surgery of mitral incompetence · diastolic thrill and there is a lift over the right ventricle....

POSTGRAD. MED. J. (I96I), 37, 666

SURGERY OF MITRAL INCOMPETENCEC. N. BARNARD, M.D., Ph.D.

Cardiothoracic Surgeon, Senior Lecturer, Department of Surgery.

V. SCHRIRE, M.B., Ph.D.(Cape Town), M.R.C.P., F.R.C.P.E.Cardiologist, Senior Lecturer, Department of Medicine, Groote Schuur Hospital, and

University of Cape Town

MITRAL valve disease has for many years beenaccepted as the commonest sequel of rheumatism,both clinically and pathologically. The develop-ment of stenosis has never been in question.Such has not been the case, however, with incom-petence, though as long ago as I849 Hope firstdrew attention to this condition. The existence ofmitral incompetence as an entity or even as animportant component of the disease was soonchallenged and early in this century, largelythrough the teachings of Graham Steell (i906),Sir James McKenzie (i9i6), Cabot (1926) andSir Thomas Lewis (I933), the diagnosis of mitralincompetence fell into disrepute. With the de-velopment of cardiac surgery, however, mitralincompetence has once more come into its own.

Three major haemodynamic disturbances of themitral valve have now been recognized. Puremitral stenosis is the commonest and most readilyrecognized clinically and pathologically (Wood,I954). The valve leaflets are fused at the com-missures and though the chordc and papillarymuscles are diseased the valve mechanism isusually not grossly abnormal. The condition isgenerally amenable to closed-heart surgery withsome form of mechanical dilator. Pure mitralincompetence is the least common and is notdifficult to diagnose. Deficiency of valve leaflettissue, dilatation of the annulus or a combinationof both is generally present, but the valve me-chanism remains relatively normal so that repairunder cardiac by-pass is generally possible. Thecombination of stenosis and incompetence isfrequently encountered but varying amounts ofeach component produce a spectrum of hbmo-dynamic conditions. On the one hand dominantstenosis with minimal incompetence lends itselfto closed-heart surgery, whereas dominant in-

From the Departments of Surgery and Medicine,University of Cape Town and Groote Schuur Hospitaland Cardiac Clinic, Council for Scientific and IndustrialResearch Cardiopulmonary Group, Groote SchuurHospital.

competence with trivial stenosis is amenable toopen-heart surgery. Where both severe stenosis\and severe incompetence are present the valvestructures are generally grossly disorganized andanything short of complete valve replacement isprobably ineffective. Pre-operative assessmentof the exact hwmodynamic situation may be ex-tremely difficult even with the help of cardiaccatheterization and angiocardiography.Though by far the commonest, rheumatism is

not the only cause of organic mitral incompetence.Bacterial endocarditis, usually subacute, frequentlycomplicates mild rheumatic mitral valve diseaseaccentuating valve scarring and destruction, orvalves may be affected de novo. Surgically-produced mitral incompetence is not rare andoccasionally the resulting incompetence is sosevere that the patient is worse off after valvotomythan before. Lastly, congenital mitral incompe-tence, with or without other heart defects, maybe encountered, the most common example beingthat associated with the cleft mitral valves ofendocardial cushion defects (partial common atrio-ventricular canal). Mitral incompetence due tofibroelastosis or endomyocardial fibrosis is beyondthe scope of this discussion.

In this paper we wish to record the clinicalrecognition, surgical approach and preliminaryoperative results in rheumatic mitral incompe-tence, surgically-induced mitral incompetence,and congenital mitral incompetence.

Rheumatic Mitral IncompetenceOur patients represent a group of highly

selected cases from a large clinic draining an areawhere rheumatic heart disease is common (Schrire,I958) and where 330 closed-mitral valvotomieshave been performed, I25 during the two yearsunder review. Eleven patients were chosen foropen-heart surgery. Selection was based on theclinical assessment of pure incompetence in ten(confirmed in every case) and dominant re-stenosiswith slight incompetence in one. No patient was

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BARNARD and SCHRIRE: Surgery of Mitral Incompetence

FIG. i.-Pre- and post-operative phonocardiograms in a patient with severe mitral incompetence. Atrial fibrillation ispresent prior to, and sinus rhythrm after surgery. At the mitral area (MA) prior to surgery (A) there is a pansystolicmurmur, a soft opening snap (OS), a loud third sound (3) and a short mid-diastolic murmur. The systolic murmurcontinues beyond the aortic component of the second sound, which is obscured at the mitral area but shown at asynchronously recorded tracing, taken at the fourth left intercostal space (4LS). Splitting of the second sound isnormal. After surgery (B) the systolic murmur has practically disappeared; the opening snap is soft; the thirdsound has disappeared and a short mid-diastolic murmur remains.

advised surgery in whom the lesion was thoughtto be mixed stenosis and incompetence withgrossly disorganized valves. In every case dis-ability was increasing progressively despite fulland active medical therapy (Grade 3 or 4), andseveral patients were in the late stages of heartfailure.

