus of the left coronary artery.

Blocks of tissue were excised from theproximal part of the aorta and pulmonaryartery, the left and right atria, the mid-dle portion of the interventricular septum,the subauricular papillary muscle of theleft ventricle, the mitral and tricuspidvalves, the circumflex ramus of the leftcoronary artery, the descending paraconalramus of the left coronary artery, thedescending subsinous ramus of the leftcoronary artery, and the circumflex ramusof the right coronary artery. The tissueswere sectioned and stained with hematoxy-lin-eosin, Verhoff's Elastic and Masson'sTrichrome stains.The right atrium was normal; however,

the endocardium of the left atrium and

left ventricle was thickened. It varied from0.7 to 1.5 mm. in depth. Lymphocytes werescattered throughout the endocardiumwhich consisted of two definite layers. Thesuperficial layer contained irregularly ar-ranged connective tissue fibrils while thedeeper layer consisted of larger parallelelastic fibers (Fig. 5). A few degeneratemyocardial fibers were entrapped by thedeeper layer of the endocardium.The circumflex ramus of the left coro-

nary artery and the descending subsinuousramus of the left coronary artery were notremarkable. The adventitia of the circum-flex ramus of the right coronary arteryand the descending paraconal ramus of theleft coronary artery were infiltrated withlymphocytes, neutrophils, and increasedamounts of connective tissue.

There was an increase of connective tis-sue in the interstices and perivascular areasof the interventricular septum and subauri-cular papillary muscle of the left ventricle.Several areas were noted in the subauri-cular papillary muscle where myocardialfibers had undergone necrosis, phagocytosis~~~~~~~~~~~~~~~~~. .. .. .. .. ...Fig. 5. Section of the endocardium of the left atrium(Case 1) Verhoff's elastic stain; X58.5. Diffuse thicken-ing of the endocadium, consisting of two layers; anouter loosely arranged layer and an inner denser layer;remanent of degenerative myocardial fibers are locatedat the junction of the two layers.

Vol. 28 -July, 1964 171

Fig. 6. Crossection of the subauricular papillary mus-cle (Case 1) Hematoxylin and Eosin' stain; X43.3. Anincrease of connective tissue in the interstitial and peri-vascular arcas; some of the myocardial fibers have un-dergone necrosis, phagocytosis and fibrosis.

Fig. 7. Same section as figure 6; X103.7. A band of ma-ture connective tissue is noted in the center of thissection.

and connective tissue replacement (Fig. 6& 7).A thickening of the epicardium of the

apex was accompanied by edema, and in-creased amounts of connective tissue. Theconnective tissue of this area was infil-trated with lymphocytes and neutrophils.Several arterioles in the interventricularseptum and subauricular papillary musclewere conspicuous because of hypertrophy ofthe media.The mitral and tricuspid valves, as well

as the pulmonary artery and aorta, wereessentially normal.

CASE No. 2

The second case, a three month old maleAberdeen Angus calf, entered the Vet-erinary Large Animal Clinic with a historyof intractable diarrhea. The animal diedand was presented to the Department ofVeterinary Pathology for necropsy.

The animal weighed 61 Kg. The wall ofthe small intestines was congested and ab-normal amounts of mucus were present inthe lumen. The lungs, liver, spleen and kid-neys were congested.The heart was enlarged and globular in

form. Weights and measurements of theheart and great vessels are listed in Table1. The left atrium and left ventricle weredilated. The endocardium of the left atriumand left ventricle was diffusely thickenedand presented a white, opaque appearance.Rugae were noted on the endocardium of

the left atrium, 2 cm. dorsal to the parietalcusp of the mitral valve. They were inter-preted to be the result of regurgitation ofblood into the left atrium. The mitral valvewas essentially normal. Coronary ostia wereabsent in the wall of the aorta.The right ventricle was dilated and the

parietal cusp of the tricuspid valve con-tained one hematocyst 0.2 cm. in diameter.The foramen ovale and the ductus arterio-sus were closed. The pulmonary veins andvenae cavae were anatomically normal.An oblate spheroid ostium was noted in

the wall of the pulmonary artery (Fig. 1).It was located 1.4 cm. dorsally to the mid-dle of the left cusp of the semilunar valveand measured 1.1 cm. at its widest margin.Immediately, two vessels originated fromthe ostium.

