THE SURGICAL AND PATHOLOGICAL ANATOMY OF THE
`MITRAL VALVE
`
`BY
`R. C. BROCK
`
`From the Thoracic Unit, Guy's Hospital
`
`Received July 14, 1952
`
`The great practical importance that mitral valve disease has now assumed in surgery demands a
`consideration of the anatomy and function of the normal valve and the pathological anatomy of the
`Observation on many normal and diseased specimens and direct study of the valve
`diseased valve.
`at some 150 operations has made it clear to me that much that is now taught is quite unacceptable.
`The revision and extension of existing knowledge has often been seen in the development of the
`surgery of all parts of the body; relatively recently we have seen the great expansion of pulmonary
`surgery and the corresponding intensive study of pulmonary anatomy and pathology.
`In considering valvotomy for the relief of mitral stenosis we are too inclined to concentrate our
`attention on the valve cusps, forgetting that they are but one part of the valve mechanism. Although
`the complex nature of the valve mechanism is well known it seems to be largely ignored in dealing
`with the diseased valve, which is often approached as merely a fibrous, obstructing diaphragm with
`a small hole that must be made larger. The popular conception of the valve in mitral insufficiency
`seems to have no logical or scientific basis and is wholly unsatisfactory.
`The valve mechanism extends over a distance of some 5 cm., and a lesion may affect all parts of
`it or one part more severely than another. A lesion at any level can seriously interfere with the
`mechanism, and it is not always the actual valve cusps that are most seriously affected.
`
`THE NORMAL MITRAL VALVE
`The normal mitral valve consists of the atrio-ventricular fibrous ring to which the cusps gain
`their attachment, of the two cusps, and of the papillary muscles with their chorde tendinee.
`The
`two cusps are anteromedial and posterolateral, being so arranged
`that the axis of the valve orifice is directed obliquely forwards from
`right to left (Fig. 1, 18, and 22).
`The anteromedial or aortic cusp is much the larger and the more
`important in that during ventricular systole it receives a great part of
`the stream of emergent blood which it prevents being driven back
`into the left atrium and helps to direct into the aortic outlet.
`The posterolateral cusp fulfills a secondary and supporting part
`in the closing of the mitral orifice in ventricular systole.
`Thepapillary muscles are typically two in number and lie opposite
`the intervals between the valve cusps; they arise from the ventricular
`wall at about the junction of the apical and middle thirds, one being
`anterolateral and one posteromedial.
`Both muscles are situated
`in the lower inflow portion of the left ventricle; the anterolateral
`one arising from the concavity of the anterolateral wall of the
`489
`
`FGarr1ngemDiaaofthe mitral
`cusps.
`
`7_
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 1 of 25
`
`

`

`R. C. BROCK
`AO0
`ventricle and the posteromedial from the junction of the septal and posterior surfaces.
`Each
`muscle may be a single papilla or may be split to a greater or lesser degree so that it is either
`Rusted et al.
`notched at its apex, deeply grooved along its sides, or bifid.
`Extra muscles may exist.
`(1951) have recently analysed the arrangement of the paillary muscles in 250 hearts.
`
`1N,_ *
`
`FIG. 2.-Diagram of the arrangement of the papillary muscles and chorde
`tendinee. Each muscle and its tendons controls the corresponding half of
`the opposing cusps.
`The chorda? tendinee pass from each papillary muscle to gain attachment to both valve cusps in
`such a way that the anterolateral muscle and its tendons control the anterolateral half of the valve,
`and the posterolateral muscle and its tendons control the corresponding posterolateral half.(Fig.
`2, 3, and 5). The chorde tendineae are of three orders, according to Quain (1929).
`(1) Those which are inserted on the free edge of the cusps. They are numerous delicate threads
`which arise from the other cords near the cusp margin, and often form a fine network before they are
`attached to it.
`(2) Those which are inserted at intervals on the ventricular surface of the cusp near its free edge,
`which they pass over to the attached border.
`They are distinctly thicker than the chordce of
`group 1, and those attached to any one cusp
`are derived from two different papillary muscles
`or from one papillary muscle and the wall of
`the ventricle.
`(3) The short, broad fibres that stretch
`across the perivalvular groove from the ven-
`tricular wall to the under surface of the cusp
`near its base and run along the cusp a short
`CRIXa_wvdistance towards its free margin.
`The Critical Areas of Tendon Insertion
`Although the arrangement of the chorde
`tendinew can be correctly described in this
`fashion, the total- picture presented is too
`complex-too complete-for practical pur-
`It needs simplification.
`poses.
`Study of the
`arrangement has impressed me with the essential
`importance of the direct or primary attach-
`ment of the tendons.
`The primary attachments are two on each
`
`Reproduced from an article in
`FIG. 3.-The mitral valve.
`the Guy's Hospital Reports, by T. Wilkinson King, 1840.
`
`,
`
`,
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 2 of 25
`
`