Clinical Features of Pure MitralIncompetence

Females outnumbered males by 6 to i, and theage ranged from I7 to 44 with the majoritybetween 20 and 30 years. A history of at leastone attack of rheumatic fever, often several, waspresent in all but one patient. Subacute bacterialendocarditis occurred in three patients, one ofwhom had several attacks. Symptoms due topulmonary congestion were present in everypatient, all but two having paroxysmal cardiacdyspncea. Angina pectoris was present in twopatients and systemic embolism in one. Althoughpalpitation was not a major complaint, patientswere always aware of the hyperdynamic over-active left ventricle. The first observation madein the post-operative period was the disappear-ance of the pounding in the chest.

Atrial fibrillation was present in every patient,tricuspid incompetence, jugular venous distensionand hepatomegaly in half. The pulse was usually

normal in most patients, though on occasion aslight collapsing element was noted. Hypertensionwas absent.

Palpation was of the greatest value. In everypatient considerable left ventricular enlargementwas present with an overfilled hyperdynamicthrust in the fifth or sixth intercostal space usuallybeyond the anterior axillary line. A systolic thrillwas often present. Rocking movement of thechest suggested an aneurysm of the left atrium inthree patients. Right ventricular over-activity wasabsent in most subjects.

Auscultation revealed a loud (Grade 3 to 4 ofsix grades) pan-systolic murmur in every case,maximal at the apex radiating widely into theaxilla and left base posteriorly and medially tothe parasternal area. The murmur commencedwith the first sound which was often drownedand continued through or beyond the aortic com-ponent of the second sound. A third sound washeard and recorded in every case, followed by ashort, soft (Grade I to 2 of four grades) mid-diastolic murmur. An opening snap was heard intwo and recorded in four subjects (Fig. i) anddid not correlate strictly with the mobility of theanterior mitral cusp nor with operability (Nixon,Wooler and Radigan, I960).

Trivial aortic incompetence was present in onesubject clinically and in three at surgery. In one,

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POSTGRADUATE MEDICAL JOURNAL

FIG. 2.-Electrocardiogram in mitralincompetence showing atrialfibrillation and digitalis effecton severe left ventricularhypertrophy.

moderate aortic incompetence was present, and inone there was aortic stenosis and incompetencewith a gradient of 50 mm. across the aortic valve.Significant tricuspid incompetence was presentin two patients though transient tricuspid mur-murs occurred more often.The electrocardiogram confirmed the presence

of atrial fibrillation in every patient and in onlyone was this the sole abnormality. One patienthad complete right bundle branch block and theremainder showed digitalis effect on left ven-tricular hypertrophy (Fig. 2). The presence ofleft ventricular overload excludes any significantmitral stenosis in the absence of other causes ofenlargement such as aortic incompetence. Trac-ings taken during sinus rhythm showed left atrialhypertrophy.

Radiologically gross or aneurysmal enlargementof the left atrium was found eight times (Fig. 3).Such a finding strongly suggests dominant mitralincompetence though we have encountered giantleft atrial enlargement at necropsy in the presenceof pure tight stenosis. Left ventricular enlarge-ment was present in all patients, indicating severemitral incompetence. Valve calcification was notseen.

Mixed Stenosis and IncompetenceThough only one patient with this combination

was submitted to surgery in this series, thephysical signs are well known. Pure mitralstenosis is associated with an apex beat in thenormal site, tapping in quality with a diastolicor pre-systolic thrill, a lift over the outflow tract

of the right ventricle and a palpable pulmonarysecond sound. The characteristic auscultatoryfindings are loud first sound, second sound fol-lowed by opening snap, diastolic and pre-systolicmurmurs producing an unforgettable cadence.Systolic murmurs are generally absent unless theyhave radiated from the tricuspid or aortic valves.In pure mitral incompetence, on the other hand,the apex is displaced outwards, left ventricular intype, thrusting hyperdynamic in quality, asso-ciated with systolic thrill, little lift over the rightventricle and an impalpable pulmonary secondsound. The characteristic auscultatory findingsare a pan-systolic murmur, starting with the firstsound which is not accentuated, continuingthrough to the second sound, and a third soundfollowed by diastolic murmur which is short andsoft. Occasionally an opening snap is also heard.When both stenosis and incompetence are

present the signs consist of a combination of thetwo. The apex is usually left-ventricular with adiastolic thrill and there is a lift over the rightventricle. There is a pan-systolic murmur asso-ciated with a third heart sound and loud mid-diastolic murmur. The greater the stenosis themore the signs resemble pure mitral stenosis, andvice versa.The electrocardiogram usually shows left atria]

hypertrophy when sinus rhythm is present.There may be no evidence of ventricular hyper-trophy, right or left ventricular hypertrophyRadiological examination is usually not of grealhelp in determining the nature of the dominanivalve lesion.

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FIG. 3.-A-D X-rays from four patients with severe mitral incompetence showing moderate to gross cardiomegaly.marked left atrial and left ventricular enlargement. Hilar congestion of varying degree is also present.




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FIG. 4.-Pulmonary wedge tracing showing a raisedpulmonary venous pressure with a CV wave of45 mm. and a brisk Y descent characteristic ofsevere mitral incompetence. Atrial fibrillation ispresent.

Cardiac Catheterization andAngiocardiography

Special investigations were unnecessary and notperformed in any of our subjects. In the majorityof patients, pure or dominant stenosis, or pure ordominant incompetence can be recognized with ahigh degree of accuracy. When in doubt catheteri-zation may sometimes be of help. Right heartstudies (Fig. 4), with or without exercise, generallygive equivocal results precisely in those caseswhere help is most needed. Left atrial pressurecurves, measurement of the gradient across themitral valve and dye dilution curves are also fre-quently inconclusive. The most promising investi-gation is left ventricular angiocardiography orcineangiocardiography which gives a roughquantitative assessment of the degree of mitralincompetence present.