One vessel, corresponding to the leftcoronary artery, was directed to the leftand measured 1.2 cm. in circumference. Itcontinued for 1 cm. then trifucated intoan anterior septal ramus, a descending para-conal ramus and a circumflex ramus. Thecontinuation of the circumflex ramus wasthe same as in the first case.The other vessel, corresponding to the

right coronary artery, followed a course tothe right between the pulmonary artery andaorta. After proceeding for 1.5 cm. theright coronary artery gave origin to asmall septal artery and the main branchcontinued as the circumflex ramus.The heart was sectioned and stained for

histologic examination as in the previouscase.The histopathological lesions noted in this

case were similar in many respects to thoseobserved in the first case. The circumflexramus of the left coronary artery, the cir-cumflex ramus of the right coronary ar-tery, the descending paraconal ramus of theleft coronary artery, the descending sub-sinous ramus of the left coronary artery,

Can. J. Comp. Med. Vet. Sci.172

the right atrium, the aorta and mitral valvewere not remarkable. The intima and mediaof the pulmonary artery were separatedby bands of edematous connective tissue,within which were located islands of gran-ular basophilic staining material. This find-ing was interpreted to be mucoid degenera-tion. The endocardium of the left atriumand left ventricle was thickened with elas-tic connective tissue fibers. Several areaswere noted where Purkinje fibers weretrapped in the subendocardium of the leftventricle by edematous connective tissue.Within these areas macrophages, plasmacells and lymphocytes were observed. Dif-fuse fibrosis was noted within the myocar-dium of the left atrium, left ventricle andthe subauricular papillary muscle of theleft ventricle.

DiscussionSeveral features of these cases of anoma-

lous origin of the coronary arteries of cat-tle are different from those previously de-scribed. Apparently these are the firstreported instances of anomalous origin ofboth coronary arteries from the pulmonaryartery in cattle. Several explanations maybe suggested for the absence of descrip-tions of this anomaly. It would be an easymatter to overlook this anomaly unless it wasspecifically being sought and the possibili-ty exists that it has been seen and not re-ported. The most plausible explanation,however, is the relative lethal characterof A.O.B.C.A. as compared with A.O.R.C.A. Of the 4 reported cases of A.O.R.C.A.in cattle all survived to at least 6 years ofage. The benign nature of A.O.R.C.A.'28' hasbeen referred to in reports of this condi-tion in man. The longest survival of 5 casesof A.O.B.C.A."20' in man was 10 days. Con-sequently, many animals with A.O.B.C.A.would be expected to die at an early ageand would not be brought to necropsy.

Since both the foramen ovale and ductusarteriosus were closed, the survival of thesecond case to three months of age is dif-ficult to explain. Either the ductus arterio-sLis and the foramen ovale were patent anddeath ensued soon after they were closedor the bovine myocardium is able to func-tion for a considerable length of time eventhough the oxygen concentration of theblood is subnormal.These cases are unique also, because of

the lack of cirsoid aneurysms of the coro-nary arteries and absence of extensive anas-

tomosis between the right and left coronaryarteries. Cirsoid aneurysms were a com-mon feature of four reported cases ofA.O.R.C.A. (10,20,31 & 32) in cattle and anasto-moses were described in 3 of these cases.(10,31 & 32) Cirsoid aneurysms and anastomosesoccurs in many instances of A.O.L.C.A. inman. (5 & 11)

Since both coronary arteries originatedfrom the pulmonary circulation in thesecases it would be tempting to conclude thatthe absence of a pressure difference be-tween the right and left coronary arterieswas responsible for the lack of the develop-ment of cirsoid aneurysms and extensiveanastomoses. Cirsoid aneurysms have beenobserved in cattle'272 in which the originof the coronary arteries was normal.

In the rabbit, prior to the development ofthe coronary arteries, the myocardium isnourished by blood from the intertrabecularspaces,(" and, presumably, this is truefor the bovine embryo. Thus, it is tentativelyconcluded that a difference in pressure be-tween the coronary arteries is important.However, arrest of development of the coro-nary system (i.e. persistence of the primi-tive intertrabecular spaces) must also beconsidered to explain the development ofcirsoid aneurysms and anastomoses.The histological findings associated with

anomalous origin of one or both coronaryarteries have been described.'10"'2"1519' &

An interesting finding in these cases isthe thickened endocardium of the left atriaand left ventricles estimated to be 5-10times normal. The histological observationsof the endocardium reported here are simi-lar to endocardial fibroelastosis which hasbeen seen in man, 4 & 22) cattle, (29 & 130) dogsand cats.") Endocardial fibroelastosis ac-companied by A.O.L.C.A. has been reportedin man, 4' and it has been suggested thatchronic hypoxemia may be responsible forendocardial fibroelastosis. However, itwould be more appropriate to classify thelesions of the endocardium, reported here,as subendocardial necrosis.The lesions associated with anomolous

origin of one or both coronary arteries fromthe pulmonary artery have been inter-preted"' to result from either low perfu-sion pressure or low oxygen content of theblcod delivered to myocardial tissues. Con-sequently, the ventricle supplied by theanomalous coronary artery should havemore extensive lesions than the contra-