`

`491
`SURGICAL AND PATHOLOGICAL ANATOMY OF THE MITRAL VALVE
`cusp, being situated about 2 cm. apart; these I have termed the critical areas of tendon insertion,
`for reasons which will become apparent later.
`These areas are depicted in Fig. 4 and 5 and are seen to be formed by those tendons that arise
`from the very summit of the papillary muscles and gain the most direct attachment to the valve
`These tendons are often slightly thicker and stronger, and clearly must exercise the most
`cusps.
`powerful selective action on the cusps since they are in the line of the direct pull of the papillary
`muscles. The more obliquely placed tendons which gain insertion on each side are of a secondary
`supporting nature.
`The disposition or shape of the cusps is such that there exists, fundamentally, a distal or central
`The critical areas of tendon in-
`horizontal portion and two lateral or receding oblique portions.
`
`FIG. 4.-Diagram to show the probable mode of closure of the mitral cusps.
`The thicker chordee tendineae are those in the direct line of pull from the
`papillary muscle to the cusps. The small inset indicates the critical areas of
`tendon insertion thus formed; in these areas the cusps are held most
`tightly together.
`
`FIG. 5.-Photograph of bullock's heart opened to show the mitral cusps. The arrangement of the tendons from
`each papillary muscle controlling half of each cusp is well shown. The large, prominent cusp is the anteromedial
`or aortic, and the critical areas of tendon insertion should be noted with the central blood pathway between.
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 3 of 25
`
`

`

`R. C. BROCK
`492
`sertion are at the junction of the horizontal part and the lateral receding parts of the valve cusps.
`Most of the oblique or secondary tendons are inserted in relation to the lateral parts of the cusps;
`This
`fewer pass medially to what may be termed the central pathway of the valve (Fig. 3 and 5).
`It is true that the shape of the free edge of
`is especially so in the case of the anteromedial cusp.
`the cusps may be described as semicircular or semi-ovoid, but the above suggested resolution into
`a somewhat arbitrary transverse or horizontal distal central portion and the two lateral receding
`portions is of great practical importance and, I think, aids clarity of understanding.
`
`THE CLOSURE OF THE NORMAL MITRAL VALVE
`Although the mode of closure of the mitral valve may appear to be fairly obvious and simple,
`it is a good policy to take nothing for granted but to re-examine the existing conceptions from time
`Actually, there is room for considerable difference of opinion in the exact mode of closure
`to time.
`of the valve.
`It is almost certain that the two cusps come together along their opposing surfaces, being driven
`into this position by the rise in pressure during ventricular systole (Fig. 4). The anterior cusp is
`15-18 mm. long at its middle part and the posterior cusp is 10-12 mm. The extent of their probable
`contact can be judged from the observation (Quain, 1929) that the area of the atrioventricular
`orifice is 855 sq. mm. in a man and the surface area of the two cusps is 1868 sq. mm. The pro-
`portion of valve area to orifice area, therefore, appears to be from 1: 1 5 to 1: 2-2. The overlap
`may, in fact, be more than this, because when the ventricle contracts the A-V ring is reduced in
`circumference and the area of the orifice is correspondingly reduced.
`On the other hand Quain does not state the conditions under which these measurements were
`obtained, although presumably in the cadaver, and we must make allowance for much variation
`in the degree of contraction and dilatation of the heart and mitral orifice that may be present,
`Nature is always prodigal in
`whether caused by disease or by rigor mortis affecting the heart muscle.
`her reserve and it may well be that the overlap described above pertains to quiet resting conditions
`of the healthy heart, but is greatly lessened during exercise or illness, especially when the heart
`muscle is affected by the disease.
`A possible alternative mechanism of closure is that the orifice is closed entirely by the anteromedial or
`aortic cusp forcing the much smaller posterolateral cusp against the posterior wall of the ventricle (Fig. 6).
`It is doubtful if this is the usual mechanism, but it may well happen
`sometimes; it is unlikely to occur, if the A-V ring is at all dilated.
`In systole the inflow portion of the left ventricle is tightly contracted
`so that its cavity is almost completely obliterated, but sufficient
`space remains postero-inferiorly for the hydrostatic pressure to reach
`the ventricular aspect of the posterolateral cusp and force it away
`from the wall of the ventricle. The greater part is in contact with
`the opposing surface of the aortic cusp and its " free " area must
`be small. When the finger is introduced into the left atrium during
`an operation for mitral stenosis, the anteromedial cusp is usually
`very easily felt billowing upwards into the atrium like a sail filled
`with the wind; it is much more difficult to feel the posterolateral
`cusp, and, indeed, its presence has often rather to be assumed by
`judging the distance that lies between the actual mitral orifice
`and the posterior part of the A-V ring.
`Lutembacher (1950) describes the mechanism of closure as a
`bunching up in which the valve cusps, the chordce tendinee, and the
`papillary muscles come together in such a way that the closure of
`the orifice is aided and secured by an actual interlocking or inter-
`opposing of these structures, and he describes and depicts specimens
`in such a way as to indicate that the partly cockled-up mitral orifice
`in mitral stenosis actually occupies grooves on the papillary muscles.
`
`FIG. 6.-Diagram to show a possible
`alternative mode of closure of the
`mitral valve in which the postero-
`wall of thepventricle by the antero-
`medial cusp.
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 4 of 25
`
`