Post-operative Mitral IncompetenceGross post-operative mitral incompetence fol-

lowing closed mitral valvotomy is fortunately rare.In our experience this has become commonersince the introduction of the mechanical dilator,particularly in cases with re-stenosis. Clinicalrecognition is easy. In the first place the surgeon

is generally immediately aware of the fact thathe has produced too much incompetence by tear-ing a cusp or opening a commissure too widely.Secondly, the post-operative course is stormy,with the patient developing pulmonary congestionand heart failure and responding poorly to treat-ment. Lastly, the signs of severe mitral incom-petence with a left ventricular thrusting apex anda loud pan-systolic mitral are immediately evident.There were two patients with intractable heart

failure in this series, in one of whom incom-petence had developed following a second valvo-tomy for re-stenosis.

Congenital Mitral IncompetenceWe have had no experience with isolated con-

genital mitral incompetence (Starkey, 1959; Talner,Stern and Sloan, I96I), but have encounteredmitral incompetence which did not require sur-gical interference in association with correctedtransposition (Beck, Schrire, Vogelpoel, Nellen andSwanepoel, I96I) and secundum type atrial septaldefect. The most common and most importanttype of congenital incompetence is that en-countered in endocardial cushion defects, partialor complete (Edwards, I960). Sixteen patientswith acyanotic, partial or complete endocardialcushion defects have been submitted to surgery.The clinical features of these conditions aredescribed elsewhere (Sellors and Somerville,I96I; Barnard and Schrire, I96I).

Anatomy and PathologyNormal mitral valve closure is effected mainly

by the freely mobile anteromedial leaflet; thiscusp is much longer than the posterolatpral one.Since its chorcle are only attached to the peripheralzone, a triangular area at the base, whioh is muchthinner, is left free to billow towards the cavity ofthe left atrium during systole. The shorterposterolateral cusp with its chordae inserted morewidely on its ventricular surface moves only ashort distance into the valve orifice during systole.It acts mainly as a ridge or shelf against whichthe anteromedial cusp abuts to effect closure(Brock, 1952; van der Spuy, 1958). The move-ment of the leaflets is activated by the differencein hydrostatic pressure between the atrium andthe ventricle. It is passively restrained by theanchoring chordie and papillary muscles. Theseanchors are protected to some extent from thefull force of ventricular systole by the mutualsupport the two cusps give to each other (Fig. 5).Although several different pathological lesions

may result in incompetence of the mitral valve,the essential cause is deficiency of leaflet tissue,either absolute or relative, or a combination ofboth. An absolute deficiency of leaflet tissue may

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N3ARNARD and SCHRIRE: Surgery of Mitral Incompetence

FIG. 5.-Cycle of normal mitral valve movement, showing the valve starting in the closed position,then opening and the subsequent closing. Note the free mobility of the anteromedial leafletwhilst the posterolateral one provides only a passive ridge (from 'A Surgical Approach toMitral Insufficiency'. C. N. Barnard, M. B. McKenzie and V. Schrire, Brit. J7. Surg., 48,655-662, I96I).

FIG. 6.-Congenital cleft of the anteromedial leaflet of the mitral valve (A), as seen in endocardialcushion defects, showing the abnormal restraints a, b and c. Acquired perforation of theanteromedial leaflet of the mitral valve (B) following acute bacterial endocarditis (from'The Surgical Correction of Endocardial Cushion Defects'. C. N. Barnard and V. Schrire,Surgeryr 49, 4, 500-509, ig6i. Published by C. V. Mosby Co., St. Louis).

result from a cleft, perforation or tear of a cusp(Fig. 6), but more commonly from rheumaticscarring of the cusps. The posterolateral leafletof the mitral valve is more susceptible to theravages of the rheumatic process (Fig. 7). How-ever, this may be more apparent than real because

of the greater length of the anteromedial cusp.Thus the same degree of rheumatic involvementof both leaflets from their free margins to theirbases will involve only one-third of the antero-medial leaflet while the posterolateral cusp willbecome almost completely rigid. In such a case,

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FIG. 7.-Cycle of incompetent mitral valve movement showing the extensive scarring of theposterolateral leaflet and the immobility of the anteromedial leaflet.

although the middle and basal thirds of theanteromedial leaflet remain thin and flexible, theshelf provided by the posterolateral leaflet is lost.With each systole the anteromedial leaflet over-rides the posterolateral one and incompetenceresults.

Relative deficiency may be due to dilatationof the annulus. The two leaflets are thus movedfarther apart and although there may be noactual loss of leaflet tissue, the distance the cuspshave to move to meet is too great for the tissueavailable. Inflammatory changes in the junctionaltissue causing thickening, shortening and fusionof the chorde with limitation of cusp mobilitywill also result in relative deficiency of cusptissue.

Surgical TechniquesIn his approach to mitral incompetence, irre-

spective of the letiological factor, the aim of thesurgeon should be to restore any relative orabsolute deficiency of leaflet tissue that may exist.This can usually be achieved by one or more ofthe following techniques:

A. Repair of cleft, hole or tear in mitralleaflets which may be present.

B. Mobilization of the anteromedial cusp.C. Provision of a posterior shelf or support to

the anteromedial cusp.D. Insertion of a complete prosthesis.