Vol. 28-July, 1964 173

lateral ventricle. The degree of develop-ment of either low perfusion pressure oxpoorly oxygenated blood would be contin-gent upon to what extent anastomoses haddeveloped and the pressure difference be-tween the pulmonary circulatory system andthe arterial circulatory system. For in-stance, it is common knowledge that rever-sal of flow from the pulmonary artery tcthe aorta occurs in some cases of patentductus arteriosus. If extensive anastomoseQare present, essentially the same hemody-namic situation would exist with anoma-lous origin of one coronary artery from thEpulmonary artery. In one instance of A.O0L.C.A.'7' in man, it was calculated that 30%of the cardiac output was being shuntedfrom the aorta to the pulmonary artery.One would expect that the most extensivElesions would be observed with A.O.B.C.A,because the total blood supply to the myo-cardium would be venous and delivered atsubnormal pressures. In addition, becausethe left coronary artery supplies a majorportion of the myocardium, more extensivemyocardial lesions would be observed withA.O.L.C.A. than with A.O.R.C.A. prior tcdevelopment of reversal of flow. If anasto-moses exist, this is evident because inA.O.R.C.A. oxygenated blood would flowthrough a large portion of the myocardiumsupplied by the left coronary artery beforebeing shunted to the right coronary artery.With A.O.L.C.A. a smaller part of themyocardium would be supplied with oxy-genated blood by the right coronary arterybefore being shunted into the left coronaryartery. One would expect, however, that thedifferences in the extent of the myocardiallesions between the two anomalies would beless evident after reversal of flow, becausethe myocardium would be supplied withrelatively unoxygenated blood regardless ofwhich artery was anomalous in origin.

It follows then that extensive anasto-moses are essential for prolonged survivalwith A.O.L.C.A. and less essential withA.O.R.C.A., if survival can be equated withthe severity of the lesions. In general, onewould anticipate that individuals with A.O.R.C.A. would survive longer than those withA.O.L.C.A., and, subsequently, the life ex-pectancy of those with A.O.B.C.A. would bethe shortest. This is apparently true 7,11 & 28)in man. Either low perfusion pressure orlow oxygen content of the blood suppliedto the myocardium is equivocally responsi-ble for the myocardial lesions observed with

anomalous origin of the coronary arteries.Comprehensive discussions of the tera-

togenic theories of anomalous origin of thecoronary arteries are given elsewhere.(1,16,17 & 28) Those theories that are quotedmost often include:

(a) Deviation of the septum which div-ides the truncus arterious in such amanner that normal coronary pri-mordia"' are included with the pul-monary artery rather than the aorta.

(b) Displacement of coronary primordia") to that part of the truncus ar-teriosus destined to become the pul-monary artery.

(c) Persistence of accessory anlagen(14 & 15 located in the pulmonary ar-tery with the involution of normalanlagen in the aorta.

Objection to the theory of septal devia-tions have been discussed.(81' First, coron-ary anlagen appear after division of thetruncus arteriosus has been completed.Furthermore, with septal deviation onewould expect the pulmonary artery to belarger than the aorta. An enlarged pulmo-nary artery is seldom describedt281 in re-ports of these anomalies. The theory of per-sistent accessory coronary anlagen offers asound embryological basis for the explana-tion of anomalies of the coronary arteries.

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6. CHRISTENSEN, N. O., and DALGARSRD-MIKKEL-SEN, S. Te tilfaelde af kronisk ektasi af en kos o-nararterierne vet paa kongenitalt grundlag opstasetkommunikation til hojre ventrikel hos oksen. Med-lemsbl Danske Dyrlaegefor. 28: 187-211, 1945.

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21. PREUSS, Z. Zur nomenklatur am herzen. Anat. Anz.103: 20-37, 1956.

22. PRIOR, J. T. and WYATT, T. C. Endocardial fi-broelastasis: A study of eight cases. Am. J. Path.20: 26-29, 1950.

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Gluconeogenesis in the Lactating CowBecause of a suggestion that the large

amounts of lactose synthesized by the dairycow make demands upon the animal that arepartly met by the conversion of protein intocarbohydrates the present experiment wasdone with a view to establishing the extentto which the gluconeogenetic process operatedin the normal lactating animal. Such a processof gluconeogenesis would lead to the libera-tion of ketogenic amino acids (leucine, lysine,isoleucine, phenylalanine and tyrosine) andthese could be broken down to ketone bodies.This in turn might contribute to the ketosisobserved in cows suffering from acetonemia.A mixture of C14 labelled amino acids was

given intra-venously to a lactating dairy cowand the appearance of C14 in various consti-tuents of blood and milk was followed for a

subsequent 16 hours. About 9 per cent of thelabelled amino acids was converted to milkprotein but the milk lactose also became radio-active to an extent indicating that about 12%of the lactose was formed by gluconeogenesisfrom protein. The ketogenesis accompanyingthis process would lead to the synthesis of 50to 60 g. per day of ketone bodies. In a normalcow this would rapidly equilibrate with acetylcoenzyme A and would be oxidized. However,in a cow suffering from acetonemia it maynot be possible for it to make sufficient Co Aavailable to effect the conversion of acetoace-tate. This would contribute considerably to theincreased level of ketone bodies in the ace-tonemic animal.

Hunter, G. D. and Millson, G. C. Res. Vet.Sci. 5: 1, 1964.

Vol. 28 -July, 1964 175