`

`SURGICAL AND PATHOLOGICAL ANATOMY OF THE MITRAL VALVE
`493
`This is a conception reached by inspection of the dead contracted heart; from what the finger feels when
`I have felt the mitral valve functioning on some 150
`inside the contracting heart it cannot be a true one.
`occasions and the aortic cusp at least has always been forced or billowed towards the atrium; it has never
`been gripped or bunched up within the orifice.
`Although it is difficult to feel the posterolateral cusp billowing out, it would be strange if it
`did not do so in conformity with the aortic cusp, for the very presence of the musculo-tendinous
`mechanism indicates that this is the action of the cusp in systole.
`It cannot fail to be forced upwards
`and backwards in this manner unless it is entirely protected from the high ventricular systolic
`pressure by complete apposition with the posterior wall of the ventricle.
`There ig little doubt that the aortic cusp is the main factor in effective closure of the orifice and
`the posteromedial cusp occupies a subsidiary or adjuvant function in sealing a narrow and probably
`variable posterior crescent of the orifice. The variability of its apposition with its fellow cusp
`in varying degrees of cardiac activity or dilatation has already been mentioned.
`According to Quain the distance between the apex and the base of the left ventricle does not
`shorten during contraction of the ventricle; the atrioventricular region moves upwards and back-
`wards, but the length of the cavity remains constant.
`This makes it easier to understand how the
`comparatively small contraction of the papillary muscles is able to ensure efficient closure of the
`Actually, all that is needed is quite a small tensing of the chorde tendinew to prevent the
`valve.
`cusps being blown open into the atrium. The apposition of the cusp surfaces ensures their water-
`tight closing, but the pressure-resisting mechanism comes from the musculo-tendinous support
`and its neuromuscular co-ordination with ventricular systole.
`The mode of insertion of the
`tendons from one papillary muscle to each of the opposing cusps increases the efficiency of' the
`mechanical closure of the valve.
`The important, indeed fundamental, part played by the papillary muscle mechanism was
`dramatically, albeit tragically, emphasized for me in one unfortunate operative experience (Brock,
`After dividing the stenosed orifice in a case of mitral stenosis I tried to reach the aortic
`1950).
`I had just reached the
`valve. by passing the index finger around the aortic cusp of the mitral valve.
`valve with the finger-tip when something gave way and immediately severe mitral regurgitation
`occurred; a powerful regurgitant stream of blood could be felt entering the atrium, the walls of
`which could be seen to distend freely with each ventricular systole.
`Clearly the high ventricular
`pressure was being transmitted directly to the left atrium.
`I thought that the aortic cusp had been
`torn transversely across its substance. The patient, unable to tolerate this severe acute mitral
`incompetence, died some 48 hours later and autopsy revealed that the anterolateral papillary
`muscle had been torn from its ventricular attachment; the simple mechanical apposition of the
`two cusps had not been enough to prevent the severe and fatal regurgitation.
`During ventricular diastole the papillary muscles and the tendons are lax and the cusps float
`During ventricular systole the valve cusps are
`open before the stream of blood from the atrium.
`flung tight together and the papillary muscles and tendons become taut and straight; the maxi-
`mum, the most powerfully supported, closure must occur in relation to the critical areas of tendon
`insertion already described. At the height of systole the tendons passing from the summit of each
`papillary muscle direct to these two critical areas on the valve cusps must be tense and parallel
`and very close to one another (Fig. 4); in contrast with during diastole when they are lax and directed
`outwards towards the wide open margins of the orifice.
`At these two critical areas the cusps must
`be held together very tightly indeed; the significance of this will become apparent when we consider
`Sokoloff et al. (1950), as a result of a study and survey of the chorde
`the state of the diseased valve.
`tendinew in 200 hearts of all ages, have shown that the more centrally placed chordc of the anterior
`cusp are thickened and more powerful in every heart and this can be noted at all ages and in animals
`(bovine) when rheumatic infection can be excluded.
`The changes are less marked in the chordx
`of the posterior cusp, as would be expected.
`I have always been intrigued by the difference in size between the A-V
`The size of the mitral orifice.
`orifice and that of the aorta or pulmonary artery. The explanation that first suggests itself is that this is related
`2L
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 5 of 25
`
`