A. REPAIR OF CLEFT, HOLE OR TEAR IN MITRALLEAFLETSA hole or tear in one or other leaflet of the

mitral valve resulting in an absolute deficiency ofleaflet tissue can be repaired by direct suture orthe use of a plastic patch. However, the correc-tion of mitral regurgitation from a cleft antero-medial leaflet as found in endocardial cushion

defects often needs more than the simple suturedescribed by certain surgeons (Cooley, Kirklinand Harschbarger, 1957; Cooley, Latson andKeats, 1958; McGoon, DuShane and Kirklin,1959; Barnard, Phillips, De Villiers, Casserley,Hewitson, Van der Riet and McKenzie, 1959).In most of these cases free mobility of the antero-medial leaflet is not present and before completecompetence can be restored mobilization of thecusp is necessary (vide infra).

B. MOBILIZATION OF THE ANTEROMEDIAL CUSPAs the anteromedial cusp is the 'main flap' in

the closure of the mitral orifice during systole,free mobility of this leaflet is essential. The freemovement can be prevented by fusion of thecommissures, rigidity of the leaflet or sub-valvularfibrosis. Thus to give maximum mobility, thefollowing avenues can be explored:

(i) Separation of fused commissures.(ii) Removal of calcium from the leaflet.(iii) Treatment of sub-valvular changes inter-

fering with cusp mobility.

(i) Separation of Fused CommissuresAlthough commissural separation either by

blunt or by sharp dissection may increase themobility of the anteromedial cusp, this manceuvremay increase regurgitation if performed whenthere is annular dilatation. In these circumstancesthe fusion of the two leaflets at their commissuresprevents further annular dilatation and acts as anannuloplasty (vide infra). When this restraint isbroken the two cusps move further away fromeach other, thus increasing the distance whichthe anteromedial leaflet has to extend to close theorifice. Commissurotomy is only of value whenthe annulus is normal in size or smaller thannormal.

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FIG. 8.-Congenital cleft mitral valve after closure bydirect suture showing the abnormal restraints (a,b and c) preventing free mobility of the centraltrigone (from 'The Surgical Correction of Endo-cardial Cushion Defects'. C. N. Barnard andV. Schrire (I96I): Surgery, 49, 4, 500-509. Pub-lished by C. V. Mosby Co., St. Louis).

(ii) Removal of Calcium from the AnteromedialLeaflet

Free mobility of the trigone of this leaflet maybe prevented by plaques of calcium. Once theserigid areas are broken up by gentle crushing andthe bits of calcium carefully removed, the leafletwill again swing freely like a sail with ventricularsystole.

(iii) Treatment of Sub- Valvular ChangesPreventing Cusp MobilityAs discussed in the section on the normal

anatomy and function of the mitral valve, thechordx of the anteromedial leaflet are attachedonly to the periphery of the cusp allowing freemobility of the central trigone. In most cases ofendocardial cushion defects, abnormal restraintsof the cleft tie this portion of the valve down(Edwards, I960; Barnard, I96I; Barnard andSchrire, I96I) (Fig. 8). These prevent freemobility of the trigone and therefore, even aftercareful suturing of the cleft, regurgitation willpersist unless these restraints are divided and thecusp is mobilized.

In incompetence following rheumatic valvu-litis, chordo-papillary fusion restricts the move-

ment of the anteromedial leaflet. An attemptshould be made to free the cusp by breakingdown these adhesions. Direct finger-tip pressuremay sometimes suffice but it may be necessary toseparate the papillary muscles by sharp dissection.In some cases the shortened, retracted chordwe ofthe posterolateral leaflet can be divided, allowingmore mobility of the chordae of the anteromedialleaflet. This will not cause inversion of theposterolateral cusp during ventricular systole assevere fibrosis will have made this cusp a passiveridge.

C. PROVISION OF A POSTEROLATERAL SHELFWHICH WILL EFFECT CLOSURE AND PROVIDESUPPORT FOR THE ANTEROMEDIAL CUSPThe importance of the provision of a postero-

lateral shelf in the treatment of mitral insuffi-ciency has been recognized by many workers.Substances such as pericardial tubes (Moore andSchumacker, I953), vein grafts (Henderson andLaw, 1953) and tendon grafts (Glover, Henderson,Martutti and Gregory, 1952) have been placedin the posterior commissure to provide such ashelf in the area where regurgitation is maximal.Ridged Ivalon sponge (DeWall, Warden, Lilleheiand Varco, 1956; Glenn, Gentsch, Hume andGuilfoil, I956) a mobile Ivalon sponge sling(Johns and Blalock, I954), and a baffle of lucite(Harken, Block, Ellis and Dexter, I954) have beenplaced in the mitral orifice with the same objectin mind. Approximation and elevation of theposterior aspect of the mitral valve will have thesame effect, and this has been attempted usingpericardial strips (Bailey and Bolton, 1956), veinslings (Sakakibara, 1955), and silk sutures (Kayand Cross, 1955; Nichols, I957). The use of anartificial cusp in place of the posterolateral leafletwas suggested by Brock in I952, and reported byGott and others in I957. All these procedureshave the same common aim in that they attemptto provide a buttress against which the antero-medial cusp can meet and close during ventri-cular systole.