`

`R. C. BROCK
`494
`This may be so except that nature could just as easily have made the
`to the lower pressure in the atrium.
`atria slightly more powerful without interfering with any venous reservoir or volume-regulating function
`After all the blood has only to be expelled into the lax ventricular cavity during the long
`they may possess.
`diastolic filling period; the atria do not have to maintain a systemic or even a pulmonary blood pressure
`such as the ventricles must do.
`I do not believe that the real difference in size between the atrial and the aortic orifices is anything like so
`great as appears. The explanation is that only a part of the A-V channel functions as a true pathway for the
`blood; this soon becomes apparent when the mechanism of the normal mitral valve is considered more closely.
`Quain gives the size of the aortic and the mitral orifices in mm. as follows:
`Aortic orifice:
`26 mm. in diameter, 530 sq. mm. in area
`Mitral orifice:
`32 mm. in diameter, 855 sq. mm. in area
`We are thus faced with an apparent difference in size which is indicated by the diagram shown in Fig. 7.
`The mitral orifice has not been depicted as a circle in spite of the figures given above, for in fact it is usually
`not circular during life.
`If, instead of simply superimposing the two " orifices " in this way, we consider them in the form shown
`in Fig. 8, we obtain a different conception which is best explained by developing the diagram further to pre-
`That is, a distal horizontal or central portion
`sent the basic structure of the mitral valve already mentioned.
`and two receding lateral portions; at the junctions of the central and lateral portions are the critical areas of
`tendon insertion (Fig. 8 B).
`
`A
`B
`FIG. 8.-Diagram to illustrate the suggested mode of con-
`struction of the mitral pathway.
`
`FIG. 7.-Diagram to contrast
`the relative size of the
`aortic
`mitral
`and
`the
`orifices.
`We may now return to a diagrammatic representation of the mitral orifice from above (Fig. 9) with
`Although the orifice may be thought to open as a simple oval,
`the valve in the open and in the closed state.
`it will be seen that this is, in fact, not so. The part of the valve orifice that matters is what I would term
`the central channel and it is formed by the opening of the distal, horizontal, central portions of the cusps.
`The receding lateral portions serve merely as hinges, allowing the central portions to open and close.
`In-
`deed, the two " lateral " parts of the valve channel on each side 'of the central channel are largely filled
`in, when open, by the numerous chordie tendineze radiating, fan-wise, upwards and outwards from the
`papillary muscles (Fig. 3). The tendons passing to the borders of the central channel are fewer and are
`disposed so as not to interfere with the blood pathway.
`It will thus be seen that the effective orifice of the mitral valve is much smaller than would at first appear,
`and is much more closely related to that of the aortic orifice. The apparent difference in size is due entirely
`to the essentially different mechanisms in the opening and closing of the aortic valve and the mitral valve.
`McMillan et al. (1952) have recently demonstrated that the functional aortic outlet at the valve level is
`triangular and not actually circular.
`
`THE DISEASED MITRAL VALVE
`It is usually taught that in the milder forms of rheumatic infection the edges of the mitral cusps
`become thickened and distorted and some incompetence results; and that with a more severe
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 6 of 25
`
`