If incompetence persists after the surgeon hasfully mobilized the anteromedial leaflet, it meansthat the anteromedial flap is still not capable ofmoving across the valve orifice to close againstthe posterolateral shelf. The leak can only becorrected or lessened now by providing such ashelf. Improvement in valve function underthese circumstances can be achieved either bybringing the existing shelf nearer to the antero-medial cusp or by building an artificial postero-lateral ridge.

(i) AnnuloplastyThis operation for the correction of mitral

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FIG. 9.-Metal moulds and dumb-bell-shaped immobile pros-theses (from 'A SurgicalApproach to Mitral Insuffi-ciency'. C. N. Barnard,M. B. McKenzie and V.Schrire (I96I): Brit. J. Surg.,48, 655-6X).

regurgitation was reported by Gott and others(I957), Lillehei, Gott, DeWall and Varco (I957),Kay, Nogueira and Zimmerman (1958), andothers. Competence is achieved by approxi-mating the anteromedial cusps and the postero-lateral buttress, thus shortening the distance theanteromedial leaflets must move before closingthe mitral orifice. In this way one compensatesfor the loss of leaflet substance. The operationcan only be performed when annular dilatation ismainly responsible for the leak and there is notmuch loss of leaflet substance. When the annulusis normal or smaller than normal in size, thismaneuvre will result in stenosis of the valve.

In performing annuloplasty, silk mattresssutures are placed through the anteromedial andposterolateral portions of the annulus at one orboth commissures, taking care not to damage thecircumflex coronary artery, the proximal portionof the great cardiac vein or the coronary sinuswhich are closely related to the posterolateralportion of the ring. These stitches are tightenedwith the heart beating and when the two portionsof the annulus have been sufficiently approxi-mated to produce competence, the stitches aresecurely tied over a pillow of compressed Ivalonsponge to prevent them from tearing out at alater date.

(ii) The Building of a Posterolateral RidgeThis will take the place of the shortened,

ineffective mural leaflet, especially if the antero-medial cusp is still freely mobile as is so oftenfound. The operation has had considerablesuccess. The function of the mural leaflet canbe replaced either by an immobile or a mobileprosthesis.

(a) Immobile Prosthesis. Gott and others (I957)and Lillehei and others (1958) reported the useof an immobile prosthesis of compressed poly-

vinyl sponge. Cylindrical metal moulds in severalsizes were made and an assortment of polyvinylcylinders prepared and sterilized. At operation asuitably-sized cylindrical prosthesis was selectedand by means of three or four vertical mattressstitches of No. 2 silk secured against the ventricularsurface of the posterolateral portion of the mitralannulus. In this way a buttress against whichthe aortic mitral leaflet could close was provided.We prefer the use of dumb-bell shaped Ivalon

prostheses for the same purpose (Fig. 9). Thesehave the advantage that the prosthesis can be soplaced that the widest portiontof the dumb-bellis situated at the area where separation of the twocusps is greatest and the thinner portion wherethe separation is not so great, thus minimizingthe possibility of stenosis of this area. Further-more, from our laboratory and clinical experiencewe believe that the prosthesis should be securedagainst that part of the annulus which faces themitral orifice and not on its ventricular surface(Fig. io). As already pointed out, in long-standing mitral incompetence the anteromedialleaflet tends to prolapse into the atrial cavity dueto loss of support from its mural leaflet. There-fore, during ventricular systole, the anteromedialleaflet rises higher than it should so that theleaflet will overshoot the prosthesis if it is posi-tioned on the ventricular surfaEe unless the pros-thesis is very large. In the latter case theprosthesis may actually produce stenosis. In thelast five patients, a dumb-bell shaped prosthesiswas secured in the correct position with four tofive vertical No. i silk mattress sutures, each tiedover an Ivalon bar. The results to date havebeen the best so far achieved.

(b) Mobile Prosthesis. Where both the antero-medial and posterolateral leaflets have beenextensively destroyed and scarred by the rheu-matic process, resulting in little mobility of the

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FIG. Io.-Diagram illustrating the incorrect (A) andcorrect (B) insertion of the prosthesis.

anteromedial leaflet, an immobile prosthesis willnot correct the incompetence without producingstenosis. A mobile prosthesis is required in thistype of case. It should not interfere with the

valve orifice during diastole and should bulge upduring systole to effect closure of the valve.Such a prosthesis has been developed in ourlaboratory and its use in animals is teing observed(Fig. i i).

D. INSERTION OF A COMPLETE PROSTHESISIn our experience there has never been any

need to replace the mitral valve completely inpure mitral incompetence. Where a mixed lesionwith marked stenosis and incompetence is present,both leaflets may be so destroyed and immobilizedthat very little valvular function can be obtainedby the manceuvres described above. Completevalvular replacement will be the ideal answer tothe problem. To date the results obtained whenthe mitral valve is completely replaced by someform of plastic valve have been very discouraging(Levowitz, Lovette, Leone, Ratan, Magovern andKent, I960).

ResultsRheumatic Mitral IncompetenceThere were eight patients operated upon by

one of us (C.B.) with no mortality. Annuloplastywas performed on two. The first had an initialexcellent result with return to complete normalityboth subjectively and objectively although priorto surgery she had been incapacitated with chroniccongestive cardiac failure (Barnard, McKenzieand Schrire, I96I). Five months later signs ofmitral incompetence returned and progressed.Symptoms and congestive cardiac failure wereprecipitated by recurrence of atrial fibrillationI7 months after surgery. Death resulted fromquinidine toxicity during attempted conversion to

FIG. i i.-Cycle of mobile prosthesis showing the valve in the closed position, then opening andthe subsequent closure. Note that the valve orifice is not obstructed during diastole (from'A Surgical Approach to -Mitral Insufficiency'. C. N. Barnard, M.' B. McKenzie and V.'Schrire, 'Brit. Y.' Surg., 48, 655-66-2, I96I). :

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FIG. 12.-Tracing A shows an elevated left atrial pressure (LAP) mainly due to a CV wave of44 mm. Hg. After surgery the pressure has dropped to 8/4 mm. Hg. Tracing B shows anelevated LAP mainly due to a CV wave of 30 mm. Hg. After surgery the pressure has halvedand the CV wave is now only 5 mm. Hg. Tracing C shows an elevated LAP with a CV waveof I5 mm. Hg. After surgery the pressure has halved with a V wave of 4 mm. Hg.

sinus rhythm. Necropsy showed recurrence ofgross annular dilatation with severe mitral incom-petence but no suture disruption. The secondpatient was in the last stages of cardiac failurewith enormous cardiomegaly (Fig. 3a) prior tosurgery. Within three weeks after annuloplastyand insertion of a baffle (Fig. i2a) he had re-covered remarkably. While convalescing at homehis symptoms suddenly recurred, ' post-peri-cardiotomy syndrome ' with pericarditis developedand catheterization showed return of gross mitralincompetence (Fig. 4). At re-operation, threemonths after the first, the annuloplasty was foundto have torn. Following surgery he developedstaphylococcal bacterial endocarditis, cerebralembolism and died.

Six patients have had mitral valve repair witha dumb-bell shaped Ivalon prosthesis. The pres-sure recordings in the left atrium taken immedi-ately post-operatively (Fig. 12) have shown astriking fall in left atrial pressure with disappear-ance of the mitral incompetent CV wave in all.The follow-up period varies from a few weeks totwo years. Sinus rhythm has been restored byquinidine and maintained in four patients.Marked improvement has been present in everycase subjectively, and in all but one objectively(Fig. i). Two patients are virtually symptom-free.The one patient with dominant stenosis and

some incompetence has made a remarkable

response and is well two years after surgery.Inadequate valvotomy in 1953 was followed byopen-heart procedure in 1959 at which the com-missures were divided and the calcium removedfrom the cusps which were then mobilized.

Post-operative Mitral IncompetenceBoth patients had incapacitating symptoms and

one was in intractable congestive failure. In thefirst mitral valvotomy had been performed sixyears previously and pure incompetence had beenproduced which was repaired with an Ivalonprosthesis. Following surgery the patient re-married and was travelling abroad greatly im-proved a year later. The second patient had aninadequate valvotomy in I952 with relief ofsymptoms until 1956. Re-valvotomy for tightstenosis in I960 with a mechanical dilator resultedin tearing of the anterior cusp. Six weeks laterthe tear in the leaflet was repaired and com-missurotomy completed with moderate improve-ment.

Congenital Mitral IncompetenceThere were i i patients with endocardial cushion

defects without ventricular septal defects and threewith ventricular septal defects (Barnard andSchrire, I96I) operated upon by one of us (C.B.).All subjects had -cleft mitral valves with varyingdegrees of mitral incompetence.- There was otie

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death in the latter group. The importance ofmobilization of the mitral leaflets and cutting theabnormal restraints was not appreciated in thefirst three patients. One died 48 hours aftersurgery of gross mitral incompetence, one hassevere mitral incompetence aggravated by sub-acute bacterial endocarditis 2 years later and onehas persistent severe mitral incompetence withbreakdown of the atrial septal repair. Sinceappropriate treatment of the mitral incompetencehas been instituted only one of the nine re-catheterized one year after surgery has hkemo-dynamic mitral incompetence or any intracardiacshunt of any consequence.

Summaryi. Mitral incompetence is now a well recognized

sequel of rheumatic fever. Usually it is associatedwith stenosis, the degree of stenosis and incom-petence differing from patient to patient. Thisresults in a hiemodynamic spectrum varying fromdominant stenosis with slight incompetence onthe one hand to dominant incompetence withslight stenosis on the other, and all grades of thetwo between.

2. Pure mitral incompetence without stenosis isthe least common. It can be recognized clinicallywith as much accuracy as can pure mitral stenosis.The left ventricle is enlarged, there is a loud pan-systolic murmur, a third heart sound and a shortmid-diastolic murmur. The electrocardiogramshows left ventricular hypertrophy ard left atrialhypertrophy (if atrial fibrillation is absent) andthe X-ray shows enlargement of the same twochambers.

3. The presence of both stenosis and incom-petence of the mitral valve can be recognized bythe combination of the signs of each, but in manycases it is difficult to assess the part played byeach component. Angiocardiography promises tobe the most useful investigation in solving thisdifficulty.