`

`495
`
`SURGICAL AND PATHOLOGICAL ANATOMY OF THE MITRAL VALVE
`infection the valve cusps adhere, the orifice becomes contracted, and
`Examples are depicted in text-books of valves, said
`stenosis follows.
`to be incompetent, in this lesser state of thickened, distorted edges.
`In this way many students gain the impression that mitral incompetence
`results from a mild rheumatic valvitis, and stenosis from a more severe
`This is an erroneous simplification; a high degree of mitral
`attack.
`stenosis can be caused by a relatively mild attack of rheumatic valvitis;
`in contrast, true mitral incompetence is usually caused by the most
`severe grades of damage to the valve. The condition of the thickened.
`deformed edges with no fusion of the cusps is, almost certainly, of little
`or no functional significance.
`Study of diseased mitral valves teaches that considerable varieties
`Although a clinical state of " mitral
`and degrees of valvitis occur.
`stenosis " may be present, the actual condition of the valve mechanism
`varies greatly from case to case and with corresponding differences in
`The valve orifice may
`the degree of benefit that can follow operation.
`be equally small in two cases, but in one the valve cusps may be thin
`and almost normal and a successful valvotomy will restore an almost
`normal valve; in the other the whole valve structure may be so altered,
`so rigid and fibrous, that no more than a partial restoration of function
`is possible.
`It is necessary to draw attention to the loose use of the terms mild
`or severe mitral stenosis. The picture often conveyed, and intended,
`by such expressions is that the actual degree of contracture of the orifice
`This is not in accordance with
`may be slight, moderate, or severe.
`operative experience; the mitral orifice in stenosis is almost always a
`experience;
`operative
`small oval about 1 cm. x 05 cm.; in a small percentage of cases it may
`be very much smaller and is then usually circular, as little as 04 cm.
`in diameter.
`It is, however, not possible to explore case after case and observe
`the almost standard small orifice, 1 cm. x O.5 cm., without being
`The same small orifice is
`impressed by its occurrence and significance.
`It is
`found in cases with mild symptoms or with severe symptoms.
`not the mitral stenosis that is mild or severe; it is the resulting
`The' anatomical variation in the size of the hole is slight; the clinical variation of
`disability.
`It would seem that a certain minimal size of valve orifice must be reached
`symptoms is considerable.
`before clinical disability is likely.
`First, just because a patient has early
`This has an important practical bearing for two reasons.
`symptoms of mitral stenosis it is not to be assumed the orifice is only mildly contracted; at operation
`it will be found little or no different from that found in a severe case. The patient with mild symp-
`toms can expect to receive just as much mechanical relief by valvotomy as one with severe symptoms.
`Second, the anatomical occurrence of this virtually " standard " type of orifice in mitral stenosis
`demands an explanation based on sound pathological anatomy.
`
`FIG. 9.-Diagram to show the
`mode of action of the mitral
`cusps. The true functional
`central
`pathway
`is
`the
`portion; the lateral portions
`serve as hinges allowing the
`~~~~~~~~~~~~~close.
`central part to open and
`thickened
`The
`chordie tendinem indicate
`thecriticalareasof insertion;
`lateral to these the pathway
`is closed by the lattice work
`of the supporting oblique
`Note the effective
`tendons.
`central pathway is much
`closer in size to that of the
`aortic pathway; cf. Fig. 7.
`
`THE MECHANISM OF PRODUCTION OF MITRAL STENOSIS
`Rheumatic inflammation occurs firstly and chiefly along the margins of the valve cusps; if the
`cusps remain separate and only the margins are affected, the final result is merely some permanent
`thickening and mild distortion of the edges of the cusps, a condition of no functional importance.
`The significant-event in the-production -of mitral stenosis is the;fusion of the valve cusps and this
`It must be
`occurs, fundamentally, at the two opposing critical areas of tendon insertion (Fig. IOA).
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 7 of 25
`
`