4. Mitral incompetence may develop or beaggravated by surgery for mitral stenosis. Thesurgeon is usually immediately aware of thedynamic disturbance produced and the patient'ssymptoms and signs soon confirm this im-pression.

5. Congenital mitral incompetence producesthe same hiemodynamic disturbance as incom-petence of rheumatic etiology or following bac-terial endocarditis. It is most commonly asso-ciated with endocardial cushion defects. Murmursare usually present but interpretation is oftendifficult. The electrocardiogram provides themost important clue to the diagnosis.

6. Normal mitral valve closure is mainly effected

by the freely mobile anteromedial leaflet whichcloses on the less mobile posterior cusp. Incom-petence of the mitral valve is produced by defi-ciency of leaflet tissue due to loss of tissue, todilatation of the annulus or a combination ofboth. Surgery is designed at correcting thisdeficiency.

7. Clefts, holes or tears in the leaflets can berepaired by direct sutures or a plastic patch.Mobilization of the cusps can be achieved byseparation of the fused commissures and removalof calcium. Abnormal restraints present in thecleft valves of endocardial cushion defects mustbe severed and chordopapillary fusion and sub-valvular adhesions in rheumatic valves freed torestore mobility.

8. Most important of all is the provision of aposterolateral shelf which will effect closure andprovide support for the anteromedial cusp. Thiscan be achieved by annuloplasty or by using aprosthesis made of plastic material providing abuttress against which the anteromedial leafletcan close. The correct positioning of the pros-thesis is of the greatest importance. The antero-medial leaflet tends to prolapse into the atrialcavity due to loss of support from the posteriorcusp. The prosthesis should be placed againstthat part of the annulus which faces the mitralorifice and not on the ventricular surface. Inthis way it can act as an efficient buttress sup-porting the relatively normal anterior cusp.

9. In mixed stenosis and incompetence withgross disorganization of the valves, mobilizationof the leaflets and provision of a prosthetic buttresscannot correct the incompetence without produc-ing stenosis. The only satisfactory treatmentappears to be partial or complete replacement ofthe valve cusps. At present a satisfactory pros-thetic valve is not available and much work stillneeds to be done to solve this problem.

IO. The results achieved in pure rheumaticmitral incompetence are reported. Annuloplastywas found to give excellent but only temporaryimprovement and has thus been abandoned.Repair of the valve with a dumb-bell shaped Ivalonprosthesis, provided it is large enough, has giventhe best and longest maintained improvement.

ii. The importance of mobilizing the mitralvalves freely in endocardial cushion defects andthe severance of all restraints has been furthersubstantiated.

NOTE.-Since this was written, four patients ingrade 4 heart failure due to rheumatic mitralincompetence have had successful surgical repair.

We wish to thank Professor J. H. Louw of theDepartment of Surgery, University of Cape Town, for

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678 POSTGRADUATE MEDICAL JOURNAL November g961his encouraging support of our work, and the technicalstaff of the Marais Laboratory, Mr. C. C. Goosen,Mr. C. J. Lockett and Mrs. V. M. Commell, for theirexcellent work. We are grateful to the Medical Super-intendent of Groote Schuur Hospital, Dr. J. G. Burger,for permission to publish. Certain illustrations are

reproduced by permission of the publishers of the BritishJournal of Surgery and Surgery. Thanks are also due tothe Council for Scientific and Industrial Research andthe City Council of Cape Town, and to the Dr. C. L.Herman and Fourcade research grants for financialsupport.

IR FRmRwENChBAILEY, C. P., and BOLTON, H. E. (i 956): Criteria for and Results of Surgery for Mitral Stenosis, N. Y. med. J., 56, 649.BARNARD, C. N. (I961): Abnormal Restraints of the Cleft Anteromedial Leaflet of the Mitral Valve in Endocardial

Cushion Defects, Brit. med. J7., i, 719.-, PHILLIPS, W. L., DE VILLIERS, D. R., CASSERLEY, R. D., HEWITSON, R. P., VAN DER RIET, R. L., and McKENzIE,

M. B. (1959): Some Experiences with Intracardiac Surgery Using the Helix-reservoir Bubble Oxygenator withTotal Cardio-pulmonary By-pass, S. Afr. med. J., 33, 789.and SCHRIRE, V. (I961): The Surgical Correction of Endocardial Cushion Defects, Surgery, 49, 500.McKENzIE, M. B., and SCHRIRE, V. (196I): A Surgical Approach to Mitral Insufficiency, Brit. J. Surg., 48, 655.

BECK, W., SCHRIRE, V., VOGELPOEL, L., NELLEN, M., and SWANEPOLL, A. (I96 i): Corrected Transposition of theGreat Vessels, Brit. Heart J., 23, 497.