`

`R. C. BROCK
`496
`emphasized that in an appreciation of this simple fact lies the correct understanding of the pro-
`duction, the anatomy, and the technical operative treatment, of mitral stenosis.
`It is in these areas that the inflamed cusps are held most tightly together in systole; once cross
`adhesion has occurred, important, secondary changes follow, for the hinge-like action of the lateral
`In other words, the opening of the central pathway in
`parts of the valve cusps is at once lost.
`diastole is prevented; the valve cusps cannot move apart, held as they are by the cross fusion at these
`critical sites. The central pathway-functional lumen of the valve-must inevitably remain partly
`open if life is to continue, but its size is inevitably no more than a shallow oval formed between the
`two areas of adherence at the critical points (Fig. lOB).
`To the outer side of each critical area, i.e. on each side of the central pathway, the valve lumen
`is now functionless, it does not form part of the main blood channel from atrium to ventricle, and
`
`X XS.^r
`A
`B
`FIG. 10-Diagram to show suggested mode of adherence and fusion of the cusps and
`consequent production of mitral stenosis.
`In A the inflamed cusps adhere first of all
`at the critical areas.
`In B complete cross fusion of the critical areas has occurred,
`and also secondary adherence of the commissures.
`
`as already pointed out, it really exists only to allow complete opening of the central part of the valve
`lumen or pathway in diastole.
`Once the two lateral components are prevented from opening in
`this way by the cross fusion of the critical areas of tendon insertion it is inevitable that they should
`completely fuse together since there is no powerful direct stream of blood to keep them apart.
`In this way the two " commissures " are formed; i.e. the cusp margins are fused from the atrial ring
`up to and including the two critical areas of tendon insertion (Fig. lOB).
`The commonly accepted notion that stenosis arises from progressive fusion of the cusps, begin-
`ning at the periphery and extending inwards, is quite erroneous.
`Cases of mitral stenosis with
`partial lateral adherence of the cusps with non-adherence of the " critical " areas just do not occur.
`It is true that the orifice may be eccentrically placed and one commissure may be much shorter
`than the other or both may be very short, but this is due to variation in the focal incidence of the
`infection which may produce a more severe degree ofinflammation in one place and therefore greater
`local contracture.
`Once cross adhesion of the critical areas and secondary adhesion of the commissures has
`occurred, a state of mitral stenosis inevitably results. The degree of stenosis must clearly depend
`on the size of the oval aperture that is subtended between the fused critical areas.
`In the
`earlier stages, or in cases in which the valvitis is mild, this central lumen may be rather
`larger than in other circumstances, but is neVer likely to be more than about 1-5 cm. x 075 cm.
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 8 of 25
`
`