BROCK, R. C. (1952): Surgical and Pathological Anatomy of Mitral Valve, Ibid., I4, 489.CABOT, R. C. (1926): ' Facts on the Heart'. Philadelphia: J. B. Saunders.COOLEY, J. C., KIRKLIN, J. W., and HARSCHBARGER, H. G. (1957): The Surgical Treatment of Persistent Common

Atrioventricular Canal, Surgery, 41, 147.COOLEY, D. A., LATSON, J. R., and KEATS, A. S. (1958): Surgical Considerations in Repair of Ventricular and Atrial

Septal Defects Utilizing Cardio-pulmonary By-pass: Experience with 104 Cases, Ibid., 43, 2I4.DEWALL, R. A., WARDEN, H. E., LILLEHEI, C. W., and VARCO, R. L. (I956): Prothesis for Palliation of Mitral Insuffi-

ciency, Dis. Chest, 30, 133.EDWARDS, J. E. (I960): The Problem of Mitral Insufficiency Caused by Accessory Chordm Tendineae in Persistent

Common Atrioventricular Canal, Proc. Mayo Clin., 35, 299.GLENN, W. W. L., GENTSCH, T. O., HUME, M., GUILFOIL, P. H. (I956): Surgical Treatment of Mitral Insufficiency

with Particular Reference to Application of Vertically Suspended Graft, Surgery, 40, 59.GLOVER, R. P., HENDERSON, A. R., MARTUTTI, R., and GREGORY, J. (I952): Surg. Forum, 178,GOTT, V. L., DEWALL, R. A., GONZALEZ, J. L., HODGES, P. C., VARCo, R. L., and LILLEHEI, C. W. (1957): The Direct

Vision Surgical Correction of Pure Mitral Insufficiency by Use of Annuloplasty or a Valvular Prosthesis, Univ.Minn. med. Bull., 29, 3, 69.

HARKEN, D. E., BLOCK, H., ELLIS, L. B., and DEXTER, L. (1954): The Surgical Correction of Mitral Insufficiency,J. thorac. Surg., 28, 604.

HENDERSON, A. R., and LAW, C. L. (1953): Surgical Treatment of Mitral Insufficiency: Experimental Use of Trans-planted Pericardium in Dogs, Surgery, 33, 858.

JOHNS, T. N. P., and BLALOCK, A. (I954): Mitral Insufficiency: Experimental Use of Mobile Polyvinyl SpongeProsthesis, Ann. Surg., 140, 335.

KAY, E. B., and CROSS, F. (1955): Surgical Treatment of Mitral Insufficiency, Surgery, 37, 697.I NOGEUIRA, C., and ZIMMERMAN, H. A. (1958): Direct Vision Correction of Mitral Insufficiency, Ibid., 44, 325.

LEvoWITZ, B. S., LOVETTE, J. B., LEONE, M., RATAN, R. S., MAGOVERN, G. J., and KENT, E. M. (I960): Total ProstheticReplacement of the Mitral Valve: An Experimental Study (Abstracts of the 33rd Scientific Sessions of theAmerican Heart Association), Circulation, 22, 779.

LEWIS, SIR THOMAS (1933): 'Diseases of the Chest'. London: Macmillan.LILLEHEI, C. W., GOTT, V. L., DEWALL, R. A., and VARCO, R. L. (1957): Surgical Correction of Pure Mitral Insuffi-

ciency by Annuloplasty Under Direct Vision, J.-Lancet, 77, 466.(I958): The Surgical Treatment of Stenotic or Regurgital Lesions of the Mitral and Aortic

Valves by Direct Vision Utilising a Pump-oxygenator, J. thorac. Surg., 35, 154.MCKENZIE, SIR JAMES (I9I6): 'Principles of Diagnosis and Treatment of Heart Affections'. London: Oxford

Medical Publications.MCGOON, D. C., DUSHANE, J. W., and KIRKLIN, J. W. (1959): The Surgical Treatment of Endocardial Cushion

Defects, Surgery, 46, i85.MOORE, T. C., and SHUMACKER, H. B. (1953): Unsuitability of Transventricular Autogenous Slings for Diminishing

Valvular Insufficiency, Ibid., 33, 173.NICHOLS, H. T. (1957): Mitral Insufficiency: Treatment by Polar Cross-fusion of the Mitral Annulus Fibrosis,

J3. thorac. Surg., 33, I02.NIXON, P. G. F., WOOLER, G. H., and RADIGAN, L. R. (I960): The Opening Snap in Mitral Incompetence, Brit. Heart

J., 22, 395.SAKAKIBARA, S. (1955): Surgical Approach to Correction of Mitral Insufficiency, Ann. Surg., 142, 196.SCHRIRE, V. (1958): The Racial Incidence of Heart Disease at Groote Schuur Hospital, Cape Town: II, Hypertension

and Valvular Disease of the Heart, Amer. Heart J., 56, 742.SELLORS, T. H., and SOMERVILLE, W. (I96I): The Persistent Ostium Primum Atrial Septal Defect, Postgrad. med. J.,

37, 646.STARKEY, G. W. B. (1959): Surgical Experiences in the Treatment of Congenital Mitral Stenosis and Mitral Insuffi-

ciency, J. thorac. Surg., 38, 336.STEELL, G. (I906): ' Textbook on Diseases of the Heart'. Manchester University Press.TALNER, N. S., STERN, A. M., and SLOAN, H. E. (I96I): Congenital Mitral Insufficiency, Circulation, 23, 339.VAN DER SPUY, J. C. (1958): The Functional and Clinical Anatomy of the Mitral Valve, Brit. Heart J7., 20, 471.WOOD, P. (I954a): Appreciation of Mitral Stenosis: Clinical Features, Brit. med. .i, 0O51.*-954b): Appreciation of Mitral Stenosis:- Investigations -and Results, Ibid.i, I3.

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surgery of mitral incompetence · diastolic thrill and there is a lift over the right ventricle....

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