`

`497
`SURGICAL AND PATHOLOGICAL ANATOMY OF THE MITRAL VALVE
`If the valvitis is severe, recurrent, or chronically smouldering, this central lumen is likely
`to become rapidly much smaller and with correspondingly more rigid margins. Symptoms may
`then occur early.
`If the valvitis ceases quickly and the patient is left with a small functional oval lumen some 1 cm.-
`1-5 cm. in length and with fairly supple margins, although stenosis is present, symptoms may be
`With a healthy muscle there is little doubt that considerable stenosis of the
`completely absent.
`central pathway of the mitral valve can be readily compensated for. Symptoms could appear if
`the muscle begins to weaken, but the more likely cause is a steady diminution in the size of the
`This seems to be the
`valve lumen until it reaches what might be termed the minimal effective area.
`small oval aperture most commonly seen, some 1 cm. x 0'5 cm.; if the lumen becomes smaller than
`this graver symptoms can only be forestalled by -a correspondingly greater increase in the power
`of the atrial muscle and the increased risk of its failure.
`The steady diminution in size of the central lumen towards the minimal effective area, if not
`caused by actual rheumatic infection, is inevitable from the daily wear and tear of the blood stream
`passing through the narrowed orifice, especially as the wear and tear or friction is steadily increased
`by the stronger flow of blood brought about by the more powerful contractions of the partly ob-
`By the deposition of platelets and fibrin the edges become thicker, more fibrous
`structed left atrium.
`and therefore more contracted and rigid and the orifice correspondingly smaller; verrucose pro-
`This progressive
`jections and even calcified plaques and masses add further to the obstruction.
`and relentless shrinkage of the functional central lumen over the course of the years is one main
`reason why the appearance of symptoms in mitral stenosis is closely related to increasing age
`Clearly the condition of the atrial muscle is also
`and is commnonest between 30 and 40 years.
`important in this connexion.
`Just as the edges of the valve opening are exposed to the wear and tear of the blood stream, so
`are the chorde tendinee in the direct line of pull from the papillary muscles, as these inevitably
`form part of the banks confining and directing the stream of blood issuing from the stenosed orifice.
`It would therefore be expected that these chordw should show extra evidence of thickening all along
`This is indeed so and Sokoloff et al. (1950) have drawn attention to the occurrence
`their length.
`of sclerotic changes in these central chorde tendineae, especially of the anterior cusp, in the heart
`of middle-aged subjects who were not rheumatic; the sclerosis is due to deposition of subendocardial
`collagen and affects the whole length of the chordc and more particularly the central ones which
`Magarey (1951) has also written
`are more exposed to the mechanical action of the blood stream.
`of this.
`
`MITRAL STENOSIS WITH MINIMAL VALVITIS
`The basic mechanism of valve fusion, beginning with cross adherence of the critical areas and
`extending by more gradual secondary narrowing of the central pathway, is seen most clearly in cases
`The
`in which the rheumatic infection has been confined almost entirely to the valve margins.
`patient's symptoms may be severe; the central orifice characteristically small, 1 cm. x 0 5 cm. or
`The condition of the
`even less, its edges firm and fibrous; in other words the stenosis is severe.
`valve cusps themselves, however, shows that the original rheumatic infection was not severe; or
`Although the edges of the
`at least did not affect the whole valve cusps but chiefly the margins.
`central orifice may be firm or even dense, the fusion of the critical areas is not densely fibrous, the
`commissures are often very lightly fused, and the actual valve cusps are thin, supple, and almost
`normal. Moreover, the chorde tendinee are thin and separate and once the two cusps have been
`separated (by splitting or cutting) as far as the A-V ring on each side, an almost normal valve
`mechanism is restored.
`It is noteworthy that a patient can have such a severe disability, eventually fatal, from a simple
`cross fusion of the cusps following what must have been a mild form of valvitis and that this great
`disability can be quickly relieved by a short and simple operation.
`
`Colibri Heart Valve LLC, Exhibit 2030, Page 9 of 25
`
`

`

`498
`
`R. C. BROCK
`
`MITRAL STENOSIS WITH SEVERE VALVITIS
`In the more severe grades of rheumatic valvitis the process is no longer confined to the margins
`but spreads to involve the cusps, the chorde tendinew, the A-V ring and even the papillary muscles.
`The cusps become generally thickened and fibrous so that they constitute a rigid or semi-rigid
`fibrous diaphragm with a small rigid orifice.
`Calcification may also be added, either in the form of
`light surface deposit or thick plaques or exuberant craggy masses.
`The chorde tendineee become thickened, matted together, and shortened; in extreme cases the
`fibrous reaction extends down to involve the papillary muscles, and the chorde may then be so shor-
`tened that the papillary muscles are almost directly fused with the valve cusps themselves, only a
`short thick fibrous mass intervening (Fig. 11, 12, and 13). The papillary muscle and tendons
`Occasionally calcification extends from the valve cusps
`may even adhere to the wall of the ventricle.
`and the orifice, down the chorde tendinee as far as the papillary muscles, so that a narrow calcified
`channel is formed. The fibrosis may also involve the A-V ring, which becomes smaller and rigid,
`and in some cases actually calcified.
`These facts are, of course, common knowledge, but it is necessary to consider more critically
`the precise effect on the chorde tendineae. The most important c